1
Herpesvirus kills cancercells in malignant melanomas
In 'The Lancet'
researchers from the university of Glasgow published the effect of a 'herpes simplex',
(a virus which causes 'feverlips), in malignant melanomas. Five patients got
directly injected the herpesvirus in their malignant melanoma. With all
patients the herpesvirus had killed the malignant cells and didn't infected or
destroyed at all the surrounding 'healthy cells". The strongest effect was
found with the patient who got four injections with the virus.
Oncologist Prof. Rona MacKie MD thinks the results are hopefull and promising
for the future, as she writes in The Independent. Though she said that it is
too early for definite conclusions and a lot of research and work will be done
before other and more patients will profit from this treatment and will last
al least several years before this treatment will be used in general.
2.
Additional chemo and radiation does not have any positif effect on
surviving non-small lungcancer
With thanks to Ralph Moss for next information.
Additional chemo with radiation of non-small-cell lung cancer does have any positif effect on surviving of healingproces. So are the conclusions of scientific researchers of the Eastern Cooperative Oncologygroup based on a large randomised research project with 242 patients. The results of this study are published in The New England Journal of Medicine at 26th of october 2000.
242 patients received beside radiation extra chemotherapy. Also a controlgroup of 242 patients got just radiation. In the group with extra chemotherapy (cisplatin and etoposide) the average surviving rate was 38 months. In the group with just radiation 39 months.
De official conclusion : compared with radiotherapy alone, adjuvant radiotherapy and chemotherapy with cisplatin and etoposide does not prolong survival in patients with completely resected stage II or IIIa non-small-cell lung cancer (N Engl Med 2000;343:1217-22)
The two oncologists, Desmond N. Carney, MD en Heine Hansen, MD, who did the research give the advice that additional chemotherapy with patients with totally removed tumors should not be a standard protocol. (treatment).
An other, also randomised researchproject, shows that postoperative radiation should be a contra-indication for such patients. That are the conclusions from a large scientifical trial with 2.128 patients published in The Lancet in 1998 (Lancet 1998;352:257-63).
2.128 patients received after a surgery radiation therapy. In a controlegroup also 2.128 patients received just an operation and no radiation therapy. Afterwards the researchers concluded that patiënts with radiation therapy got a higher risc to die (21%). The worst reacted patients with longcancer with an an early stage (stage I and II)
The official conclusion published in The Lancet: "Postoperative radiotherapy is detrimental to patients with early-stage completely resected NSCLC (Non-small-cell lung cancer) and should not be used routinely for such patients. ((Lancet 1998;352:257-63).
3.
Lightsigarets cause lungcancer which is more difficult to treat
Lightsigarets cause lungcancer which is more difficult to treat than 'normal' lungcancer. This conclusion is made by Dutch researchers and oncologists in a study published in the American magazine Epidemiology. Smoking light sigarets is as bad as smoking normal sigarets.
Lungspecialist dr. N. Zandwijk of the Anthonie van Leeuwen Hospïtal writes in a Dutch newspaper that people who smoke lightsigarets, which content less tar and nicotine, do inhale deeper. The need for nicotine is the base of addiction, so the need for smoking is the need for more nicotine. Through deeper inhaling the tar parts which cause cancer come deeper in the lungs and develop an adenocarcinoma. In the Netherlands 20% of the people with cancer suffer from an adenocarcinoma. A kind of cancer which is very bad to treat.. Twenty years ago 'just' 10% of all cancerpatients suffered from an adenocarcinoma. An adenocarcinoma is discovered always very late and is a big disadvantage in a succesfull treatment Dr. Zandwijk says. Another reason why nowadays more people suffer from lungcancer is because people smoke more lightsigarets than twenty years ago. Today people smoke 23/24 sigarets a day (after the introdcution of the lightsigaret) and twenty years ago people smoked 15/16 sigarets a day. Statistics show, also in the U.S.A., that after the introduction of the lightsigaret 42% of all smokers switched from 'normal' sigarets to lightsigarets with the reason it might be better for your health. Now shows this Dutch research that the effect of smoking lightsigarets in stead of 'normal' sigarets is either worse than better for your health.
4.
GTI-2501, a virus, offers hope for new cancertreatment
Embargoed until Tuesday, June 19, 2001, 4 p.m. ET
TORONTO, June 19 /CNW/ - New findings by Canadian scientists that a
common virus kills brain cancer cells growing in culture and mice are
"extremely exciting and encouraging," the Canadian Cancer Society said today. The research is funded in part by the Society.
The scientists showed that the virus - called reovirus -- was very potent in attacking human gliomas implanted into mice, as well as in specimens removed from patients. The results are published in the June 20 issue of the Journal of the National Cancer Institute.
Malignant gliomas are the most common type of brain tumour. Invasive and aggressive, they are hard to treat with current therapies.
"These findings offer the hope of an entirely new strategy for dealing with a very difficult cancer," says Maaike Asselbergs, Acting CEO of the Canadian Cancer Society, a funder of the research. "We hope this virus can achieve the same effects in clinical trials involving patients who are dealing with this type of cancer."
The scientists found that when live reovirus was injected into a
particular strain of mouse, malignant gliomas either vanished or shrank to a few remaining cells. The animals gained weight, seemed healthier and lived longer than mice treated with dead virus.
The scientists also injected reovirus into nine glioma specimens that had been surgically removed from patients. The virus infected and killed cancer cells in all the specimens.
"It's amazing that you can give something in a single injection, make an animal's tumour go away and return it to health," says Dr. Peter Forsyth, a medical oncologist and a senior author of the JNCI paper. Although the lab results are exciting, "it remains to be shown whether this approach works in patients," Dr. Forsyth says. He is hoping that clinical trials will be approved to study reovirus in glioma patients.
As a physician who sees glioma patients every day, Dr. Forsyth is excited by the possibility that the reovirus might help to change the outlook for these people. "Even with advances in surgery, radiation, chemotherapy and brain scans, people are still dying at the same rate from this disease as 20 years ago."
The reovirus "may be a potentially useful treatment for a broad range of cancers," says Dr. Patrick Lee, the paper's other senior author and the cancer biologist who first discovered the anti-cancer potential of the reovirus. To grow, the reovirus "hijacks" machinery used by cancer cells to divide and proliferate -- machinery common to most kinds of cancer cell.
The reovirus is a respiratory and gastrointestinal virus to which most people are exposed early in life. It causes mild upper respiratory tract infection and some diarrhea. The reovirus kills cancer cells but not normal cells.
Drs. Forsyth and Lee are both with the University of Calgary's Cancer Biology Research Group and the Tom Baker Cancer Centre.
In addition to the Canadian Cancer Society, other funders of the research include: the Alberta Cancer Board; Partners in Health; the Canadian Brain Tumor Foundation; and the Dr. Michael Longinotto Molecular Neuro-Oncology Fellowship Fund and Mr. Clark Smith.
The Canadian Cancer Society (CCS) is a national, community-based
organization of volunteers whose mission is the eradication of cancer and the enhancement of the quality of life of people living with cancer. The CCS is the largest charitable funder of cancer research in Canada. Excellent research is funded through a rigorous review process, managed by its research partner, the National Cancer Institute of Canada. Since 1938, the CCS has been transforming research knowledge into powerful information and programs - helping people to understand, prevent and reduce the risk of cancer.
For information about cancer, our services, or to donate call
1-888-939-3333 or visit www.cancer.ca.
/For further information: Margaret Polanyi, Manager, Communications and
Marketing (Research), Canadian Cancer Society/National Cancer Institute of Canada, (416) 934-5684; Judy Noordermeer, Senior Communications and Marketing Officer (Research), Canadian Cancer Society/National Cancer Institute of Canada,
(416) 934-5691/
Source CNW - Canada News Wire
Categories:
NWR/ON NWI/HEA MST/R/CA MST/I/HEA
More information about this you can find at:
5.
Cancervaccin very succesful with Non-Hodgkin
Cancer
Vaccine Pioneer At NYU To Review Personalized Cancer Vaccines,Pioneering
Biotherapies Are At Advanced Trials Stage
NEW YORK--(BUSINESS WIRE)--Jan. 25, 2001--Dr. Larry W. Kwak, M.D., Ph.D.,Senior
Investigator at the National Institutes of Health, will present
published findings related to work on personalized cancer vaccine
technologies, at 1 p.m. on Jan. 26, 2001, at The New York University Medical
Center (NYU). Specifically, Dr. Kwak will discuss pioneering advances in the
field of tumor-specific personalized cancer vaccines, to treat a variety of
lethal cancers.
As one example, on Sept. 27, 1999, the National Cancer Institute (NCI)
announced that, for the first time ever, results of a Phase II cancer vaccine
study demonstrated an anti-tumor effect in a small group of patients
vaccinated over a five-year period. NCI researchers reported that 18 of 20
patients vaccinated against this common blood-cell tumor remained in complete
remission an average of four years after vaccine therapy began. Prior to
vaccination, all of the patients in the Phase II study had minimal disease or
were in a chemotherapy-induced first remission.
As a result, NCI launched a large-scale, randomized, Phase III clinical trial
to test these experimental cancer vaccines, which are custom-made from
patients' own tumor cells when in complete remission after chemotherapy. The
side effects of the vaccine appear to be minor or non-existent. Its
production requires extremely unique technologies.
NYU is considering an opportunity to participate in, and play a pivotal role
in, this national Phase III trial. Currently, cancer vaccine trials are in
Phase III trials at five leading medical centers: Northwestern University
Medical School, University of Pennsylvania, Duke University, the Moffitt
Cancer Center at University of Southern Florida, and at the National Cancer
Institute in Bethesda, Maryland.
In the year 2001, an estimated 54,900 people are expected to be diagnosed with
non-Hodgkin's lymphoma. Biovest International is currently producing the
aforementioned cancer vaccines for the national Phase III trial.
6.
Extra radiation (boost) decreases chance/possibility of a relapse
of breastcancer
After 5 years 4,3 procent of the women with breastcancer who got a BOOST, got a relapse. 6,8% of the women who didn't get a BOOST, got a relapse. With young women under 40 the difference was even bigger. Without a BOOST, 20% got a relapse, with a BOOST, 'just' 10% got a relapse of breastcancer.
7.
Vitamin C produces gene-damaging compounds
Source: American Association For The Advancement Of Science (http://www.aaas.org)
and http://www.sciencedaily.com
Vitamin C Produces Gene-Damaging Compounds, Test-Tube Study In Science Reports
Vitamin C, known to be a DNA-protecting "antioxidant," is a switch hitter, also capable of inducing the production of DNA-damaging compounds, suggests a study in the 15 June issue of the international journal, Science. Mutations caused by these compounds have been found in a variety of tumors.
Such mutations can be repaired, however, and lead author Ian Blair of the Center for Cancer Pharmacology, at the University of Pennsylvania, cautioned that the study shouldn't be interpreted as a claim that vitamin C causes cancer. Nor does it question the wisdom of eating a balanced diet rich in fruits, vegetables, and whole grains, he said.
The findings, which come from test-tube experiments (in vitro), may help explain why vitamin C has thus far shown little effectiveness at preventing cancer in clinical trials, according to the Science authors.
"It's possible that vitamin C isn't working in cancer prevention studies because it's causing as much damage as it's preventing, but that's really speculation at this point. What we can say is that vitamin C clearly doesn't work when you expect it to, and now we're in a position to see if that's what's happening in vivo, [or, in living cells]" Blair said.
Some scientists have long recommended dietary supplements of vitamin C, particularly for treating and preventing cancer. But the supplements' effectiveness has been hotly debated, with critics saying they either have no effect or that they may be harmful.
"The logic being used [for vitamin C supplements] is that 'fruits, vegetables, etc. contain vitamin C; these foods prevent cancer; thus vitamin C prevents cancer," Blair said. "But our message is that it's the total diet that's important, not just one antioxidant in isolation."
(Note from us: vitamin C decreases toxicity of chemo and radiation and
increases the effects of chemo and radiation and hormonal therapies. See page cancerresearch
diagrams.)
Vitamin C is known to do beneficial work in the body, including acting as an antioxidant that "disarms" free radicals. These highly reactive ions are produced by the breakdown of oxygen, which occurs constantly in cells.
In addition to damaging DNA directly, free radicals can also act indirectly. They begin by converting linoleic acid, the major polyunsaturated fatty acid in sunflower, grape, and safflower cooking oils, as well as the major polyunsaturated fatty acid in human plasma, into another compound called a lipid hydroperoxide. When certain metal ions are present to act as catalysts, the lipid hydroperoxides degrade further, into DNA-damaging agents called "genotoxins."
These compounds react with DNA, switching one base for another in mutations that have been found in human tumors.
Scientists, including Blair and his colleagues, have suspected that vitamin C might also be capable of making lipid hydroperoxides degrade into genotoxins, in place of the transition metal ions.
To investigate, the Science authors added vitamin C to solutions of lipid hydroperoxides in the lab. They used concentrations comparable to those found in the human body, assuming a person would take 200 milligrams a day.
The vitamin was more than twice as efficient as transition metal ions at inducing the formation of genotoxins, including a particularly potent variety.
The researchers' next step is to see whether vitamin C produces significant amounts of genotoxins in intact cells, and whether they generate cancer-causing mutations.
The other members of the research team are Seon Hwa Lee and Tomoyuki Oe, of the Center for Cancer Pharmacology, at the University of Pennsylvania. Funding for this research was provided by the National Cancer Institute and the University of Pennsylvania Cancer Center.
Note: This story has been adapted from a news release issued by American Association For The Advancement Of Science for journalists and other members of the public. If you wish to quote from any part of this story, please credit American Association For The Advancement Of Science as the original
source.
8.Bicalutamide
shows drop in risk of disease progress (prostatecancer)
TORONTO, June 20 /CNW/ - A once daily dose that slows disease progression offers new hope for hundreds of thousands of men around the world diagnosed with prostate cancer each year. The first results of the largest ever trial in prostate cancer, the Early Prostate Cancer (EPC) Programme, showed that, in comparison with standard care
alone (surgery, radiotherapy or watchful waiting), bicalutamide 150mg
(Casodex(TM)) reduces the risk of the cancer progressing by 42 per cent and reduces the risk of the cancer spreading to the bones by approximately 33 per cent. In addition, in patients taking bicalutamide 150mg there was a significant delay in prostate-specific antigen (PSA) rise - a second indicator that the disease is under better control.
As with most cancers, prostate cancer patients have a better chance of survival if diagnosed early. Current standard treatment for early prostate cancer (i.e. surgery, radiotherapy or watchful waiting) is not always successful, as there is often disease recurrence or progression. The growth of prostate cancer is known to be stimulated by the male (androgenic) hormone, testosterone, and therefore the early use of an anti-androgen (a drug which blocks the testosterone receptor), in addition to standard treatment, could improve the outlook for men with prostate cancer.
A similar approach has proved very successful in the treatment of breast cancer, where the use of tamoxifen (Nolvadex(R), an anti-estrogen), in addition to standard treatment, has been shown to improve the survival of women with early disease.
"Progression of prostate cancer is associated with a number of serious complications such as anaemia, urinary obstruction, kidney failure, severe pain and pathological fractures caused by bone metastases. I believe that these first promising results from the EPC Programme will offer real hope for prostate cancer patients as we are already able to show a significant reduction in the risk of disease progression," said Dr. Yves Fradet, Professor of Surgery/Urology and Chairman of the Department of Surgery at Laval University in Quebec, and a Principal Investigator in the EPC Programme.
"These results, although requiring further follow-up to assess their impact on patients survival, already provide hope to the patients."
"The EPC Programme results are very exciting and will undoubtedly trigger discussion around the role of adjuvant hormonal therapy in the treatment of early prostate cancer. Inevitably, there will be some reservation regarding the preliminary nature of the data, which does not yet include any information on survival," said Dr. Jack Barkin, Chief of Urology at Humber River Regional Hospital in Toronto, Ontario. "Nonetheless, prolonging the time to clinical progression will result in significant benefits for patients with early prostate cancer, especially those at high risk of experiencing the morbidity
associated with disease progression."
The data will be presented on June 27th, 2001 at the Canadian Urology Association (CUA) meeting in Toronto, Ontario. The data have already been submitted to the UK regulatory authorities and will be submitted to other regulatory authorities around the world during the course of 2001. The aim of such submissions is to provide clinicians and patients with an additional treatment option for localized and locally advanced prostate cancer.
The majority of side effects reported were predicted from the mode of action of the drug. Breast swelling and breast pain were the most frequent, but in the majority of patients, these were mild to moderate, frequently resolving or improving when therapy was withdrawn.
The EPC Programme involved a total of 8,113 men with localized and
locally advanced prostate cancer and was carried out in Europe, North America, Scandinavia, South Africa, Australia, Israel and Mexico.(1) In Canada, 14 centres participated in the study and 318 patients were involved. Patients were randomized to receive bicalutamide 150mg once daily or placebo, in addition to standard care.
Despite an increase in public awareness and screening, prostate cancer does not have the same level of public recognition as other forms of cancer, such as breast cancer. Yet, it is the second most commonly diagnosed male cancer in Canada, as well as many western countries, after lung cancer.
According to the National Cancer Institute of Canada, it is estimated that nearly 17,800 new cases of prostate cancer will be diagnosed and 4,300 men will die from the disease in Canada during 2001.(2)
The Canadian leader in cancer treatments, AstraZeneca Canada Inc. has an extensive cancer drug portfolio for breast (Arimidex(R) and Nolvadex(R)), prostate (Casodex(TM), Zoladex(R)) and colorectal cancer. Committed to Canadian health care, AstraZeneca Canada Inc. currently invests over $1.5 million every week on research and development. With more than 65 ongoing basic and clinical research projects in Canada, AstraZeneca Canada Inc.'s active research and development program aims to find innovative treatments for many forms of cancer.
AstraZeneca is one of the leading pharmaceutical companies with a
formidable product portfolio spanning seven major therapeutic areas:
cardiovascular, gastrointestinal, oncology, pain control, respiratory, central nervous system, and infection. AstraZeneca's brands include Casodex(TM), Zoladex(R), Atacand(R), Losec(R), Zestril(R), Xylocaine(R), Pulmicort(R), Zomig(R) and Seroquel(R). The Canadian headquarters and manufacturing facilities of AstraZeneca are located in Mississauga, Ontario, with a state-of-the-art basic research centre based in Montreal, Quebec. Please visit our web site for more information at www.astrazeneca.ca.
(x) Casodex(TM) is a Trademark, the property of the AstraZeneca group of companies
References:
1. WA See, D McLeod, P Iversen, M Wirth. The Bicalutamide Early Prostate Cancer Program. Demography. Urol Onc 2001;vol6: 43-47.
2. National Cancer Institute of Canada, Canadian Cancer Statistics 2001, Toronto, Canada
/Editor's notes
- Men with localized and locally advanced prostate cancer (classed as T1b-4N0-1M0 (TNM 1997)) have been randomized on a 1:1 basis to receive bicalutamide 150mg (Casodex(TM)) daily or placebo in addition to their standard care. Recruitment to the programme closed in July 1998, and the study is continuing. Study endpoints include time to clinical progression, overall survival and tolerability. Patient age at
enrolment ranged from 38 to 93 years (mean 67 years).
- Bicalutamide (Casodex(TM)) is a well-tolerated, once-daily, non-
steroidal antiandrogen, currently used in treating the more advanced
stages of prostate cancer in conjunction with other hormonal treatments
(at a dose of 50 mg per day).
- Further background information on prostate cancer and its management can be found at www.prostartonline.com or by calling the Prostate Cancer Research Foundation of Canada at (416) 441-2131 and also by visiting their website at www.prostatecancer.ca./
/For further information: please contact: Karisma Communications, (416)
663-1500, Michelle Brun, ext. 231 or Alanna Fox, ext. 225; For more information on AstraZeneca Canada Inc., please contact: Kirsten Evraire, (905) 803-5732 or 1-800-565-5877 x 5732/
Source CNW - Canada News Wire
Categories: NWR/ON NWI/MTC MST/R/CA MST/I/DRG
9)
Postoperative
radiation with cervical cancer shows no positif effect on
surviving
10
Prostate
cancer and nutrition
11 NCI
starts some trials about complementary treatment
Pancreatic Cancer
Lung Cancer
Prostate Cancer
Breast Cancer
12.
BL22 succesfull in Phase I study and leukemia
NEW ORLEANS, March 27, 2001 -- Early tests in humans of a
new compound show promising results for patients with a rare form of blood
cancer say researchers at the National Cancer Institute.
13.Protein CD45
stops growth malignant bloodcells
Researchers claim 'Holy Grail'
ref="#top">
14. LDP-341
stimulates suicide cancercells
Millennium cancer drug tests advance By Naomi Aoki,
Globe Staff, 3/2/2001
15.
Researchers in India find new treatment against all kind of
cancers
Has the ultimate cancer cure arrived?
16.Gleevec
Two messages about Gleevec: Leukemia pill gets quick approval Thursday, May 10, 2001
17.
Source: www.AFXnews.com Novartis' Gleevec cancer therapy patients had relapse
18.
Lorus (Canadian Company) claims new treatment
19.
Topotecan gives hope for ovariancancer and non-small-lungcancer
20.
Vitamin C and Gene-Damagin compounds
Vitamin C Produces Gene-Damaging Compounds, Test-Tube Study In Science Reports
21.PLATO
a new radiation method for prostatecancer
- Spanish Hospital Pioneers Advanced Radiation Therapy Cancer Treatment --
22.Prostatecancer
and Cryosurgery
23 Gene
succesfull in treating leukemia
Source: http://news.bbc.co.uk/hi/english/health/newsid_1113000/1113883.stm 24.
AMAS test and breastcancer The AMAS Test (Anti-Malignin Antibody in Serum) Some sites with information about the AMAS test: http://www.alternativemedicine.com/digest/issue09/09049R00.shtml http://www.amascancertest.com/ http://members.tripod.com/~AlexisRay/index This article about the AMAS test is written at the last mentioned site: CANCER
25.
Is Kanlight the new breaktrough in curing cancer
We received this messages about
Kanglaiteand in my opinion this is very interesting news. Read also after
this message the case M. at remarkable stories no. 4.
This woman healed with help of a diet, and supplements and Chinese herbs
from an incurable pancreascancer and coloncancer with metastases in her liver.
Also the information about PC-SPES tells about Chinese herbs and PC-Spes heals
prostatecancer very well. See also at the page other alternatives the
information about PC-Spes. Also the FDA has approved 'Kanglaite'
to start trials with it. Look further in this message for a hospital adress
where people can follow a trial with Kanglaite. BEIJING, Jul 09, 2001 (Itar-Tass via COMTEX) -- For a very well and detailed story from
a woman who cured from bladdercancer with additional help from among others
Kanglaite see her story at this site: http://blcwebcafe.org/stories/pat.asp Following some quotation and a reaction from Pat on a question from
me: In mid March I leave for China for consultations with two of the top
onocologists in China, one Western MD and one Chinese Traditional Medicine.
The diagnosis is the same as my great non-communicator's, and they agree with
what I have been doing, but suggest I add the immune stimulant boosters that
they use. Kanglaite IV for 20 days and TCM herbal brews. This I do, as I went
China to find out what else I could do to keep the immune system working. They
also said to keep up the BCG maintenance. Upon my return in 30 days, I went in for the NMP22 test and it showed
nothing there. Do we get excited?
I told the doc what I had done in China, showed him the info on the
Kanglaite and told him about the weeds and things. He laughed. I followed him
into his office and told him I would have the last laugh. He told me that if
it saved my bladder and my life then, "Go for it".
One week later, Cysto. All rigged for TUR as we all expected the beast to
be back, as usual. Nothing, not one red raised area. The beast is
gone... Reaction from Pat d.d. 8 augustus 2001 on a question from me: Hello Kees, thanks for asking me to explain something about KANGLAITE Diary dedicated to the absent beast: Dateline Oregon 7/29/00: Following the news that the FDA approved
Kanglaite for the American trials:
Traditional Chinese medicine has taken a new step towards the global market. In the next message a company/hospital asks for patients to participate in
the trial with Kanglaite
-- KRO> Salt Lake City-Area Researchers Are Testing Coix Herb --
26.
Protein
decreases pain of bonecancer
27.
information about tamoxifen
We got from a visitor of this site some interesting sites which give good
information about tamoxifen. http://www.w-i-n.com/tamox.htm http://www.prostate90.com/JLeeCancer_Testosterone.htm On our page cancerresearch you can read
more about nutrition and nutritional supplements in addition of chemo,
radiation and tamoxifen.
28.
A new identified gene protects women against getting breastcancer
29.
Virus can kill
cancertumors in mice -- DJ Scientists Find Virus Can Kill Cancer Tumors In Mice --
30.
Researchers find that irinotecan in combination with cisplatin is
an effective treatment for metastatic small-lungcancer
For who can read Dutch or is able to translate Dutch in English or your own
language read the report of the
organisation Canhelp about all the
current developments of treating smallcell lungcancer and read the
story of Bert who survived till today (d.d. 18 february 2002) an
incurable smallcell lungcancer with help of a special prepared chemo and
injections with vitamins. Now he follows a vaccination programm (imunotherapy)
with help of the German professor Atzopodien. For the one who wants the adress
of this professor send us a personal e-mail. Read here the complete
studyreport about this study. Two quotes: Results The planned size of the study population was 230 patients,
but enrollment was terminated early because an interim analysis found
a statistically significant difference in survival between the
patients assigned to receive irinotecan and cisplatin and those
assigned to receive etoposide and cisplatin; as a result, only 154
patients were enrolled. The median survival was 12.8 months in the
irinotecan-plus-cisplatin group and 9.4 months in the
etoposide-plus-cisplatin group (P=0.002 by the unadjusted log-rank
test). At two years, the proportion of patients surviving was 19.5
percent in the irinotecan-plus-cisplatin group and 5.2 percent in the
etoposide-plus-cisplatin group. Severe or life-threatening
myelosuppression was more frequent in the etoposide-plus-cisplatin group
than in the irinotecan-plus-cisplatin group, and severe or
life-threatening diarrhea was more frequent in the irinotecan-plus-cisplatin
group than in the etoposide-plus-cisplatin group. Conclusions Irinotecan plus cisplatin is an effective treatment for
metastatic small-cell lung cancer. Overall Survival As of March 2001, when the final analysis was conducted, the median
overall survival was 12.8 months (95 percent confidence interval,
11.7 to 15.2) in the irinotecan-plus-cisplatin group and 9.4 months
(95 percent confidence interval, 8.1 to 10.8) in the
etoposide-plus-cisplatin group; 70 patients in the irinotecan-plus-cisplatin
group and 74 in the etoposide-plus-cisplatin group died (P=0.002 by
the log-rank test) (Figure 1). The rate of overall survival
in the irinotecan-plus-cisplatin group was 58.4 percent (95 percent
confidence interval, 47.4 to 69.4 percent) at one year and 19.5
percent (95 percent confidence interval, 10.6 to 28.3 percent) at two
years; in the etoposide-plus-cisplatin group, the rates of overall
survival at these time points were 37.7 percent (95 percent
confidence interval, 26.8 to 48.5 percent) and 5.2 percent (95
percent confidence interval, 0.2 to 10.2 percent). The risk of death
in the irinotecan-plus-cisplatin group relative to that in the
etoposide-plus-cisplatin group was 0.60 (95 percent confidence
interval, 0.43 to 0.83). Similar results were obtained in analyses
that adjusted for age, sex, performance status, and weight loss and
in an analysis that excluded the 23 patients randomly assigned to the
radiotherapy portion of the study, which was canceled.
The following is Part 2 of an excerpt from Dr. Bob Arnot's new book,
The
Prostate Cancer Protection Plan
, published by Little Brown in May 2000.
HOW BIG A VILLAIN IS THE WESTERN
DIET?
The Japanese flat-out blame the Western diet for their prostate cancer
travails: There were 5,399 deaths from prostate cancer in 1995 in Japan.
By 2015 that number will increase to 13,494. Dr. Y. Kakehi of the
Department of Urology, Faculty of Medicine, Kyoto University, concludes: "Change in dietary habit (more Western-style
diet) is
considered to be a major cause of the increase." English researchers too
have concluded that nutrition is the major risk factor associated with
prostate cancer, singling out low intake of fresh fruit, low intake of
vegetables, and low intake of whole-grain cereal, as well as excess body
fat.
The Association for the Cure of Cancer of the Prostate (CaP CURE) writes
in its white paper on nutrition: "Of all the risk factors for prostate cancer,
only nutrition seems to explain the differences in global distribution of this
disease. One hundred and twelve studies estimate that 75 percent of all
cases of prostate cancer could be prevented by changes in diet and lifestyle." Scientists from Cap CURE
conclude: "We believe, therefore, that nutrition and lifestyle practices in
lower-risk countries arrest the growth of prostate cancer so that it is never
clinically discovered."
Okay, you may say, what does all of this high-powered epidemiologic
research have to do with me? After reading the thorough research on
nutrition and prostate cancer, I have to tell you that I''m convinced. As a
physician and as a male concerned about prostate cancer, I believe this
research is the strongest indication that diet plays a big role in prostate
cancer and that there is something you
can do about your own diet to change your risk. This isn''t just a pipe dream; this could be close to the whole game. But I asked
myself: Which foods? What diet? Well, you''re in for a real treat.
There is a true treasure trove of terrific foods that can help protect you
against prostate cancer. If you're like me, you don't just want to read a lot
of wishful thinking by well-meaning advocates of alternative medicine. You
want hard facts. The hard facts, in this case, show that foods have highly
specific effects on the prostate gland. These are varied enough to give you
a range of strategies to
protect yourself. You''ll also find, as I have, that this is high-level science.
Foods have incredibly sophisticated powers, like well-designed pharmaceuticals.
Researchers are excited enough about the power of foods that they''re
already intensely investigating many of them. In fact, tens of millions of
dollars are being spent on nutritional research. The next section of the
book will present these foods and tease apart their specific actions that
can help you protect yourself against prostate cancer. You''ll be pleased to learn that virtually all of them have terrific
general health benefits, from lowering your cholesterol and your risk of
heart disease to controlling your weight and risk of other cancers. They are
also foods that will make you feel terrific, perhaps the best you have ever felt. I hope
you''ll develop the same
enthusiasm for the foods and meals in this book that I have. Tens of
thousands of men threatened with prostate cancer have already made the change. Most telling of
all, men who already have the disease are finding
remarkable changes in the state of their cancer with a rigorous change in diet.
Why? The most intriguing reason is that our bodies are designed to eat a
specific diet. Just as putting low-grade, cheap gas into a car will eventually
ruin a car engine, putting cheap fuels that we were not designed to use
into our own bodies will lead to disease. Specifically, the human prostate and the Western diet may be
incompatible. You see, through human evolution, our bodies became
accustomed to specific foods. Unfortunately, our bodies can''t turn on a
dime and acclimatize overnight to a new diet, especially one loaded with
animal fats and refined carbohydrates, almost devoid of fruits and vegetables. Human evolution marks time in the tens of thousands of
years.
The dramatic changes in our diets since the Industrial Revolution aren''t
even a tick on our evolutionary clocks. What''s the diet we as men are meant to
eat? Is it roast beef with
Yorkshire pudding, roasted potatoes, and gravy? Not if you look back into
the dawn of humankind.
For 90 percent of the last 200,000 years, we were fruit-and-vegetable eaters. Donald
Coffey, Ph.D., who is a professor in the famed Department
of Urology at John Hopkins, argues that humankind did not evolve fully
equipped to be dairy or meat eaters.
More to the point, our prostates may not have evolved to handle a diet rich
in fats. Humans came from an arm of evolution that did not eat a lot of meat. Until 2.5 million years
ago, we were mainly gatherers -- we ate
seeds and fruits and nuts. Homo sapiens first appeared 100,000 years ago, but only 9,000 years ago did we start processing and storing food and
trading it. That''s when we started down the road to eating the massive
amounts of carbohydrates that we eat today, for example, corn, wheat, rice,
barley, potatoes, and root plants. Fruit consumption dropped, since
fruits were harder to store.
And as we increasingly ate a diet rich in meat, which we cooked and even burned, we stopped eating as many fruits and
vegetables. Dairy got big
only around 3,000 years ago, and it''s then that we increased our dairy
intake. Before that we would get milk from goats and sheep, but it was
only when we bred these animals that we developed the dairy industry. "After fifty years of trying to prevent
cancer, we''ve learned that we should
go back to eating the foods we ate while we were evolving," says Dr. Coffey. He
adds, "It's not surprising that the American Cancer Society and
the National Cancer Institute make the same suggestions. They tell us to
return to the diet we ate when we were evolving: more vegetables, more
fruit, more fiber, less red meat,
less animal fat, less dairy, less barbecuing, and more aerobic exercise."
So who eats a diet closer to the one we were designed to eat? In parts of
China, people eat around 6 to 8 percent fat. Compare that to the United States, where the figure is 30 to 40 percent, much of it animal fat. "Put it
all together and you''ll figure that our lifestyle is giving us cancer," says Dr.
Coffey. I swear the reason I
feel so terrific on this diet is that it's the one we're supposed to eat, the
one we are designed to eat.
Copyright (c) 2000 Dr Bob Arnot. Reprinted with permission from the
author.
Coming Wednesday in the finale of our three-part series: The Prostate
Cancer Diet.
If you haven't read it yet, take a look at Part 1 of our series:
Asian
Diet: A Clue to Prostate Cancer
Want to know more about prostate cancer? Then check out these articles
:
on
healthAtoZ
Randomized Dietary Intervention Study of a Diet Rich in Vegetables, Fruit, and Fiber and Low in Fat in Women With Previously Treated Stage I, II or III Breast Cancer.
CAM Cancer Physician Data Query (PDQ) Summaries: The NCI's PDQ Office has produced summaries of the evidence for various CAM
therapies.
In an early clinical trial designed only to test safety of the drug, a protein-based compound called BL22, produced complete remissions in a high
percentage of patients with hairy cell leukemia (HCL) resistant to standard
therapy. The research team led by Dr. Robert Kreitman, chief of the Clinical
Immunology Section, Laboratory of Molecular Biology at the NCI presented the
preliminary data at the American Association for Cancer Research meeting here.
"With our longest follow-up at 15 months, the research is still in its
early stages," said Kreitman in a prepared statement. "But with
several patients having maintained complete remissions for more than a year,
BL22 appears promising as a treatment for patients who do not respond fully to
first-line therapies."
Hairy cell leukemia is a disease in which cancer (malignant) cells are found
in the blood and bone marrow. The disease is called hairy cell leukemia
because the cancer cells look "hairy" when examined under a
microscope. HCL represents 2 percent of all leukemias, with 600 new cases
diagnosed annually in the United States.
The research team at the National Cancer Institute (NCI) tested BL22 against
several types of blood cancer. Of the 14 patients with HCL who completed
treatment, 11 had no pretreatment antibodies to the drug, immune system
proteins that would have neutralized its effect.
Patients received one to nine 3-week cycles of BL22 at the treatment regimen's higher doses. All 11 anti-body-free patients achieved complete
remission, and no relapses occurred at a median follow-up period of seven
months. Although side effects were usually mild and cleared on their own,
several HCL patients had potentially serious side effects including swelling
and hemolytic uremic syndrome -- a condition involving rupture of red blood
cells, anemia, low platelet count, and kidney failure - all of which resolved.
BL22 is a protein compound created by the fusion of two components: a fragment of a monoclonal antibody and a fragment of a toxic substance
manufactured by Pseudomonas bacteria. The monoclonal antibody fragment binds
to CD22, a protein present on the surface of leukemia cells, which allows
entry of the toxic fragment into the leukemia cell. Inside the cell, the toxin
splits off and exerts its lethal effect, killing the malignant cell.
BL22 was developed at NCI for preclinical use by Kreitman; Dr. David
Fitzgerald, chief of the Biotherapy Section at the Laboratory of Molecular
Biology; and Dr. Ira Pastan, chief of the Laboratory of Molecular Biology.
Since the early 1990s, two standard treatments for HCL have been available,
each with a high rate of complete remission (70 percent to 85 percent) in
previously untreated patients. However, various studies have found a 13
percent to 50 percent incidence of residual disease after use of these
therapies. In the BL22 study, sensitive tests detected malignant cells in
blood, bone marrow, or elsewhere in only one (9 percent) of the patients in
complete remission.
According to Kreitman, an important characteristic of the responding patients
was the absence of pre-existing antibodies to the Pseudomonas toxin, which
might develop after exposure to the bacteria, possibly through something as
simple as a cut, and neutralize the cancer-killing effect of the drug. Some 5
percent of the population has significant levels of antibodies to Pseudomonas.
Even after treatment with BL22, however, most leukemia patients do not develop
the antibodies.
Among the 29 patients who finished treatment, complete responses were seen
only in the HCL group. Partial or marginal responses occurred in patients with
chronic lymphocytic leukemia (CLL), and responses improved with additional
treatment cycles.
The NCI team expects to complete the phase I trial of BL22 and begin enrolling patients for multi-center phase II trials this year. In these
upcoming safety and efficacy studies, BL22 will be investigated in several
trials, including one for HCL and others investigating its use in CLL,
non-Hodgkin's lymphoma, and pediatric leukemias.
American Association for Cancer Research (AACR) press release from the Annual
Meeting, Mar. 24-28, 2001, New Orleans, La.
Prolific Toronto team tags a protein as the off switch of the immune
system
Tom Arnold
National Post
James Pattyn, Saturday Night
Dr. Josef Penninger says the new discovery, his 126th published findin to date, came on a hunch. "In 1993," he says, "somebody told me
that we know all about [protein] CD45 and we will never find anything new
about it." He thought otherwise.
A team of Canadian scientists has discovered the "Holy Grail" of the
signalling process the human body uses to control its immune system, a finding that could one day halt the development of cancer, diabetes,
arthritis and heart disease.
Researchers have discovered that the protein CD45 contains a master switch capable of turning off hormones and proteins in the immune
system. The switch could help shut down growth of diseases, stave off viral infections and prevent rejection of transplanted organs.
"It is the Holy Grail of the body's cellular signalling system,"
said
lead researcher Dr. Josef Penninger, an immunologist at the Amgen
Institute and the Ontario Cancer Institute, a research centre at
Princess Margaret Hospital in Toronto. "Our cells rely on the delicate
balance of communications signals to grow normally and produce blood cells.
However, when a signal cannot be stopped, the cells overgrow and we run
into trouble. We have discovered that it is CD45 that sends the 'ceasefire'
signal to cells."
Dr. Penninger called the finding one of his most important discoveries: "People understand very much how you turn on a cell but people have had
not much idea about how the master off switch works. Everyone was looking for
it. Finding this out is kind of like the ultimate prize in this field."
The research is published in today's issue of Nature, an international
journal. It is Dr. Penninger's 126th scientific finding to be published.
It marks the sixth major discovery to emerge from the same Canadian labin less
than two years. Dr. Penninger's recent research has attracted headlines around the world.
"It's an important step in that it identifies a new function for
CD45,"
concluded Dr. John Cambier, chairman of the department of immunology at the
University of Colorado Health Sciences Center and the National Jewish Medical
and Research Center in Denver. He is considered an international expert on
CD45.
"I'm not sure that I would consider it the Holy Grail of understanding
regulation of cell growth. But nonetheless the observations are very
important because they do illustrate a new function in regulation of
growth."
The human body contains tens of thousands of CD45, a protein that sits on the surface of red and white blood cells. First discovered 13 years
ago, it was believed the protein played a limited role with two
different types of cells.
"We set out to find additional function of CD45 just based on the idea that there must be something else," Dr. Penninger said of his 13-member
team.
"In 1993 somebody told me that we know all about CD45 and we will never
find anything new about it," Dr. Penninger said.
The researchers genetically engineered mice that could not make the
protein so they could compare how these mice and normal mice fared against a virus.
"If there's a virus infection, our lymph nodes are swelling up but when
the virus is killed the system must be shut down," said Dr. Penninger.
"For some people it doesn't. And if you cannot stop the system, what we
get is tumours because the cells overgrow, or auto-immune diseases like
diabetes or multiple sclerosis because our cells cannot stop attacking."
Scientists will now look to develop a drug capable of switching off the
protein, he said. For instance, since most cancers require particular cells to
grow, he said, a new drug that will interfere with the protein and turn off
CD45 could halt the proliferation of cancerous cells.
Dr. Arthur Weiss, an immunologist at the University of California in San
Francisco, called the discovery "interesting and provocative. I've heard rumours about it. It is an unexpected and interesting finding."
Dr. Penninger has emerged as a leader in Canada's research community. He came
to Toronto from Austria in 1990 to work with Dr. Tak Mak, a well-known immunologist. By 1993, he had his own lab.
Last year, he discovered the molecule that regulates movement of white blood cells, a major finding that could one day lessen the likelihood of
heart attack, stroke and dying from the flesh-eating disease. His lab also solved the genetic mystery of how a common, contagious cold virus
carried by 70% of the human population triggers heart disease. The findings will help predict who is at serious risk of cardiovascular
disease and how it can be prevented.
Based on positive results from earlier tests, Millennium Pharmaceuticals Inc.
yesterday said it is moving a cancer-fighting drug known as LDP-341 into the
second of three phases of human testing generally required before seeking
regulatory approval.
The Cambridge biotechnology company said the drug triggers cancer cells to
self-destruct, possibly paving the way for a new class of cancer medications
with fewer side effects than traditional chemotherapies.
If the drug proves effective, the company said, it expects LDP-341 to become
a cornerstone of its oncology program. Cancer is one of three disease areas
(the others are inflammatory and metabolic disorders) for which Millennium is
working to discover and develop drugs and predictive tools.
Aside from Campath, another cancer therapy, LDP-341 is the most advanced drug
in the company's pipeline, and it is the most advanced of the drugs owned
entirely by Millennium. The proceeds from Campath, which is awaiting approval
by the US Food and Drug Administration, will be split among Millennium, Ilex
Oncology Inc., and Schering AG. Millennium picked up both cancer drugs when it
acquired LeukoSite Inc. in late 1999.
Julian Adams, Millennium's senior vice president of drug discovery and
pre-clinical development, said the clinical trial will test the effectiveness
of LDP-341 as a treatment for multiple myeloma, a cancer marked by the
excessive growth of plasma cells.
More than 40,000 Americans have the disease, and about 11,000 die from it
each year, according to the Multiple Myeloma Research Foundation. The cancer
is difficult to cure - killing more than one in four patients within five
years of diagnosis.
Eventually, Adams said, the company hopes the drug will prove useful either
on its own or combined with chemotherapy in treating a variety of cancers,
including leukemia and non-Hodgkin's lymphoma as well as breast, colon,
prostate, and lung cancers.
Ten clinical trials for the drug - some run by the company and others by
researchers at the National Cancer Institute - are set to begin this year.
''We're very excited about the promise of this drug,'' Adams said. ''But we
don't want to mislead patients. We've got a lot of work ahead of us to show
if this is going to be an effective treatment in cancer.''
LDP-341 works by binding to a chamber within the cell, called a proteasome,
which rids the cell of excess or unwanted proteins. By blocking the
proteasome from doing its work, the drug triggers the cancer cell to commit
suicide, a reaction known as apoptosis, or programmed cell death, Adams said.
Healthy cells are less sensitive to the drug, Adams said, creating ample
opportunity for the drug to kill cancer cells without changing the normal
function of healthy cells. As a result, he said, the drug seems to cause only
mild side effects.
In earlier tests involving nearly 150 people, he said, the drug did not cause
the severe side effects associated with traditional chemotherapies such as
nausea, hair loss, and bone marrow damage. Adams said it also has shown
promise in treating patients who have not responded to other existing
treatments.
Naomi Aoki can be reached by e-mail at naoki@globe.com.
This story ran on
page C14 of the Boston Globe on 3/2/2001.
© Copyright <http://www.boston.com/globe/search/copyright.htm> 2001
Globe Newspaper Company
PTI
(Hyderabaad, May 28)
INDIAN CANCER researchers have taken a giant step on the road to discovering the
ultimate cancer cure by developing a drug that selectively targets the cancer
cells without harming the healthy ones.
Researchers in Kolkata claim that patients in "very advanced stages"
of cancer for whom all other treatments had failed have been brought back to
"excellent" health with the help of a drug formulation they have
developed after research spanning more than a decade.
"We have what we think magic bullet against cancer," says Manju Ray, a
biochemist at the Indian Association of the Cultivation of Science (IACS) where
the drug was developed under a project funded by the Department of Science and
Technology and the Council of Scientific and Industrial Research.
Most currently available anti-cancer drugs are toxic because they also damage
the normal cells. Ray says the IACS formulation, containing "Methylglyoxal"
as the lead ingredient, combats only the diseased cells, the cherished goal of
cancer researchers worldwide. Methylglyoxal is a metabolite in the human body
produced during glucose breakdown.
Others involved in the project are Swapna Ghosh of IACS, Manoj Kar and Subhankar
Ray of the University College of Science, and Santajit Datta, a medical
practitioner. Results of human trial conducted by them with the new drug have
recently appeared in the Indian Journal of Physics.
While Americans are going ga-ga with their new anti-cancer drug "Glivec"
- that was featured on the cover of May 28 issue of Time magazine - the
low-profile, cash-strapped Kolkata researchers have been working quietly for
over a decade shunning publicity until they obtained proof from human trials
nine weeks ago.
According to their published paper, the Methylglyoxal-based forumulation had
"a dramatic positive effect on the patients".
For instance, the condition of 11 out of the 19 patients treated - most of them
in a very advanced stage when the treatment began -- are now stated to be in
"excellent physical condition". Five are in stable condition and only
three died during the course of the study.
Since the submission of the paper, the number of patients treated has crossed 40
mark with more than 70 per cent success, according to Manju Ray.
Most remarkable fact, according to the scientists was that Methylglyoxal was
successful against different types of cancer unlike "Glivec" which
targets only the chronic myeloid leukemia.
Those whose health returned to "excellent" condition after treatment
with Methylglyoxal included patients in "a very advanced stages" of
colon cancer, acute myeloid leukemia, non-Hodgkin's lymphoma, and cancers of
ovary, breast, liver, lung, bone, gall bladder, pancreas and oral cavity.
The patients were inducted for the trial, from January to June 2000, after
obtaining permission from the Drug Controller General of India, the scientists
said. The drug was administered orally for about six months with gradual
reduction of daily dosage from the initial 25 milligrams per kilogram of body
weight.
Researchers said development of the drug was preceded by years of basic research
involving human cancer cells in culture and animal experiments that showed that
Methylglyoxal selectively killed the cancer cells without affecting normal cells
by exploiting "a very significant" biochemical difference between the
two.
Explaining the mechanism of action, the scientists said cancer cells required a
large amount of energy providing substance called ATP (Adenosine-5-Triphosphate)
for survival.
"Methylglyoxal inactivates the enzyme (Glyceraldehyde-3- Phosphate
Dehydrogenase) needed for ATP production in cancer cells and thereby starves
them to death. Normal cells remain unaffected."
Manju ray said that chemists knew Methylglyoxal molecule for about four decades
and its anti-cancer effects in animals had also been studied. "But
surprisingly, no one bothered to initiate further research leading to human
trials," she said.
The researchers said concern in some quarters about safety of Methylglyoxal were
not borne out from the clinical trials, which showed that in combination with
protective agent like Ascorbic Acid and vitamins, the drug Methylglyoxal had no
major toxic effect. They said there was scope for further enhancing the drug's
efficacy.
Gleevec, an enzyme-targeting drug resulting in large part from OHSU research, is
heralded as a new type of cancer treatment
Friday, May 11, 2001
By Joe Rojas-Burke of The Oregonian staff
A pill that has halted a form of leukemia in 90 percent of study patients gained
federal approval Thursday, and cancer researchers called it the beginning of a
new era of precision drugs that will lack the brutal side effects of most
chemotherapy agents.
"What we've done gives us a glimpse to the future of all cancer therapies,"
said Dr. Brian Druker, a professor of medicine at Oregon Health and Science
University. Druker, working with scientists at Novartis Pharmaceuticals in
Switzerland, developed the drug. It will be sold under the name Gleevec in the
United States and Glivec in other countries. The U.S. Food and Drug
Administration approved the drug after only two months of review, a near record.
Health and Human Services Secretary Tommy Thompson took the unusual step of
announcing the approval at a news conference in Washington.
Clinical trials have shown only that the drug works against chronic myeloid
leukemia, a disease that strikes about 4,500 Americans each year. But the new
pill demonstrates for the first time that it is possible to repair a fundamental
defect that triggers normal cells to multiply out of control as cancer cells. By
contrast, standard cancer treatments indiscriminately kill cancerous and normal
cells that are rapidly dividing. "Gleevec offers proof that molecular
targeting works in treating cancer, provided that the target is correctly chosen,"
said Dr. Richard Klausner, director of the National Cancer Institute. That has
ignited an intensive effort to find the targets for treating other forms of
cancer and to develop drugs that reach those targets, he said.
Before Gleevec, patients with chronic myeloid leukemia, or CML, faced
limited treatment choices. The disease causes an enormous multiplication of
white blood cells. With standard therapy, usually including a drug called
interferon alpha, half of patients die within six years after diagnosis. A bone
marrow transplant can cure the disease, but some patients die during the risky
operation. Many patients are too frail to face the risk. And often patients lack
a suitable marrow donor.
Sima Schorr of Portland, a registered nurse and mother of two, couldn't find a
bone marrow donor. Her leukemia was diagnosed about six years ago, when she was
42. Taking interferon, she said, "You're really poisoned, dead flat-out."
Then that drug stopped working.
Schorr became one of the first patients to volunteer for the human tests of
Gleevec, which were run by Druker, the OHSU physician and professor. Within
weeks of taking three pills a day, her blood counts began returning to normal.
On Thanksgiving Day, one year after she entered the trial, Druker called her
with stunning news: Laboratory tests could no longer find any cells with the
defective chromosome that causes the leukemia.
"I just got lucky, finally, boom!" Schorr said. "Everything,
instead of
adversity and sadness, became excitement and insane amounts of hope." A
year later, Schorr remains free of all signs of the disease and is considering
going back to work as a hospital nurse.
"Spectacular success"
In one clinical trial, reported in April in the New England Journal of
Medicine, Gleevec restored normal blood counts in 53 of 54 patients whose
leukemia had become resistant to interferon. Fifty-one of the patients remained
healthy one year later, and most reported only a few minor side effects.
"I can't think of another cancer drug that has shown such spectacular
success in a group of people that had failed all other treatment," said
Dawn Willis, scientific programs director for the American Cancer Society
Despite the excitement, Klausner and others say many questions about Gleevec
remain unanswered. The drug has produced remission in thousands of patients, but
will it continue to do so long enough to increase life span? Can patients stop
taking the drug after they've remained cancer-free for some length of time? Will
it work against other, more common types of cancer?
For patients newly diagnosed with CML, experts say, it's too early to know
whether Gleevec is a better treatment choice than a bone marrow transplant or
interferon. "You're going to see wide-ranging recommendations," Druker
said.
Gleevec has produced higher remission rates than interferon in three
short-duration, early-phase clinical trials, according to the National
Cancer Institute.
Trials against other cancers
Several clinical trials are under way to test the drug against other forms of
cancer, including glioma, soft tissue sarcoma and gastrointestinal stromal
tumors. Druker says Gleevec probably won't be effective against many other
cancers. Rather, he expects researchers in years to find comparable drugs that
target errors specific to each type of cancer. "If we can do this for one
cancer, we can do it for all cancers," Druker said. "Our pace of
discovery is going to be quickened."
Dr. Daniel Vasella, president of Novartis, says he expects to begin
shipping, Gleevec, also called STI571, next week. U.S. shares of Novartis rose
$2.65, or 6.8 percent, on Thursday to close at $41.65 on the New York Stock
Exchange. OHSU, although instrumental in the development of Gleevec, has no
patent rights and no claim to royalties from sales. Druker says, though, that
the university's role in the discovery will help its Oregon Cancer Institute
attract research grants and talented scientists.
Novartis says a one-pill-a-day regimen will cost $2,000 to $2,400 monthly, which
company officials say is comparable to current cancer treatments.
Vasella says the company is setting up a program to make the treatment
available on a sliding scale for people with incomes below $100,000 a year, and
free for those who earn less than $40,000.
WASHINGTON - A new drug that helped more than 90 percent of patients
with a rare form of leukemia won government approval Thursday.
Gleevec works by blocking chemical signals sent by cancerous cells
and researchers hope it will also prove useful against a form of
stomach tumor and perhaps other types of cancer as well.
Health and Human Services Secretary Tommy Thompson said the drug is
based on the principle of molecular targeting, killing leukemia cells
while leaving normal white cells alone.
"We believe such targeting is the wave of the future," he said.
The results of clinical trials of the drug, formerly known as STI-
571, generated excitement among cancer researchers.
Chronic myeloid leukemia, a relatively rare disease, is caused by a
protein produced an abnormal chromosome. It leads to a huge increase
in the number of white blood cells in the body, which can interfere
with the functioning of other organs. The disease kills about 2,300
Americans annually.
In clinical trials financed by the manufacturer, Novartis
Pharmaceuticals, more than 90 percent of patients in the first phase
of CML saw their cancer go into remission within the first six months
of taking the pill. The findings were presented in December at a
meeting of the American Society of Hematology.
A study of patients in the second phase of the disease showed more
than 90 percent responded positively to the treatment. In 63 percent,
the cancer went into remission. The trials involved 530 first-phase
and 230 second-phase patients.
The early success has propelled researchers to test the drug on
almost 3,000 patients around the world.
"This is not a miracle drug," but it is a model for future cancer
study because it targets the cause of the disease without damaging
other cells, Edward Benz, president of the Dana-Farber Cancer
Institute at Harvard Medical School, said at the hematology meeting.
Gleevec blocks a signal that the abnormal protein sends out,
preventing the abnormal growth and production of other cancerous
cells.
Currently the only treatments for CML are bone marrow transplants,
which can be dangerous, or interferon, which can extend a leukemia
patient's life by up to two years but can have side effects that
cause about 20 percent of patients to stop using it.
Gleevec has been studied on humans for only about two years, so how
long it will prolong a patient's life is not yet known. But it has
had few side effects.
LONDON (AFX) - More than half of late-stage patients with chronic myeloid leukemia who initially benefited from treatment with Novartis AG's Gleevec have seen their cancer return within six months, an often-fatal relapse, the Wall Street Journal Europe reported, citing a study.
A University of California at Los Angeles team, which studied 11 patients who had developed resistance to Gleevec, found two types of alterations in the genetic machinery of cancerous cells that help explain their ability to counteract the drug, the report said.
In six of the 11 patients, the found that cancerous blood cells exhibited a single mutation in the abnormal gene responsible for CML, altering the shape of the resulting protein in such a way that Gleevec can no longer bind to it.
In a second group of three patients, the researchers found that the cancer cells had somehow each produced multiple copies of the aberrant BCR-ABL gene, according to the group's findings to be published today in the journal Science, the Journal reported.
The U.S. Food and Drug Administration approved Gleevec last month.
Novartis was cited as noting that Gleevec remains an effective treatment for patients with less-advanced forms of CML, a rare form of leukemia estimated to strike roughly 9,000 people in the U.S. and Europe every year, the report said.
Noone at Novartis was immediately available to comment to AFX News.
For more information and to contact AFX: www.afxnews.com and www.afxpress.com
-The Company’s third anti-cancer drug commences clinical trial program -
JUNE 11, 2001
--------------------------------------------------------------------------------
TORONTO, CANADA – June 11, 2001 - Lorus Therapeutics Inc. (TSE: LOR; OTCBB: LORFF) announced today that it has started treating its first patients with its anti-cancer antisense drug, GTI-2501. The Phase I dose-escalating trial of GTI-2501 is underway at the University of Chicago Medical Center.
The Phase I clinical trial will enroll patients with solid tumors or lymphoma for which no effective therapy is currently available or whose cancer has not responded to conventional or standard therapies. The trial has been designed to establish the recommended clinical Phase II dose as well as look at the safety profile of GTI-2501. The Company also plans to monitor the drug’s activity during the treatment cycle.
“The pre-clinical results with GTI-2501 are very promising and we are extremely pleased to begin our clinical trial program in patients with different tumor types,” said Dr. Jim A. Wright, president, Lorus. “We think there is great potential for this drug to provide patients with an effective treatment that is safe and less toxic than alternative therapies.”
Lorus previously reported the approval of its Investigational New Drug (IND) submission for GTI-2501 by the U.S. Food and Drug Administration. In pre-clinical testing, Lorus reported that GTI-2501 demonstrated significant anti-tumor activity properties when investigated in standard mouse models with a variety of different human cancers. The results were promising as they revealed complete tumor regression in all mouse models with human tumors derived from kidney and breast cancers. Following the tumor regression, no kidney tumor re-growth occurred, even after the treatment was stopped. Earlier investigations in animals also showed that the drug is well tolerated. Lorus is anticipating similar safety and activity profiles in this first phase of human trials.
GTI-2501 is the Company’s third drug to enter clinical trials. Lorus is preparing for multiple Phase II clinical trials with its lead antisense drug GTI-2040, the first of which is to involve patients with renal cell carcinoma. A Phase III clinical trial with Virulizin® in patients with advanced pancreatic cancer is planned for later this year.
redistributed by University of Bonn, Medical Center
CANCER FACTS National Cancer Institute National Institutes of Health
The Food and Drug Administration (FDA) has approved topotecan, the first of a new class of drugs to treat patients whose advanced ovarian cancers have not responded favorably to standard treatments. Topotecan works by interfering with an enzyme, topoisomerase I, that uncoils DNA before cell division by creating and resealing nicks in the DNA. Altered function of the enzyme eventually leads to tumor cell death.
"The approval of topotecan is significant because it is the first of a
series of drugs with a new mechanism of action, which opens the door to the development of unique methods of treatment," said Edward Sausville, M.D., Associate Director of the National Cancer Institute's (NCI) Developmental Therapeutics Program. "This approval re-emphasizes the importance of natural products and their derivatives in the search for better cancer treatments."
Topotecan, to be marketed as Hycamtin-R by SmithKline Beecham
Pharmaceuticals, is derived from the bark of a Chinese tree known
scientifically as Camptotheca acuminata. In 1958, Monroe Wall, Ph.D., then at the Department of Agriculture, and the late Jonathan Hartwell, M.D., of NCI discovered the antitumor activity of extracts from this plant in the course of a screening project for a natural source of steroids to make cortisone. In 1966, with the support of NCI's Natural Products Branch, Dr. Wall and Mansukh Wani, Ph.D., successfully isolated the active ingredient, camptothecin, from bark extracts.
Clinical trials using a soluble salt of camptothecin began in the early
1970s, but the drug proved too toxic for clinical use. Following these
discouraging results, camptothecin research continued slowly and efforts focused on discovering how the drug killed cells. Still hoping to harness the antitumor activity in a better-tolerated chemical form, NCI funded research to find less toxic derivatives of the compound.
By the early 1980s, scientists at NCI and other institutions had discovered that camptothecin caused DNA and RNA damage, which eventually led to tumor cell death. Scientists at SmithKline Beecham then approached Johns Hopkins University researchers, and in parallel trials, both teams tested camptothecin samples from NCI for their ability to inhibit a second topoisomerase enzyme, topoisomerase II, an enzyme present in all cells at a constant level.
Johns Hopkins' scientists were conducting research on topoisomerase II
inhibitors, and camptothecin shared similar properties with many of the
known topoisomerase II blockers. It was found, however, that camptothecin strongly inhibited topoisomerase I, rather than topoisomerase II. This discovery was important because the drug -- based on the presence of the enzyme in high levels in tumor cells -- might be more selective for tumor cells.
Efforts to modify camptothecin for clinical use were quickly renewed, and scientists belonging to a National Cooperative Drug Discovery Group (NCDDG), sponsored and coordinated by NCI, were able to successfully alter camptothecin. By 1990, topotecan had been semisynthesized by SmithKline Beecham, the industrial partner in the NCDDG. In addition, several other modified camptothecins, such as irinotecan, had been synthesized by research teams at NCI and other institutions.
Topoisomerase I, the target enzyme of these new agents, exists in both
normal and tumor cells and appears to take advantage of the growth rate
difference between them. Researchers are not sure why, but there are two possible explanations. Topoisomerase I is most vulnerable in cells at a stage of the cell cycle known as the "S" phase. In this phase, cells copy their DNA while preparing to divide; therefore, the target enzyme is present more frequently and at a higher concentration. Since rapidly-proliferating tumors have a greater percent of cells in "S" phase, compared to normal, slow-growing cells, tumors are more susceptible to the action of topotecan.
A second explanation might be that rapid metabolic processes of tumor cells enable greater influx of the drug.
Whatever the mechanism, topotecan has had positive trial results. In a
series of clinical trials supported jointly by NCI and SmithKline Beecham, the compound showed activity against a variety of solid tumors including ovarian cancer, small-cell lung cancer, and others. In trials conducted in Europe by the European Organization for the Research and Treatment of Cancer, topotecan was shown to have similar antitumor activity against a variety of tumor types.
In later Phase III trials, examining topotecan as second-line therapy
against ovarian cancers, response rates were 10 to 15 percent among patients who had not previously responded to standard treatment and 25 to 30 percent among patients who had responded to first-line therapy. In one study, comparing topotecan and taxol for the treatment of advanced, recurrent ovarian cancer, topotecan showed a 20 percent response rate, whereas taxol had a 12 percent response rate. According to some researchers, topotecan is as significant as taxol in terms of a unique mechanism of action and novelty of approach.
Response rates as high as 39 percent also have been seen in Phase III trials using the drug as a first-line treatment for small-cell lung cancer. Future studies will look at how topotecan performs when used in combination with other drugs, such as
cisplatin.
Vitamin C, known to be a DNA-protecting "antioxidant," is a switch hitter, also capable of inducing the production of DNA-damaging compounds, suggests a study in the 15 June issue of the international journal, Science. Mutations caused by these compounds have been found in a variety of tumors.
Such mutations can be repaired, however, and lead author Ian Blair of the Center for Cancer Pharmacology, at the University of Pennsylvania, cautioned that the study shouldn't be interpreted as a claim that vitamin C causes cancer. Nor does it question the wisdom of eating a balanced diet rich in fruits, vegetables, and whole grains, he said.
The findings, which come from test-tube experiments (in vitro), may help explain why vitamin C has thus far shown little effectiveness at preventing cancer in clinical trials, according to the Science authors.
"It's possible that vitamin C isn't working in cancer prevention studies because it's causing as much damage as it's preventing, but that's really speculation at this point. What we can say is that vitamin C clearly doesn't work when you expect it to, and now we're in a position to see if that's what's happening in vivo, [or, in living cells]" Blair said.
Some scientists have long recommended dietary supplements of vitamin C, particularly for treating and preventing cancer. But the supplements' effectiveness has been hotly debated, with critics saying they either have no effect or that they may be harmful.
"The logic being used [for vitamin C supplements] is that 'fruits, vegetables, etc. contain vitamin C; these foods prevent cancer; thus vitamin C prevents cancer," Blair said. "But our message is that it's the total diet that's important, not just one antioxidant in isolation."
Vitamin C is known to do beneficial work in the body, including acting as an antioxidant that "disarms" free radicals. These highly reactive ions are produced by the breakdown of oxygen, which occurs constantly in cells.
In addition to damaging DNA directly, free radicals can also act indirectly. They begin by converting linoleic acid, the major polyunsaturated fatty acid in sunflower, grape, and safflower cooking oils, as well as the major polyunsaturated fatty acid in human plasma, into another compound called a lipid hydroperoxide. When certain metal ions are present to act as catalysts, the lipid hydroperoxides degrade further, into DNA-damaging agents called "genotoxins."
These compounds react with DNA, switching one base for another in mutations that have been found in human tumors.
Scientists, including Blair and his colleagues, have suspected that vitamin C might also be capable of making lipid hydroperoxides degrade into genotoxins, in place of the transition metal ions.
To investigate, the Science authors added vitamin C to solutions of lipid hydroperoxides in the lab. They used concentrations comparable to those found in the human body, assuming a person would take 200 milligrams a day.
The vitamin was more than twice as efficient as transition metal ions at inducing the formation of genotoxins, including a particularly potent variety.
The researchers' next step is to see whether vitamin C produces significant amounts of genotoxins in intact cells, and whether they generate cancer-causing mutations.
The other members of the research team are Seon Hwa Lee and Tomoyuki Oe, of the Center for Cancer Pharmacology, at the University of Pennsylvania. Funding for this research was provided by the National Cancer Institute and the University of Pennsylvania Cancer Center.
VEENENDAAL, The Netherlands, June 28 /CNW/ -- Nucletron BV, an
international leader in radiotherapy, announces the first clinical treatments
combining the advanced inverse planning features of the PLATO treatment
planning system with a Siemens linear accelerator.
The Radiotherapy Department of the Virgen Macarena Hospital
chose precise
Intensity Modulation Radiation Therapy (IMRT) for the treatment of a patient
with prostate cancer. The IMRT technique allows the hospital to improve
local
tumor control and decrease adverse side effects of the treatment. The
treatment was designed using inverse treatment planning on the Nucletron PLATO
system, allowing higher radiation dose to be given to the tumor and minimising
dose to radiation sensitive organs. IMRT is of interest in the treatment
of
prostate cancer because of the proximity of radiation sensitive organs that
are difficult to avoid using conventional treatments.
The treatment was the first to use the Nucletron planning
system linked
with a Primus linear accelerator from Siemens. The linear accelerator is
equipped with a multi-leaf collimator (MLC) which shapes and modulates the
intensity of the radiation beam during the treatment. The complex
sequence of
movements of the MLC is calculated on the PLATO planning system and
transferred electronically to the control system of the linear accelerator.
In IMRT, the treatment radiation beams are divided into a
series of small
fields, whose irregular shape is determined by the multi-leaf collimator.
Accurately modeling the combined effect of many small, irregular fields in
order to provide independent verification of the PLATO treatment planning
system and treatment on the linear accelerator is a major step towards the
routine application of this new treatment method.
The clinical implementation of the IMRT technique, with a
satisfactory
degree of confidence, has been possible thanks to the scientific background of
the research group of the Sevilla University (Medical Physiology and Biophysic
Department) in close collaboration with the Virgen Macarena Hospital.
This
team has a wide experience on dosimetrical verification of complex
Radiotherapy treatments by means of Monte Carlo calculation. Prof.
Sanchez-Doblado and Dr. Leal said, "IMRT has been an exciting challenge
to be
checked in the new ITP module. The agreement between PLATO and Monte
Carlo
simulation has been very gratifying."
Before performing treatments of this complexity, the
hospital performed
extensive verification tests on all elements of the planning and treatment
chain. Dr. Rafael Arrans and Dr. Rosello of the Radiophysics Department
said,
"This [treatment] has been possible after verification of the high level
of
agreement between the calculation results given by the planning system and
experimental methods carried out on anthropomorphic phantoms and simulated by
Monte Carlo technique. A discrepancy of only 0.6% was found on the reference
point between the dose proposed by PLATO and the measurement of an ion
chamber."
The close agreement between calculated and measured doses
is in agreement
with studies at other hospitals using Nucletron PLATO in combination with
linear accelerators manufactured by Elekta and Varian.
Dr. Luis Errazquin and Dr. Areste from the Radiotherapy
Department
commented further, "In spite of its complexity, the application of this
technique has not been so time-consuming as to affect the normal number of
treated patients at the linear accelerator."
Nucletron also produces planning and treatment systems for
brachytherapy,
used for the treatment of prostate and other cancers. With brachytherapy,
radioactive sources are positioned in the tumour to be treated, also giving a
highly conformal dose distribution. "Nucletron is proud of its
innovations in
radiotherapy products that help fight cancer. The clinical use of
PLATO's
inverse treatment planning software in Sevilla and other centres demonstrates
that these new and complex techniques can be widely used to benefit patients,"
said Rudolf Scholte, Managing Director of Nucletron.
The Sevilla group has a large number of international
scientific
publications related to Medical Physics and maintains close links and
collaborations with important European radiotherapy centres. The group
has
organised several seminars and conferences. Currently they are
organising a
workshop on "Verification of IMRT" that will take place in Sevilla
during
September 2001.
Executive Director of the Cancer Research Institute Robert L. Durkee said, "This is a great new opportunity for men who, after radiation therapy has failed, really have very few options."
Each year, approximately 30 percent of the 180,000 men diagnosed with prostate cancer undergo radiation therapy as a primary treatment, of which approximately 22,000 men, have recurrence of the disease. For these men, secondary treatment with cryosurgery can stop the progression of the disease and improve long-term survival, according to a study published in the journal Urology (January 2000).
The study of men who were unsuccessfully treated with radiation therapy for prostate cancer showed that nearly two years following treatment with cryosurgery, 97 percent of these men were disease free, meaning they had a prostate specific antigen (PSA) score of less than 4.0 ng/mL. Of these patients, 60 percent had an undetectable PSA, or a score of less than 0.1 ng/mL.
Patients who undergo cryosurgery typically spend one night in the hospital and can return to daily activities within a week. An advanced form of cryosurgery developed by Endocare called targeted cryoablation was used in the Urology study. This procedure combines cryosurgery with ultrasound and temperature monitoring, enabling physicians to visualize the freezing process and thereby improve safety and efficacy.
"Cryosurgery -- both as a primary treatment and as a salvage treatment for men with recurring prostate cancer -- can result in long-term cure rates and has very few complications. Also, unlike other procedures, cryosurgery can be performed on older men or those who may have pre-existing health problems," said Dr. Aaron Katz, assistant professor of urology at Columbia Presbyterian Medical Center of New York-Presbyterian Hospital. "This is another breakthrough for men
who have been unsuccessfully treated with radiation therapy."
Endocare Chairman and CEO Paul Mikus applauded the Medicare action.
"We believe this is a tremendously important coverage decision and great news for the thousands of male Medicare beneficiaries suffering from prostate cancer," Mikus said. "Now these men have another, proven option after radiation therapy."
About Endocare
Endocare, Inc. -- www.endocare.com -- is a vertically integrated medical device company that develops, manufactures and markets cryosurgical and stent technologies for applications in oncology and urology. The company has initially concentrated on developing devices for the treatment of the two most common diseases of the prostate, prostate cancer and benign prostate hyperplasia. The company is also developing cryosurgical technologies for treating tumors in
other organs, including the kidney, lung, breast and liver.
This release contains forward-looking statements. These statements are subject to risk and uncertainties including, but not limited to, those discussed in the Company's most recent Annual Report on Form 10-K, Quarterly Report on Form 10-Q and other filings with the Securities and Exchange Commission. Such risk factors include, but are not limited to, limited operating history of the Company with a history of losses; fluctuations in the Company's order levels; uncertainty regarding market acceptance of the Company's new products; uncertainty of
product development and the associated risks related to clinical trials; the rapid pace of technological change in the Company's industry; the Company's limited sales, marketing and manufacturing experience; the ability to secure and protect intellectual property rights relating to the Company's technology and the ability to convince health care professionals and third party payers of the medical and economic benefits of the Company's products. The actual results that
the Company achieves may differ materially from any forward-looking statements due to such risks and uncertainties. We undertake no obligation to revise or update publicly any forward-looking statements for any reason.
For further information please contact investors, Matt Clawson of Allen & Caron, Inc., matt@allencaron.com, www.allencaron.com, or media, Len Hall, len@allencaron.com, both of Allen & Caron, Inc., 949-474-4300, for Endocare, Inc.; or Paul Mikus, President and CEO of Endocare, Inc., 949-595-4770.
Gene find sparks hope for new leukaemia
treatmentsLONDON, Jan 15 (Reuters) - British
scientists said on Monday they havedeveloped immune system cells that can recognise and kill leukaemia cellswithout damaging healthy ones.Dr Hans Stauss, one of the researchers at Hammersmith Hospital and ImperialCollege in London who engineered the cells, said they could form the basisfor new treatments for the deadly blood cancer."The principle we have developed can be applied to almost all forms ofleukaemia and could signal a huge step forward in how we treat the disease,"Stauss said in a statement.The immune system T-cells recognise a marker, or label, on the cancerouscells produced by a gene called WT-1. The label allows them to pick out anddestroy the cancerous cells."What makes this work even more exciting is that our findings can also beapplied to solid cancers, such as breast or lung cancer, where there issimilar over expression of WT-1. The possibilities for new treatments areenormous," Stauss added.He and his colleagues were able to engineer the immune cells afteridentifying the WT-1 gene during six years of research into leukaemia.Early tests of the immune cells have been promising. The scientists said theyhope to begin clinical trials with leukaemia patients within two years."To the best of our knowledge, this is the first time in the world thatanyone has identified a target which allows T-cells to selectively destroycells that cause leukaemia," said Professor Robert Winston, the director
ofresearch and development of London's Hammersmith Hospital which isparticipating in the research.Each year 18,000 people in Britain are diagnosed with leukaemia or a relatedblood
cancer.
by Steven D. Edelston, M.D.
In 1974, Dr. Samuel Bogash (MD, Ph.D.) discovered a new antigen located on all cancer cells. He and his researcher / wife, Eleanor Bogash, MD,
founded Oncolab to do this test for research and later clinical purposes.
Dr. Bogash is a Harvard-trained research neurochemist. He discovered that the outer coating on cancer cells contain sugar molecules over an inner layer of protein (glycoproteins). Cancer cells bump into each other and the outer layer is ground off-exposing the inner protein layer and the malignin antigen.
It took Drs. Bogash seven years to determine that the antigen was on all cancer cells, not just brain cancer which they were originally studying.
Due to cell recognition, our immune system spots Malignin. When it sees
this foreign protein it produces antibodies to destroy it-Anti-malignin
antibodies. This is what is measured in the study; it is our body's
defense against cancer. By 1988, Dr. Bogash showed that the anti-malignin antibody killed cancer cells in the test tube.
Greater than 95% of patients with cancer have AMAS levels above 135. AMAS levels below 135 are seen in normal individuals who do not have cancer. Sometimes there is doubt about the test (borderline numbers) and at these times the test needs to be repeated and followed up at certain intervals.
Normal levels of AMAS are seen in successfully treated cancer patients and in patients who never had cancer. Cases of advanced or terminal cancer may also have normal levels or even very low normal. The clinical status of the patient must be correlated with the AMAS test result.
The test is patented and the FDA has approved it. The test is available
for use in several areas related to cancer:
1.Cancer Screening Test. Today a check-up in your physician's office
includes a history, a physical examination and selected laboratory tests aimed at detecting potential problems including cancer. It will now include an AMAS test, and thus might defer using a chest X-ray,
proctoscope, CT scan, pap smear, and even mammography. These cancer
screens will not be needed unless the AMAS test is abnormal.
2.A Cancer Monitoring Test. After cancer has been treated both the patient and the doctor want to know if the cancer has been cured or if some malignant cells are still in the body. The AMAS test can answer this dilemma. If there is cancer present, the AMAS test remains elevated.
3.In Differential Diagnosis. At times a shadow on a chest X-ray or a spot in the liver or kidney on a CT scan are suspicious for cancer and only a biopsy can tell. That is an invasive procedure. The AMAS test can tell you if the tissue is malignant. If the AMAS is normal, the lesion in question is not a cancer.
To date, over 1000 patients with breast cancer have been studied using the AMAS test. It has been used to tell if the cancer has been cured. New data suggests that the breast cancer cannot be said to be in remission unless the AMAS test returns to normal. AMAS has found breast cancer as small as a pencil dot long before a mammogram can show it.
The AMAS detects all common cancers and the uncommon ones too. Studies on more than 6000 patients show the sensitivity of AMAS to be greater than 95%. The false positive rate and false negative rates are about 1% of the total, making the specificity about 99%.
Contact info for those interested:
Oncolab
36 The Fenway
Boston, MA 02215
Tel = 800 922- 8378
Early detection is allegedly the key factor in surviving this disease. However, statistics published by associations such as the American Cancer Society contradict this well-marketed advice: They state that 90% of all cases of breast cancer as being "early detection." If that was true, and early detection is the "key to survival," then why is it the second biggest killer among women in nearly every age group? Clearly, the TREATMENT of breast cancer needs to be considered a major factor in this mortality rate.
However, early, accurate detection will enable us ALL to choose our
treatment methods with greater variety of options. A blood test known as the Anti-Malignin Antibody in Serum, (AMAS) test is the best diagnostic aid available for early, accurate detection of cancer. A simple blood test, it can detect ALL types of cancer, regardless of site or tissue type affected, even if the tumor is as small as a pencil dot, up to three years before (traditional) clinical diagnosis or the appearance of symptoms, with 95- to 99% accuracy. In 1977, the FDA permitted marketing of this test, (under "Target Reagent" not AMAS.) Medicare and many other insurance companies are paying for the test. It permits confirmation of diagnosis while dramatically reducing or eliminating typical cancer-related procedures, including: PSA's, mammograms, biopsies, x-rays, sonograms, and PAP smears.
Use of this test will enable cancer survivors to find peace of mind
concerning their status after treatment and can reduce the need for harmful follow-up procedures such as chemotherapy and radiation. It can also allow survivors to obtain health insurance sooner than the typical 1- to 5 year waiting period.
The AMAS test is superior to all aforementioned procedures because it
detects an antibody, anti-malignin, present at the onset of cancer. Typical tests, like the Prostate Specific Antigen, PSA, detect antigens, which are not present until a tumor is large and in an advanced state! As for mammograms, their improved ability to 'read' tissue masses has only produced more "uncertain diagnosis," which results in more procedures, such as the biopsy. Do the math: a biopsy costs $1,500, the AMAS test: $135. Is it any wonder this test, which will revolutionize the business of cancer, has been kept a secret??
The test was developed by Harvard neurochemist Dr. Samuel Bogoch. His
lab, Oncolab, is the only lab in the country offering an AMAS test. He has made it possible for you to get the AMAS test anyway by obtaining a FREE AMAS test shipping kit: 1-800-9CA-TEST. It is required to do the AMAS test. The kit will arrive in approximately 7-10 days. In it, clinical studies and data to support this remarkable test. If you want to get an AMAS test, order the kit, THEN bring the clinical data to your doctor. Chances are, s/he will not have heard of the test. Do not be discouraged if they resist. Either persist, or find a new doctor to approve of your local blood draw. (Even a chiropractor can approve a blood draw!)
"A breakthrough in medical science...the AMAS test is a repeatable,
highly accurate test for early detection and monitoring of cancer."
Dr. Gordon Pedersen
PhD, Toxicology/Immunology
Program Director
Inter-American Society of Chemotherapy
Finding a lab:
This can be challenging because about 1% of our population knows about
the AMAS test. It is vital that you NOT ask the blood lab, "Do you do the AMAS test?" Only Oncolab does the AMAS test. Instead, read the technician's instructions found on the bottom of your doctor's authorization form, (in kit.) Fax a copy to the local blood lab and ask if they will do the test according to those AMAS test specifications.
Cancer survivors should use the test quarterly until their antibody
levels have returned to normal. "High risk" individuals also includes
smokers, those exposed to toxins, from housekeepers to nuclear plant
workers, and, surprisingly, the obese. Yes, obesity has been found to be a greater risk factor for cancer than having a family history of cancer.
Objections:
Several doctors have asked me, "If this can detect a tumor as small as
a pencil dot, how do we know where to treat the tumor? How do we locate it?" Dr. Bogoch informed me that when the AMAS test comes back elevated, a doctor and patient have a more serious 'chat' about the patient's health. Often, they are able to pinpoint where other diagnostic tests should be run.
A common misconception is that we are "always" fighting cancer. This
theory has not been proven. Many people have a normal AMAS test, disproving this theory. (A direct correlation between the presence of cancer and the anti-malignin antibody has been established with 3,315 double-blind studies.)
If a small tumor has been detected, you are urged to enhance your
immune system so it can produce antibody needed to combat the disease. More on such products later...
A unique anti-cancer medicine, called "Kanlight", has appeared in China. It is the world's only anti-tumour injection based on vegetable substances. Spokesman for the "Kanlight" Pharmaceutic Company of Zhejiang Province Xiong Shaowen told Itar-Tass by telephone on Monday that "this is the most effective and promising medicine
against cancer, on which great hopes are now being pinned".
Clinical tests of the medicine were started in the United States, but practical studies are to be continued in Russia in September. After the medicine is patented, it is planned to set up a joint Sino-Russian enterprise to develop and produce "Kanlight". Shaowen noted that the delegation of Russian scientists, which visited China a short while ago, had evinced great interest in the new medicine.
It was developed as a result of many-years-long studies, carried out by Li Dapeng, a staff member of the Zhejiang Institute of Chinese Medicine, who is also foreign member of the Russian Academy of Sciences. The medicine proved very effective when it was tested in China, especially in treating grave forms of malignant tumours, when surgical interventions are no longer possible. "This is an important breakthrough in the fight against cancer," the company's spokesman
believes. It is worth noting that "Kanlight" is a large pharmaceutical
enterprise, which has subsidiaries in all the provinces of China.
The origin of the medicine is linked with a dramatic episode. When the
laboratory, where it was developed, caught fire several years ago, the author of the medicine rushed into the blazing building, risking his life to save the formulas and notes from the flames.
By Alexander Zyuzin
(c) 1996-2001 ITAR-TASS. All rights reserved.
(please notice the correct spelling).
I am including my dear friend Wendy's name in this email as I wish her
to check out your website as well....you see she has put together the
bladder cancer website and resides in Amsterdam....she may be of help to
you ...and maybe you can be of help to us...
I am not so sure my story belongs on your website as Kanglaite is not
the cure, but enables a person's imune system to become so strong that
the imune system actually does any "curing" and or allowing the body
to
cause it to eliminate the disease for the time being....
nothing dramatic here, just some good old Chinese medicine being refined
into another level to allow the body to assimilate it more efficiently
to allow the body to work harder.....
Kanglaite is still not readily available here in the USA, there are
trials going on for safety at this time.....in China, the kanglaite has
been used for quite some time without any side affects that have been
notable.
I will be glad to explain or type in what the usage /dosage sheet says
for you and send it in a few days.....
but you must remember, unless there are doctors with access (because
their respective countries have approved the use of Kanglaite), the
patients will not be able to get it without travel to China and having
an appointment.......it is an IV infusion that the patient may bring
home to have done, but then again, the patient must have a doctors
approval to have an IV nurse to the infussions for 20 days..(1 bottle
per day for non emergency and 2 bottles a day for 20 days if there is a
pretty intense need.
I am not in a position to obtain appointments for people to see my
doctors in China, they are very busy.....and there are a few that will
just approve the kanglaite for use, but charge much more than the
regular price....just like the USA.....not a good practice...
so you may not wish to really put this information out there yet, or to
make sure that this isn't the magic bullet or the cure all....it helps
folks get thru chemo, it is healing in that it makes the immune system
stronger.....
you let me know.
pat
I have now logged 3 more trips to Beijing since the last posting to Tales from
the Trenches and earned 3 10,000 frequent flyer mile certificates for China,
completed the requisite 23 BCG treatments, 40 days of Kanglaite IV days and
proudly proclaim18 months free of the beast...I would say that this has been a
year of large achievements.
Kanglaite injection, an anti-cancer Chinese traditional medicine, has been approved by the Food and Drug Administration of the United States to be used for clinical human experiment, according to sources with the State Administration of Traditional Chinese Medicine.
This is the first time that a traditional Chinese medicine has been approved for clinic experiment in the USA, the sources said.
Last month, the injection, invented by Zhejiang Kanglaite Pharmaceutical Co Ltd in Hangzhou, East China's Zhejiang Province, went through a four-month clinical experiment on 15 to 18 volunteers in a hospital located in Salt Lake City, Utah in the USA.
All the data will be studied and analyzed before new rounds of experiments are allowed to start and before it is licensed for sale, according to Li Dapeng, the medicine's researcher.
The first group of people who received the injection as part of the clinical experiment have showed satisfactory results, and the medicine is considered effective and safe, said Li.
Kanglaite injection is developed from the liquid distilled from the seeds of Job's tears, which is a kind of herbal medicine.
It is targeted to effectively kill cancer cells while upgrading the immune capacity of the human body.
In China, the medicine has been used in thousands of clinical experiments and by more than 200,000 tumour patients. The results show that the medicine is effective in its anti-cancer actions and has no apparent side effects.
The active compound, production techniques and prescriptions of the medicine have received patent certificates in countries like the USA, Japan and the European Union.
The medicine enjoys the largest sales volume among Western and traditional Chinese anti-cancer medicines in China.
Despite China's long history of the use of traditional Chinese medicines, the country's export volume of them accounts for less than 5 per cent of the world's sales volume of traditional Chinese medicine.
Jun 05, 2001 (The Salt Lake Tribune - Knight Ridder/Tribune Business News via COMTEX) -- The Huntsman Cancer Institute on Monday launched a small-scale human trial of a cancer drug derived from a Chinese herb that, if proven safe, could win approval from U.S. regulators.
The cancer-fighting compound -- called a "Kanglaite injection" -- is a liquid derived from a medicinal herb called coix seed.
Huntsman is working with the Salt Lake City-based arm of a Chinese company to perform the trials as part of the new drug application to the Food and Drug Administration.
"Coix has been used in traditional China for a thousand-plus years," said Richard Wheeler, associate director of clinical research at Huntsman.
But it has just been over the past decade that Kanglaite (pronounced
"kayng-light") injection's tumor-suppressing and palliative effects have caught the attention of cancer doctors worldwide, he said.
"It's already been shown to be beneficial to patients in the regression of the cancer, improved appetite, reduced pain and improved sense of well-being," Wheeler said.
Kanglaite-U.S.A., a wholly owned subsidiary of Zhejiang Kanglaite Pharmaceutical of eastern China, is working with Huntsman to put the drug through the investigational phase, known as Phase One clinical trials.
After researchers have measured different doses and compared their safety with patients' responses to the new drug, larger studies may be organized under other phases.
The Phase One group -- some 15 to 18 patients -- will get Kanglaite
intravenously every day for 21 days. Some test subjects will get higher doses than others, and each set of patients will be evaluated to determine if they improve and if they suffer from drug-related side effects.
The trial will be conducted on an outpatient basis through Huntsman and should take five months to complete, Wheeler said.
Patients who qualify for the trial most likely will be in the advanced stage of cancer, or what Wheeler called the "solid tumor" phase. By that measure, "most of them will have lung, colon cancer and etc., but it's not limited," he said.
Patients are still being accepted for the trial, and those interested should talk with their oncologists or call the Huntsman toll-free hot line at 1-888-424-2100.
Kanglaite-U.S.A. President John L. Harmer, the former California lieutenant governor under Ronald Reagan, was traveling in China this week and could not be reached for comment, a spokesman said
Bone cancer causes two kinds of pain: a dull ache that grows over time and intense pain brought on by movement. If it has spread to the spine, even breathing hurts.
The vast majority of bone cancers have spread from the breast, prostate, lung or colon or other areas into bones. Only 2 percent start in the bone, Mantyh said.
Bone-destroying cells, called osteoclasts, usually work in balance with cells which create bone. But something secreted by the tumor cells - scientists don't know just what, but are working to find out - kicks the osteoclasts into "hyperdrive," Mantyh said.
"If a normal person would have, say, 10 osteoclasts, these patients have a thousand. They're bigger and more active than you'd ever find in a normal person," he said.
Osteoprotegerin does nothing to the tumor cells, but cancels their effect on osteoclasts, he said.
Mantyh said the osteoclasts also seem to hypersensitize nerves which carry pain stimuli to the brain. Even a gentle touch can cause excruciating pain.
In mice, that extreme
sensitivity can be tested by stroking a foot with the end of a very thin fishing line, or by shining a lamp on the floor of its cage, to heat it slightly.
The osteoprotegerin studies are very exciting, said Dr. Richard Payne, chief of pain and palliative care services at Memorial-Sloan Kettering Cancer Center and a professor of neurology and pharmacology at Cornell Medical College.
http://www.innerself.com/Health/tamoxifen.htm
These articles from Sherrill Sellman which you can read on above sites are
based on the theory of dr. Lee (http://www.johnleemd.com)
His first book is called "What your doctor didn't tell you about
menopause"
At another site of dr. Lee you can also read about a creme for prostatecancer:
http://www.nexusmagazine.com/HormoneHeresy
http://www.nexusmagazine.com/hormone2
3.
On the next sitepages of the Life Extension Foundation you can find more
information about tamoxifen/nolvadex and a non-chemical product named
Indole-3-Carbinol.
http://www.lef.org/magazine/mag99/may99-cover
http://www.lef.org/magazine/mag99/june99-cover#continue
http://www.lef.org/magazine/mag99/oct99-report1
http://www.lef.org/prod_desc/item00456
http://www.naturalhealthconsult.com/Monographs/Indole3Carbinol
http://www.lef.org/magazine/mag99/may99_abs
a gene that protects against breast cancer
Quebec City, August 9, 2001 - A team of Quebec researchers, led by Dr. François Rousseau of the Human and Molecular Genetic Research Department (HMGRD), Hôpital Saint-François d'Assise Research Centre, Centre hospitalier universitaire de Québec (CHUQ), has made a major breakthrough in the field of breast cancer by identifying a gene that protects against this disease. This discovery is reported in the August 2001 issue of the prestigious scientific journal Cancer Research, a reference publication for this field.
The gene identified by Dr. Rousseau's team is AR, an androgen receptor coding gene. Along with other genes, AR is part of the genetic baggage of all human beings, both men and women. However, this gene can present in different forms, called variants. The researchers have succeeded in identifying certain variants of this gene which provide women with greater protection against breast cancer. Approximately 15% of women present with a form of AR that is associated with a 50% decrease in their risk of developing breast cancer. Conversely, 85% of women present with the other form of AR that makes them twice as susceptible to developing breast cancer than women with the protective variant.
"These results are of great interest as they indicate that a gene involved in the action of androgen, a hormone of well-known importance in men, plays a significant role in women's risk of developing breast cancer. Given that 85% of women carry the non-protective variant of the AR gene, this discovery could benefit a large number of women," explains Dr. François Rousseau, associate professor at Université Laval's Faculty of Medicine and director of this research at the Hôpital Saint-François d'Assise Research Centre. "This breakthrough is all the more significant as it enables a better understanding of sporadic breast cancers, i.e. non-hereditary." Sporadic breast cancers represent 90% of all cases of breast cancer.
Scientists have already identified certain genes, specifically BRCA1 and BRCA2 which play a role in hereditary cancers. "Although these results are based on fairly large sample of over 700 women, they must be confirmed with another group of people," said Dr. Rousseau.
The research work leading to this discovery was done in collaboration with other researchers in the region, including Dr. Jacques Brisson of the Population Health Reseach Group and the Breast Disease Centre at Hôpital Saint-Sacrement (CHA), and Dr. Éric Dewailly of the CHUQ Community Health Research Group. The research was funded by the National Cancer Institute of Canada, Health Canada and the Canadian Genetic Diseases Network of Centres of Excellence.
Commercial partner: SignalGene working on a new drug
This discovery is part of an agreement reached in 1999, between CHUQ and the Montreal biopharmaceutical company SignalGene, which holds the exclusive marketing rights for this discovery. Dr. Michael Dennis, President and CEO of Signal Gene, congratulated the scientists and partners on the publication of these results in a renowned scientific journal. "This validates the genomic approach we are taking in collaboration with our academic and hospital colleagues, in order to identify the genetic factors involved in diseases linked to steroidal hormones such as breast cancer. Our Drug Discovery and Development team is also working on the development of small SARM-type (selective androgen receptor modulators) molecules which may constitute a future prophylactic treatment for breast cancer."
If this work provides the expected results, Dr. Rousseau estimates it would be possible to reduce the number of breast cancer cases by up to 40%. "Although there are still many stages to go through, this discovery is highly promising, especially as we already know a great deal about the functioning of this male steroidal hormone receptor, which will speed up the functional genomic research work," explains Dr. Rousseau, researcher at the HSFA Research Centre, CHUQ.
Dr. Rousseau's team, in collaboration with Dr. Brisson of the Centre hospitalier affilié universitaire de Québec and the company SignalGene, is currently recruiting a new group of 1,000 women with breast cancer and 2,000 healthy control subjects to corroborate these results and identify the other genes involved in sporadic breast
cancers.
Source: Pierre Lafleur
Communications department
Centre hospitalier universitaire de Québec
Tel.: (418) 525-4387
NEW YORK (Dow Jones)--Scientists have wiped out tumors in mice using a common virus that apparently tricks cancer cells into self-destructing.
It is too early to know if the approach might work in humans. Many treatments that look promising in mice prove disappointing when they are tested on people. However, the research sheds light on something scientists have noticed for years: Some viruses harm cancer cells but leave normal, healthy cells unscathed.
The research involves a virus that is believed to be harmless to humans, and a gene called p53 that normally suppresses tumors. In most cancer patients, the p53 gene is defective. The virus apparently zeroes in on that flaw.
Peter Beard, a professor of virology at the Swiss Institute for Experimental Cancer Research in Epalinges, said his team found that the explanation involves an unusual hairpin-like portion of the virus' DNA.
When a cancer cell encounters the virus, it apparently interprets the hairpin structure as damage to its own DNA. The cell tries to rid itself of the damage and ends up self-destructing. As part of their research, the Swiss team injected human colon cancer cells
into a group of laboratory mice, followed by the virus two days later. Only two of the 12 rodents later formed tumors. In mice with existing colon cancer tumors, injections of the virus eliminated tumors in six of the 10 rodents.
The findings were reported in Thursday's issue of the journal Nature.
Beard said his team hopes to pinpoint the precise feature on the hairpin structure that sends cancer cells to their death. If they can do that, he said, it may be possible to specially engineer the virus or even develop a drug mimicking its effects.
The p53 gene mutation that the virus exploits is present in nearly 60% of all human cancers. It is the same vulnerability that also makes cancer cells prone to chemotherapy and radiation treatment, Beard said.
(END) Dow Jones Newswires 30-08-01
0549GMT(AP-DJ-08-30-01 0549GMT)