Chemotalk Newsletter

Chemotalk Newsletter, Vol. 18:  October 1, 2009

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Hello, Everyone...

When I started this newsletter, I hoped it would evolve into more than strictly medical news about the diseases or conditions treated with chemotherapy. There are other very important factors with variables that affect our treatment. In keeping with the mandate of providing as much newsworthy accurate information as possible, I'm beginning with a story that ran in the September 2nd issue of The New York Times.


By Andrew Pollack

SAN DIEGO - Pfizer's fortunes in the past were built on cardiovascular drugs, like the cholesterol buster Lipitor and the blood pressure pill Norvasc.

But the future of Pfizer, the world's largest pharmaceutical company, may rest in a cluster of buildings on a bluff not far from the Pacific Ocean. It is here that Pfizer has amassed about 1,000 researchers for an all-out effort to develop drugs for cancer, a disease the company once largely ignored.

Virtually every large pharmaceutical company seems to have discovered cancer, and a substantial portion of the smaller biotechnology companies are focused on it as well. Together, the companies are pouring billions of dollars into developing cancer drugs.

Two industry trends are driving the push. Recent scientific discoveries have suggested new targets for cancer drug researchers. And as drug companies see profits beginning to wane from mainstays like Lipitor, the high prices that cancer drugs can command have become an irresistible lure.

About 860 cancer drugs are being tested in clinical trials, according to the pharmaceutical industry's main trade group. That is more than twice the number of experimental drugs for heart disease and stroke combined, nearly twice as many as for AIDS and all other infectious diseases combined, and nearly twice as many as for Alzheimer's and all other neurological diseases combined.

But for all the industry's spending and effort, only a trickle of new cancer drugs make it to market. Last year there were two, and this year there has been only one.

And even some of those drugs offer only a few months at most of extra life or tumor stabilization despite prices that often reach thousands of dollars a month. The drug Tarceva, which costs about $3,500 a month, was approved as a treatment for pancreatic cancer because it improved survival by 12 days.

The battle to treat cancer has become, as a commentary in a leading journal put it, a "grinding war of the trenches."

Why? Experts say the same factors that attract drug companies to the cancer business help explain the slow progress.

One reason is scientific. Studies are rapidly revealing the genetic changes in cells that cause cancer and spur its growth. That is providing drug companies with dozens of molecules, or "targets", that drugs could block.

But those same studies have shown that cancer is devilishly complicated.. There are so many aberrant molecules in a tumor that blocking just one or two is like trying to stop all traffic in Manhattan with a roadblock at a single intersection.

Tumor cells, like bacteria, can develop resistance to drugs. Some experts believe that drugs that kill most rumor cells do not affect cancer stem cells, which can regenerate the tumor.

And even two people with breast cancer, or two people with lung cancer, might have two very different diseases on the molecular level, so a drug that works for one might not work for the other.

"Cancer is not a single disease," said Robert A. Weinberg, a cancer biologist at the Whitehead Institute and the Massachusetts Institute of Technology. "It's really dozens, arguably hundreds of diseases."

The other reason for the drug makers' interest is financial. Patients are often desperate, and insurers risk outrage by denying payments for a cancer drug, even if the odds say it will have little benefit. That has allowed pharmaceutical companies to charge thousands of dollars a month for cancer medicines. Such prices can make drugs for even rare cancers, or drugs that do not work very well, into big money-makers.

Take Erbitux, developed by ImClone Systems, which costs $10,000 a month.. A study in Canada showed that as a last-ditch treatment for colorectal cancer, Erbitux lengthened lives by an average of about one and a half month compared with not treating the cancer at all. Using the price of the drug in the United States and the average length of treatment, the extra cost per patient was about $50,000.

Erbitux, which is also approved to treat head and neck cancers, recorded global sales of $1.6 billion last year, higher than all but about 70 other drugs. Last year, as part of the industry scramble into cancer drugs, Eli Lilly & Company outbid Bristol-Myers Squibb to acquuire ImClone for $6.5 billion. In 1998, there were only 12 cancer drugs on the list of the world's 200 medicines with the highest sales, compiled by the trade magazine Med Ad News. Taxol, No. 21, was the only cancer drug among the 30 drugs with sales of at least $1 billion.

The same list for last year, contained 23 cancer drugs among the top 200 - and three in the top 10. Of the 126 drugs with $1 billion in sales, 20 were for cancer.

Cancer drugs have been the biggest category of drugs in terms of sales worldwide since 2006 and in the United States since 2008, according to the market researcher IMS Health.

Such money attracts companies. "Cancer is such an emotional issue that the free market doesn't work like it does for bicycle wheels and umbrellas," said Robert L. Erwin, a biotechnology industry executive who heads the Marti Nelson Cancer Foundation, a patient advocacy group. "As long as the health care system will pay the price, the money will flow in that direction."

But Mr. Erwin and some other experts say that it is not always a good thing for patients because it can set the bar too low for drug companies.

"As long as the marketplace does not distinguish between modestly effective drugs and dramatically effective drugs, there won't be an incentive to shift resources to a greater emphasis on a larger benefit," said Dr. Neal J. Meropol, an oncologist at the Fox Chase Cancer Center in Philadelphia who has been studying drug prices.

Many executives dispute this, saying that would produce drugs offering bigger gains if they knew how. But they must balance their portfolio of experimental drugs between long shots and some drugs that have a better chance of making it to market and sustaining the enterprise.

"If you always swing for home runs, you strike out a lot," said George A. Scangos, chief executive of Exelixis, a biotechnology company with 11 cancer drugs in clinical trials. "I is not the companies' profit motives," he said. "It's largely the difficulty of hitting home runs."

With health care costs rising, there is new pressure on companies to be more selective in drugs they develop. Some experts now talk about "financial toxicity" as a side effect of cancer drug treatment, along with nausea and hair loss.

"A question is how the system can tolerate 400 new drugs on the market, all at the same price," of $50,000 a year, said Dr. Lee Newcomer, senior vice president for oncology at United Healthcare, a big insurer.

Such cost pressures, and the fact that only a handful of cancer drugs get to market each year, mean the big investments now being made into cancer drugs are likely to turn sour for many companies.

"It's the biggest bubble you've ever seen," said Dr. Mark Ratain, an oncologist at the University of Chicago.

But Pfizer is counting on cancer to help save the company. It hopes to reach $11 billion in sales of cancer drugs by 2018. That would be more than four times the category's sales last year of $2.5 billion, which represented only 5% of Pfizer's revenue.

Cancer was once unattractive for big pharmaceutical companies like Pfizer. There were relatively few patients with any one type of cancer, and they died fairly quickly. By contrast, there were millions of patients with chronic diseases like Hypertension who would take drugs for life.

Indeed, the three main cancer drugs Pfizer now sells cane to it with 2003 acquisition of a rival, Pharmacia, a deal done mainly to acquire the arthritis drug Celebrex.

But there are now many good cardiovascular drugs. Lipitor, the world's best-selling drug, will lose patent protection in 2011, and Pfizer failed to develop a successor.

So Pfizer is scaling back cardiovascular research and has made cancer drugs one of its six focus areas. About 20% of Pfizer's more than $7 billion in research and development spending is on cancer, and 22 of the roughly 100 drugs in clinical trials are cancer drugs.

"I've taken a lot of personal interest in this business unit," said Jeffrey B. Kindler, Pfizer's chief executive. "We think we are positioned to be a top leader in oncology."

Cancer research is concentrated here in San Diego, in a cluster of buildings once owned by one of the many biotechnology companies in the region. Pfizer has tried to retain some of the looser culture of entrepreneurial start-ups, like Friday afternoon beer parties. The head of the site, Catherine Mackey, a transplant from Pfizer's laboratories in Connecticut, has become an avid early-morning surfer.

The clinical trials for cancer are being overseen by Dr. Mace L. Rothenberg, an oncologist recruited this year from Vanderbilt University. He hopes Pfizer can develop those home-run drugs. "Having treated patients for 20 years," Dr. Rothenberg said, "I know their needs are not for singles."

The big thrust in cancer drug development for the last few years has been sol-called targeted therapies. These drugs aim, so far with modest success, the block aberrant molecules in tumor cells while leaving normal cells unscathed.

But even more targeted the therapies have limited impact. One reason is that most tumors are fueled by numerous, often redundant, genetic anomalies.. That means that drugs with different targets need to be used in combination.. But combinations increase both the costs and side effects of therapy. And it is difficult to test two experimental drugs in combination because of the regulatory system is geared to assessing a single drug at a time.

Another reason is that tumors differ among people. Dr. Bert Vogelstein, a cancer geneticist at Johns Hopkins, said a typical tumor might have 50 to 100 genetic mutations. But two patients with the same type of cancer might have only five mutations in common.

So even though a drug might work well for patients whose tumors have a particular mutation, when the rug is used for a broader population, it shows only a small effect.

One solution is to try to determine which patients should get which drug based on the genetic profile of the tumor.

Pfizer is moving in that direction. It plans soon to start a late-stage clinical trial of a drug for lung cancer. But the only patients in the trial will be from the 5% of so of lung cancer patients with a mutation in a gene called A.L.K.

"What we're looking for," said Dr. Rothenberg of Pfizer, "is not a small benefit in a large group, but a larger benefit in a smaller group."

For now at least, making the ballpark smaller may be the industry's best chance to hit home runs.

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(That's a lot to absorb. But after reading the previous piece, I understood a lot more about pharmaceutical companies than I did before.)

Now, for some good news!


The drug Folotyn (pralatrexate) has been approved to treat Peripheral T-cell Lymphoma (PTCL), an often aggressive form of non-Hodgkin's lymphoma, according to the U.S. Food and Drug Administration.

The drug, given accelerated approval because it treats an unmet medical need, was sanctioned for people whose disease has returned or hasn't responded to other types of chemotherapy, the agency said in a news release..

PTCL strikes fewer than 9,500 people each year in the United States, the FDA said. The disease affects T-cells, which are involved in the body's disease-fighting immune system.

Approval of Folotyn was based on clinical data showing it reduced tumor size in 27% of 109 people with PTCL who were studied. The most common adverse reactions included sores of the lips, mouth and digestive tract, low white blood cell counts, fever, nausea and fatigue.

Since the drug can harm a fetus, women taking Folotyn should avoid becoming pregnant, the FDA said. Anyone taking the drug should also take folate and vitamin B12 supplements to help reduce irritation of the mucous membranes.

Folotyn is produced by Allos Therapeutics, which is required to conduct additional studies of tumor shrinkage and life expectancy, the agency said.

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Cancer patients who receive chemotherapy are more likely to develop blood clots than other people, but now a new study says a blood-thinning drug could cut the risk in half.

Besides posing a significant risk of problems in the heart, brain and lungs, blood clots are especially difficult to treat in cancer patients and can lead to interruptions in chemotherapy. They can also greatly increase costs in patients who already face high expenses, the researchers noted in their study published online Aug. 31 in The Lancet Oncology.

Researchers haven't been certain that blood-thinning drugs could help ambulatory chemotherapy patents avoid developing the clots.

The researchers looked at 1,150 Italian patients over the age of 18 who were receiving chemotherapy for advanced lung, gastrointestinal, pancreatic, breast, ovarian, or head and neck cancer. Two percent of those who received nadroparin via a daily injection under the skin developed a blood clot during the first four months of chemotherapy, compared to 3.9% of the patients who were given placebos, the study found.

Patients with lung cancer had the highest rate of blood clots -- 8.8% among those who took placebos and 3.5% of those who took nadroparin.

"Further studies should focus on patients at high risk of thromboembolism, such as patients with lung cancer," the authors conclude. The study "supports the concept that thromboembolic events can be prevented in ambulatory patients with cancer receiving chemotherapy and this has potential implications for future therapeutic scenarios."

The study was funded by Italfarmaco, which makes nadroparin

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There isn't much to report that impacts transplant recipients. Here's some news that does.


TUESDAY, Sept. 8 (HealthDay News) -- Giving the neurotransmitter dopamine to brain-dead organ donors may help preserve the quality of their kidneys for more successful transplantation, new research suggests.

Most transplanted kidneys come from donors whose hearts are beating but who have suffered brain death, a traumatic chain of events that can damage organs and increase the likelihood of the recipient needing dialysis after surgery.

According to the study by researchers from the University Medical Centre in Mannheim, Germany, treating brain-dead organ donors with dopamine reduced the likelihood the kidney recipient would need dialysis in the first week after the transplantation.

The study is published in the Sept. 9 issue of the Journal of the American Medical Association.

In a trial that involved 264 deceased heart-beating donors, low-dose infusions of dopamine were given to the donors for an average of nearly six hours. After surgery, about 35.4% of kidney recipients whose donors did not receive dopamine required multiple dialyses before their renal function recovered, compared to 24.7% in the dopamine group.

The study also found that needing multiple dialyses increased the chances of transplantation failure in the long-term; a single, post-transplant dialysis did not.

"This study shows that pretreatment of the deceased heart-beating donor with low-dose dopamine reduces the need for dialysis in the recipient after kidney transplantation," researchers wrote.

The organ donations resulted in 487 kidney transplants at 60 hospitals in Europe between March 2004 and August 2007.

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Thanks to the newsworthiness of health and healthcare, there's a ton of information 'out there' on issues that matter to people who relate personally to chemotherapy. The following piece, also from The New York Times, concerns transplants - specifically, kidney transplants, which make up the majority of this procedure. And it has to do with costs, which affects all of us:


By Kevin Sack

SAN DIEGO - Melissa J. Whitaker has one very compelling reason to keep up with the health care legislation being written in Washington: her second transplanted kidney.

The story of Ms. Whitaker's two organ donations - the first from her mother and the second from her boyfriend - sheds light on a Medicare policy that is widely regarded as pound-foolish. Although the government regularly pays $100,000 or more for kidney transplants, it stops paying for anti-rejection drugs after only 36 months.

The health care bill moving through the House of Representatives includes a little-noticed provision that would reverse the policy, but it is not clear whether the Senate will follow suit. The 36-month limit is one of several reimbursement anomalies - along with inadequate primary care payments and incentives that encourage unneeded care - that many in Congress hope to cure.

Ms. Whitaker, 31, who describes herself as "kind of a nerd," has Alport syndrome, a genetic disorder that caused kidney failure and significant hearing loss by the time she was 14. In 1997, after undergoing daily dialysis for five years, she received her first transplant. Most of the cost of the dialysis and the transplant, totaling hundreds of thousands of dollars, was absorbed by federal Medicare program, which provides broad coverage for those with end-stage renal disease.

Despite that heavy investment, federal law limits Medicare reimbursement for the immunosuppressant drugs that transplant recipients must take for life, at costs of $1,000 to $3,000 a month.

Once Ms. Whitaker's Medicare expired, she faced periods without work and, more important, without group health insurance, which disregards pre-existing conditions. Struggling financially, she soon found herself skipping doses of anti-rejection drugs.

By late 2001, her transplanted kidney had failed, and she returned to dialysis, covered by the government at $9,300 a month, more than three times the cost of the pills. Then 15 months ago, Medicare paid for her second transplant - total charges, $125,000 - and the 36-month clock began ticking again.

"If they had just paid for the pills, I'd still have my kidney," said Whitaker, who shares an apartment in the La Jolla neighborhood with her boyfriend, Joseph D. Jamieson. "I'd be healthy, working and paying taxes."

The Medicare program is not sure how many of the country's 100,000 transplant recipients are without insurance for their immunosuppressant drugs. Officials with the National Kidney Foundation and some dialysis patients never put themselves on transplant lists because they fear that they will not be able to afford the drugs.

Currently unemployed, Ms. Whitaker is nervous that in two years she will again find herself without health coverage. She and Mr. Jamieson, who have been together five years, said they would marry if necessary so he could insure her under the group policy provided by his employer, the drug manufacturer Pfizer. But nothing is guaranteed.

"If Joe were ever to lose his job or medical coverage, I do feel it would be possible for me to find myself without insurance again," said Ms. Whitaker, who reads lips to compensate for her hearing loss. "I'm extremely nervous about whether I'm going to be able to afford my medications once my coverage runs out."

Bills have been introduced in Congress since 2000 to lift the 36- month limit and extend coverage of immunosuppressant drugs indefinitely. They have never made it to a vote, largely because of the projected upfront cost; the Congressional Budget Office estimates that unlimited coverage would add $100 million a year to the $23 billion Medicare kidney program.

But the cost-benefit analysis would seem obvious. The most recent report from the United States Renal Data System found that Medicare spends an average of $17,000 a year on care for kidney transplant recipients, most of it for anti-rejection drugs. That compares with $71,000 a year for dialysis patients and $106,000 for a transplant (including the first year of monitoring).

"It doesn't make any sense at all", Ms. Whitaker said. "Somebody's not looking at the numbers."

A provision to cover the drugs is in the sweeping House healthcare bill, which has cleared three committees. It is uncertain whether the Senate Finance Committee will include it in its bill.

Since 1973, end-stage renal disease has been the only condition specifically covered by Medicare regardless of age. In 1988, coverage was extended for 12 months to anti-rejection drugs, which had recently been developed. Congress gradually lengthened the cutoff to 36 months, and then in 2000 made the benefit unlimited for those who are at least 65 or disabled. The rationale for leaving our younger transplant recipients was simply that the money was not there, Congressional aides said.

Ms. Whitaker was married when her Medicare eligibility expired after her first transplant, and her husband was able to insure her under his group policy. They divorced in 2001, and she became uninsured until taking a job at Kinko's that provided health benefits.

Her downward spiral began the day she awoke to find that her dog had used her hearing aids as a chew toy. She could not afford replacements and had to leave her job because she was unable to interact with customers.

She lived in Seattle for a while without electricity or hot water. The bank repossessed her car, and she filed for bankruptcy. Her grandmother eventually bought her new hearing aids, and she went back to work. But she was laid off a year later.

"That's when I started stretching out the pills," she said. "I'd take one in the morning and one at night, instead of two. Toward the end, I ran out of pills and was taking nothing for a couple of months. I figured I was young and could make it until I found insurance."

She figured wrong. When she arrived at an emergency room, weak from weight loss and anemia, her doctors told her they were surprised she was not in a coma. The kidney, they said, had not been functioning at all.

"I felt really guilty because it was my mom's kidney and I broke it," Ms. Whitaker said.

Ms. Whitaker moved back to Southern California to live with her mother, and soon met Mr. Jamieson. She is seven years younger and, at 6-foot-8, stands 16 inches taller, but they had what Mr. Jamieson calls "a mutual dork synchronicity" (they share a passion for video games). He bought her a stuffed kidney, with a ureter nose, and almost immediately offered her one of his kidneys.

She declined. "I didn't want to start dating somebody and steal his kidney," she said. "That seemed kind off rude."

Several years later, she reversed course and accepted the transplant on June 10, 2008. She has suffered several minor rejection episodes, but lately has been feeling well.

The couple gets by on Mr. Jamieson's paycheck and Ms. Whitaker's Social Security benefits. With the help of financial aid, she recently completed two years at a community college and will soon start classes at the University of California, San Diego. She said she hoped a degree would help her find a job with health coverage, perhaps as an addiction counselor.

But her bigger hope is that Congress will eliminate the 36-month limit so she can pursue any job, without concern for insurance.

"My whole life is dictated by my illness, and it's such a waste," Ms. Whitaker said. "If the government is going to spend all that money to help peo0ple get a kidney, they should help you keep it."

* * *


Dose-dense chemotherapy improves survival in women with advanced ovarian cancer, Japanese researchers say.

Currently, paclitaxel and carboplatin given every three weeks is considered standard first-line chemotherapy for advanced epithelial ovarian cancer. However, dose-dense weekly treatment with paclitaxel is seen as a way to increase progression-free and overall survival in these patients, according to the new study findings.

This phase 3 study of 637 women compared the two approaches. The participants had advanced epithelial ovarian cancer, fallopian tube cancer, or primary peritoneal cancer. The 320 patients in the conventional regimen group received six cycles of paclitaxel (180 milligrams per meter squared; three-hour intravenous infusion).

The 317 patients in the dose-dense group received paclitaxel (80 milligrams per meter squared; one-hour intravenous infusion) on days one, eight and 15. Both groups received carboplatin on day one of a 21-day cycle. The patients in the dose-dense group had longer median progression-free survival than those in the standard treatment group (28 months versus 17 months), and longer overall survival at three years (72% versus 65%). This means that women in the dose-dense group had a 29% lower risk of cancer progression and a 25% lower risk of death, the authors explained.

Toxicity forced 113 patients in the dose-dense group and 69 patients in the conventional therapy group to stop treatment, the researchers noted. Severe anemia occurred in 214 patients (69%) in the dose-dense group and in 137 (44%) of the standard therapy group.

The survival benefits seen in the dose-dense group are rare in patients with advanced ovarian cancer, and this regimen offers a new treatment option for women with advanced epithelial ovarian cancer, concluded Dr. Noriyuki Katsumata, of the National Cancer Center Hospital in Tokyo, and colleagues.. The study will be published in an upcoming issue of The Lancet.

"The use of such dose-dense therapy should be decided on an individual basis together with other options for women with advanced-stage ovarian cancer," Dr. Michael A. Bookman, of the Arizona Cancer Center in Tucson, wrote in an accompanying commentary in The Lancet.

* * *

Good news for anyone who has dreaded preparing for a colonoscopy:


Tests Look for Genetic Fingerprints to Diagnose Gastrointestinal Cancers

Two new blood tests may help to make the diagnosis of colon and other gastrointestinal cancers simpler, cheaper, and less unpleasant. The tests, developed by Belgian and German scientists, look for genetic fingerprints of tumor growth in the blood. One test may also help to predict whether cancer is likely to spread.

The tests were described at a joint meeting of the European Cancer Organization (ECCO) and the European Society for Medical Oncology. ECCO President Alexander Eggermont, MD, head of surgical oncology at the Erasmus University Medical Center in the Netherlands, said that the tests may help fill a need for more convenient cancer screening. He was not involved with the work.

One in 17 people will develop colorectal cancer in his or her lifetime. It's the second leading cancer killer in the U.S. and Europe.

The risk of dying is reduced substantially if the disease is caught early, when it is most treatable. But many people shun current tests such as colonoscopy and stool sample analysis, calling them invasive or just plain nasty, says Joost Louwagie, PhD, of OncoMethylome Sciences in Liege, Belgium, which is developing one of the tests.

Louwagie and colleagues collected blood samples from 193 patients undergoing surgery for colorectal cancer and 688 people who were undergoing colonoscopies. They looked for two genes, SYNE1 and FOXE1, which have been linked to tumor growth.

"We found a high frequency of these genes in colorectal patients. The same genes occurred infrequently in noncancerous patients," said Louwagie. Overall, the test correctly identified 50% to 60% of cancers, he says. And it correctly identified more than 90% of people with no cancer.

In people with early-stage colon cancer, the test performed even better, Louwagie says. "Once validated, the new methylation test could be used as a noninvasive screening option for patients who decline or do not have access to colonoscopy or do not wish to undertake the fecal occult blood test.

"The blood sample can be taken by nurses or primary care doctors without the need for special equipment or training, leading to higher rates of patient compliance," he says. The company is talking with several larger companies about licensing rights to the test.

The second test, developed by Ulrike Stein, PhD, of the ECRC Charite University of Medicine in Berlin, and colleagues, looks for colon, rectal, and gastric cancers. The test homes in on a genetic fingerprint, S100A4, that has been linked to the development and spread of tumors.

The researchers studied daily blood samples from 185 people with colon cancer, 190 people with rectal cancer, 91 gastric cancer patients, and 51 tumor-free volunteers. "We found that S100A4 was present at significantly higher levels in the group of cancer patients, no matter whether they had colorectal or gastric cancer, than in the tumor-free control group," says Stein.

There were even higher levels in patients who cancer had spread, she says.

* * *

There's far too little good news about pancreatic cancer. Here's hope ...


Inhibiting the action of an enzyme called TAK-1 reverses pancreatic cancer resistance to chemotherapy, a finding that could lead to the development of a new way to treat the disease, researchers say. Pancreatic cancer is resistant to every currently available anti-cancer treatment.

"During the past few years we have been studying the role played by a cytokine or regulatory protein called transforming growth factor-beta [TGFbeta] in the development of pancreatic cancer. Recently we focused our attention on a unique enzyme activated by TGFbeta, TAK-1, as a mediator for this extreme drug resistance" in PANCREATIC CANCER, study author Dr. Davide Melisi said in a news release from the European Cancer Organization.

He and his colleagues developed a TAK-1 inhibitor and tested it on its own and in combination with the anti-cancer drugs gemcitabine, oxaliplatin and SN-38 (a metabolite of the anti-cancer drug irinotecan) in pancreatic cancer cell lines. They also tested the TAK-1 inhibitor combined with gemcitabine against pancreatic cancer in mice.

"The use of this TAK-1 inhibitor increased the sensitivity of pancreatic cells to all three chemotherapeutic drugs," Melisi said. "By combining it with classic anti-cancer drugs, we were able to use doses of drugs up to 70 times lower in comparison with the control to kill the same number of cancer cells. In mice, we were able to reduce significantly the tumor volume, to prolong the mice survival, and to reduce the toxicity by combining the TAK-1 inhibitor with very low doses of a classic chemotherapeutic drug, gemcitabine, that would have been ineffective otherwise," Melisi added.

The study was scheduled for presentation at the joint meeting of the European Cancer Organization and the European Society for Medical Oncology in Berlin.

"This is the first time that TAK-1 has been indicated as a relevant target for the treatment of a solid tumor and that it is a valid approach to reverting the intrinsic drug resistance of pancreatic cancer," Melisi stated. "The TAK-1 inhibitor used in this study is an exciting drug that warrants further development for the treatment of pancreatic cancer."

* * *

Finally, I'm including a piece about a new drug that performed favorably for possible use in treatment for MS. Unfortunately, the central character in the drug doesn't translate into email print. So in advance, I'm alerting you to the fact that the letter resembles a "beta", and for purposes of showing it, I'll show the drug as T_4:


Regenerx Biopharmaceuticals, Inc. announced that researchers at the Henry Ford Health System in Detroit, Michigan, demonstrated for the first time that T_4 treatment of EAE (experimental autoimmune encephalomyelitis – an animal model for MULTIPLE SCLEROSIS) significantly improves neurological functional recovery. In addition to this neurological benefit, the researchers reported a significant reduction of inflammation and induction of oligodendrogenesis (maturation of central nervous system cells associated with the formation of the nerve sheath), the control of which are important therapeutic goals.

The study entitled, “Neurological Functional Recovery after Thymosin Beta 4 Treatment in Mice with Experimental Auto Encephalomyelitis,” was published online ahead of print in Neuroscience, September, 2009. The publication highlights the statistically significant effects of T_4 treatment in EAE mice, including improvement of neurological functional recovery, reduction of inflammatory infiltrates in the brain, and increase of oligodendrocyte progenitor cells (a type of stem cell) and mature oligodendrocytes in the brain.

There is no cure for MS. While considerable progress has been made in the recent years with the development of anti-inflammatory and immunomodulatory therapies, there are currently no effective repair therapies routinely used in multiple sclerosis patients. Clinical trials have clearly demonstrated that an anti-inflammation treatment approach alone is insufficient in preventing or ameliorating permanent and accumulating MS deficits. Moreover, many medications have serious side effects and some carry significant risks. Oligodendrogenesis/remyelination is an important therapeutic goal and the subject of the research described in the journal article.

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See you next month...


And if you have any thoughts of how this newsletter could be improved, please email me directly, at

Elaine Jesmer

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