Chemotalk Newsletter, Vol. 17: September 1, 2009
September...one of the two hottest months in this part of the country. There's something really WRONG about that...
Here's the news:
WARNING FROM F.D.A. ON ARTHRITIS DRUGS FOR YOUNG PATIENTS
Federal regulators on Tuesday added stronger warnings to a group of best-selling drugs used to treat arthritis and other inflammatory diseases, saying they can increase the risk of CANCER in children and adolescents.
After more than a year of review, FDA scientists said the drugs appeared to increase the risk of cancer after they were used for more than 2-1/2 years.
The agency studied several dozen reports of cancer, some fatal, in children taking the drugs. Half of the cases were lymphomas, a cancer that attacks the immune system.
The drugs are known as tumor necrosis factor blockers and work by neutralizing a protein that, when over produced, causes inflammation and damage to bones, cartilage and other tissue. The drugs are prescribed to children with RHEUMATOID ARTHRITIS, inflammatory bowel disorder and Crohn's disease.
The drug agency will bolster the "black box" warning on the five drugs sold in the United States, including Abbott Laboratories' Humira, Johnson & Johnson's Remicade and Simponi, and Enbrel, which is marketed by Amgen and Wyeth. All the products are multibillion-dollar sellers. Enbrel was the biggest moneymaker of the group, with sales in the US of $3.4 billion last year.
The action also affects Cimzia, which was introduced in May by the Belgian drug maker UCB.
Along with updating the drugs' labels, the F.D.A. Is requiring companies to add information about cancer risks to the medication guides given to patients. The agency said it was also working with the manufacturers to further define the scope of the cancer risk.
Johnson & Johnson said in a statement that it would "coordinate closely with the F.D.A. to ensure that health care providers, patients and caregivers are properly informed."
Amgen and Wyeth said they would continue working with regulators to evaluate "the potential risks and benefits" of their drug.
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Anyone who has had chemo has - or had a disease or condition that requires monitoring. Most likely, forever. That's why this article in Parade Magazine, by Dr. Ranit Mishori, is so important:
WHEN TO CALL FOR TEST RESULTS
You go in for some tests - maybe you have some blood drawn - but never hear back from your doctor. Don't assume that means everything is okay. Believe it or not, your test results may have fallen through the cracks at your doctor's office.
Two new studies suggest it happens more often than you'd think. In one, researchers looked at 5400 patient records in 23 practices across the country. Reporting in the Archives of Internal Medicine, the authors found that for one out of every 14 tests, doctors, either failed to notify patients of abnormal tests results or didn't have a record of having informed the patient.
While some practices achieved a notification rate of 100%, others lagged far behind, failing to notify as often as 26% of the time. Practices with electronic medical-records system did no better than those with paper systems.
The second study, published in the Annals of Internal Medicine, looked at the electronic medical records of 91 patients whose CT scans recorded a widening of the aorta, an abnormal result that needs to be taken seriously. The condition was documented in the electronic records of only 42% of the group within three months; over three years, the condition showed up in the records of an additional 40%. For 18%, it never did.
Failing to recognize abnormal results or report them to patients in a timely manner can have serious consequences, leading to treatment delays, patient harm - and malpractice suits.
Make sure it doesn't happen to you. Ask your doctor how you ca expect to learn the results of a test. If they're provided online, find out how to access that information. Ask how long patients generally wait before results are posted, and whom to contact if you don't hear back from the doctor's office. Above all, understand that no news is not necessarily good news. Don't wait if you haven't received your test results. Call.
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In case you're wondering if there's ANYTHING out there that doesn't cause cancer ...
ORAL SEX CAUSE OF THROAT CANCER RISE
Experts Say They Fear Epidemic of Throat Cancer Caused by HPV Infection
Changing sexual practices have led to a dramatic rise in THROAT CANCER in the United States over the past two decades, and experts say they fear an epidemic of the disease.
The comments were made at a news conference held by the American Association for Cancer Research to discuss research into the role of the sexually transmitted human papilloma virus in head and neck cancer.
Increasing rates of HPV infection, spread through oral sex, is largely driving the rapid rise in oropharyngeal cancers, which include tumors of the throat, tonsils, and base of the tongue, said Scott Lippman, MD, who chairs the thoracic department at the University of Texas M.D. Anderson Cancer Center.
Studies of oropharyngeal tumor tissue stored 20 years ago show that only around 20% are HPV positive, Lippman said. Today it is estimated that 60% of patients are infected with the virus.
"The percentage of oropharyngeal cancers that are HPV positive is much higher now than it was 20 years ago," he said. "This is a real trend, and that is why there is concern of an epidemic given that fact that oropharyngeal cancer is increasing at an alarming rate."
Smoking and alcohol abuse were once considered the only major risk factors for these cancers, but this is no longer the case. American Cancer Society Chief Medical Officer Otis Brawley, MD, said as many as half of the oropharyngeal cancers diagnosed today appear to be caused by HPV infection.
"Changing sexual practices over the last 20 years, especially as they relate to oral sex, are increasing the rate of head and neck cancers and may be increasing the rates of other cancers as well," he said. He added that there is some evidence that oral HPV infection is also a risk factor for a type of cancer of the esophagus.
"The paradigm is changing," Lippman said. "The types of patients we are seeing now with oropharyngeal cancers are not the patients we have classically seen who were older, smokers, and have lots of other problems. These are young people, executives, a whole different population."
The experts agreed that it is critical for the public to understand that oral sex doesn't equal safe sex. The message was unofficially promoted in the early days of the HIV epidemic and it is still widely believed by many, especially teens.
Studies suggest that teens are often unaware of the risks associated with unprotected oral sex, including the transmission of HPV, chlamydia, and gonorrhea. "There is a huge public health message here," Brawley said.
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For anyone who takes tamoxifen to keep hormone-receptive breast cancer at bay, this is a very important piece of information:
ANTIDEPRESSANTS MAY THWART TAMOXIFEN'S EFFECT ON BREAST CANCER
A recent study indicates that anyone who takes tamoxifen and either Paxil or Prozac at the same time, may actually be enhancing chances that the disease will return. This finding was presented at the recent annual meeting of the American Society of Clinical Oncology, in July.
"Women should talk to their medical oncologist about what antidepressant and what hormone therapy they're on, and make sure they're not one of the ones we're worried about," said Dr. Kelly Marcom, a breast oncologist with the Duke Comprehensive Cancer Center and director of the Duke Hereditary Cancer Clinic, in Durham, N.C.
Many patients who've had BREAST CANCER take the tamoxifen to reduce their odds for recurrence. But hot flashes, a side effect of tamoxifen, can sometimes be controlled with selective serotonin reuptake inhibitor (SSRI) antidepressants such as paroxetine (Paxil) or fluoxetine (Prozac). In addition to acting upon the neurotransmitter serotonin, these drugs inhibit an enzyme called 2D6, necessary to convert tamoxifen into its main active metabolite, endoxifen.
Women with a gene mutation preventing the formation of 2D6 do not reap the same benefits from tamoxifen as women without the mutation. Additionally, drugs that inhibit the formation of 2D6 may result in lower levels of endoxifen, although the clinical implications of that remain unclear.
The U.S. Food and Drug Administration is still hasn't reached a conclusion on whether or not to add a caution about the gene variation to the tamoxifen label. Medco, a U.S. pharmacy benefits management company, reviewed the medical records of 10.7 million members of a health plan. That analysis turned up 945 women taking tamoxifen and 353 taking tamoxifen plus an SSRI/2D6 inhibitor, most commonly Prozac and Paxil.
Both groups of women, whose average age was in the early 50s, had followed similar treatment courses. Women taking both drugs had a 13.9 percent chance of their breast cancer returning over two years, vs. just 7.5 percent of those receiving tamoxifen alone; that translates into an almost twofold increase in risk.
The Medco findings should serve as a warning but not a confirmation of any real danger to patients, one expert said.* A precautionary measure would be to choose other medications.
One researcher noted that aromatase inhibitors, breast cancer-inhibiting medications which include letrozole (Femara) and exemestane (Aromasin), are possible alternatives to tamoxifen.
(*Sorry, but I strongly disagree with the expert's distinction between a warning and a confirmation. I don't think taking Paxil or Prozac with tamoxifen, is worth the risk. Anyone out there who disagrees with this perception is invited to respond, and their response will be printed here.)
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And another story about tamoxifen...**
FEMARA VS. TAMOXIFEN FOR GREAST CANCER
BREAST CANCER patients may do as well with the drug Femara as they do with tamoxifen, according to a new study.
The international study, published in The New England Journal of Medicine, included more than 6,100 postmenopausal women who had breast cancer sensitive to the hormones estrogen or progesterone.
After the women finished their breast cancer treatment, they were assigned to one of the following plans:
. Take tamoxifen for five years
. Take Femara for five years
. Take tamoxifen for two years, then Femara for three years
. Take Femara for two years, then tamoxifen for three years
The women didn't know which pills they were taking.
Tamoxifen and Femara work differently. Tamoxifen blocks the action of estrogen in the body. Femara belongs to the aromatase inhibitors class of drugs. Those drugs, which also include Arimidex and Aromasin, target the aromatase enzyme, which is needed to make estrogen.
The new study shows that over about six years, the women's odds of cancer-free survival were equally good taking Femara alone or taking either tamoxifen first and Femara later or vice versa. There was no significant difference in overall survival between women who took Femara alone compared to women who took tamoxifen alone for five years, report the researchers, who included Henning Mouridsen, MD, chair of the Danish Breast Cancer Cooperative Group.
In 2005, the researchers reported that recurrence of breast cancer in sites far from the breast was less common in women taking Femara than in those taking tamoxifen.
The new study shows that the drugs' side effects were in line with known risks; no unusual adverse events were reported. The study was funded by Novartis, the drug company that makes Femara. In the journal, Mouridsen and several other researchers disclose ties to Novartis. Femara was the only aromatase inhibitor included in the study.
(**Hopefully, the manufacturers of the aromatase drugs will come up with a formula that doesn't cause crippling side effects in one-third of women who try it, as it does now.)
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CHINESE HERB MAY HELP CONTROL SYMPTOMS OF RA
A new study published in Annals of Internal Medicine shows that a Chinese herbal remedy known as 'Thunder God Vine' may help ease symptoms in people with RHEUMATOID ARTHRITIS. The study shows that the Chinese herbal remedy Tripterygium wilfordii Hook F (TwHF), also known as "lei gong teng" (or "thunder god vine"), helped decrease joint tenderness and pain in a small group of people treated with the medicinal plant. Those who took an extract of the herb's roots experienced greater improvement in RA symptoms than those who took the anti-inflammatory drug sulfasalazine.
Although recent advancements in RA treatment have led to a greater number of available therapies, many of those therapies come with side effects that prompt some users to discontinue treatment or seek complementary and alternative treatments. Researchers say thunder god vine has been used in China for centuries to treat a variety of inflammatory diseases, and some small clinical trials have suggested that the Chinese herbal remedy may benefit people with rheumatoid arthritis.
This study, published in the Annals of Internal Medicine, compared the benefits and side effects of treatment with thunder god vine and a conventional anti-inflammatory drug used to treat RA. Researchers randomly assigned 121 people with RA to take the 60 milligrams of the Chinese herbal extract three times a day or 1 gram of the anti-inflammatory drug sulfasalazine twice a day for 24 weeks. Nearly half of the participants dropped out before the study was complete. But after 24 weeks of treatment, researchers found that a greater proportion of people in the Chinese herbal remedy group experienced at least 20% improvement on a standard measure of RA symptoms than the other group.
Researcher Raphaela Goldbach-Mansky, MD, MHS, of the National Institutes of Health, and colleagues say the study was too short to show if thunder god vine also helped to slow the progression of joint destruction from rheumatoid arthritis. But if further studies confirm these results in larger numbers of people, thunder god vine may provide an affordable natural treatment option for rheumatoid arthritis.
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INTENSE DAILY WORKOUT MAY KEEP CANCER AT BAY
Increased oxygen consumption associated with moderate- to high-intensity exercise appears to reduce the risk of cancer, a new study has found.
The Finnish study included 2,560 men, aged 42 to 61, whose leisure-time physical activity was assessed over one year. None of the men had a history of cancer, according to the report published online July 28 in the British Journal of Sports Medicine.
During an average follow-up of 16 years, 181 of the men died from cancer. Those who engaged in moderate- to high-intensity exercise for at least 30 minutes a day were 50% less likely to develop cancer compared with the other men.
The researchers found that an increase of 1.2 metabolic units (oxygen consumption) was related to a decreased risk of cancer death, especially in lung and gastrointestinal cancers, after they took into account factors such as age, smoking, alcohol consumption, body mass index, and fiber/fat intake..
"The intensity of leisure-time physical activity should be at least moderate so that beneficial effect of physical activity for reducing overall cancer mortality can be achieved," the study authors wrote in a news release.
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IN IMPORTANT EXPERIMENT, MULTIPLE SCLEROSIS SUCCESSFULLY REVERSED IN MICE
A new experimental treatment for MULTIPLE SCLEROSIS completely reverses the devastating autoimmune disorder in mice, and might work exactly the same way in humans.
The new treatment, appropriately named GIFT15, puts MS into remission by suppressing the immune response. This means it might also be effective against other autoimmune disorders like Crohn's disease, lupus and ARTHRITIS, the researchers said, and could theoretically also control immune responses in ORGAN TRANSPLANT patients. Moreover, unlike earlier immune-supppressing therapies which rely on chemical pharamaceuticals, this approach is a personalized form of cellular therapy which utilizes the body's own cells to suppress immunity in a much more targeted way. Many MS medications have serious side effects and some carry significant risks.
GIFT15 is composed of two proteins, GSM-CSF and interleukin-15, fused together artificially in the lab. Under normal circumstances, the individual proteins usually act to stimulate the immune system, but in their fused form, the equation reverses itself.
"You know those mythical animals that have the head of an eagle and the body of a lion? They're called chimeras. In a lyrical sense, that's what we've created," said Galipeau, a world-renowned expert in cell regeneration.. "GIFT15 is a new protein hormone composed of two distinct proteins, and when they're stuck together they lead to a completely unexpected biological effect."
This effect, explained Galipeau, converts B-cells, a common form of white blood cell normally involved in immune response, into powerful immune-suppressive cells. Unlike better-known T-cells, naturally-occurring immune-suppressing B-cells are almost unknown in nature and the notion of using them to control immunity is very new.
"GIFT15 can take your normal, run-of-the-mill B-cells and convert them, in a Superman or Jekyll/Hyde sort of way, into these super-powerful B-regulatory cells," Galipeau explained. "We can do that in a petri dish. We took normal B-cells from mice, and sprinkled GIFT15 on them, which led to this Jekyll and Hyde effect.
"And when we gave them back intravenously to mice ill with multiple sclerosis, the disease went away."
MS must be caught in its earliest stages, Galipeau cautioned, and clinical studies are needed to test the treatment's efficacy and safety in humans. No significant side-effects showed up in the mice, he said, and the treatment was fully effective with a single dose.
"It's easy to collect B-cells from a patient," he added. "It's just like donating blood. We purify them in the lab, treat them with GIFT15 in a petri dish, and give them back to the patient. That's what we did in mice, and that's what we believe we could do in people. It would be very easy to take the next step, it's just a question of finding the financial resources and partnerships to make this a reality."
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Policy wonks will love this one...
` PERKS POLICY FOR DOCTORS CHALLENGED
A growing number of hospitals, universities, and states are barring drug companies from buying physicians dinner, hiring them as speakers, and giving them even token gifts.
Now, a new organization of doctors - several from Boston - wants to roll back policies curbing interactions between doctors and drug company representatives, saying restrictive rules ultimately will hurt the patients they’re designed to protect.
The group, called the Association of Clinical Researchers and Educators, recently held its first conference at Brigham and Women’s Hospital (Boston) to promote “productive collaboration’’ between industry and physicians, which they say leads to better medicines and treatments. Dr. Jeffrey Flier, dean of Harvard Medical School, offered the welcoming remarks to about 200 attendees.
Flier, who is unaffiliated with the organization, will not endorse its views, said David Cameron, spokesman for the medical school, which is revising its conflict-of-interest policy. “He will welcome vigorous debate and analysis on the issue of academic collaborations with industry and encourage individuals with varied perspectives to participate in the discussion,’’ Cameron said in a written statement.
Dr. Thomas Stossel, an oncologist at the Brigham; Dr. Jeffrey Garber, chief of endocrinology at Harvard Vanguard Medical Associates; and Dr. Paul Richardson, an oncologist at Dana-Farber Cancer Institute, are among the founders of the group. Stossel said they want “to convey that there is a silent majority out there. And to restore some balance to the debate,’’ he said.
The group’s website says its long-term goals include reversing restrictive new conflict-of-interest policies and establishing chapters at universities and within medical specialty societies.
Massachusetts public health officials plan in two years to review the state’s new conflict-of-interest regulations, which went into effect July 1 and include a ban on gifts to doctors from drug and medical device companies, and Stossel said his group “wants to create an outcry against’’ the law. The law also requires drug and device companies to disclose publicly most payments made to doctors for consulting.
Partners HealthCare, which includes the Brigham and Massachusetts General Hospital, passed its own restrictions in April, which go further than the state law, banning all industry-paid gifts and meals and also forbidding doctors from traveling the country as paid members of company “speakers bureaus.’’
The association’s goals, which run contrary to the widespread movement in medicine to create more distance between doctors and pharmaceutical companies, have been widely discussed - and often derided - on healthcare blogs in the past several weeks.
Patient advocacy groups and lawmakers leading the charge for more restrictive policies say Stossel and his colleagues are misguided. Advocates of the restrictions believe drug companies, by giving doctors gifts and paying them to speak and consult, create bias in favor of their products, causing doctors to write more prescriptions for expensive new drugs even if patients don’t really need the medication or if an older, less expensive drug would work just as well.
Dr. Peter Slavin, president of Mass. General, has said that company-funded meals, gifts, and other practices don’t promote a positive image of doctors and increase healthcare costs.
“The rules benefit consumers by removing the conflicts that we know cloud judgment, and let doctors make decisions free from market pressures,’’ said Brian Rosman, research director for Health Care For All, a Boston-based patient advocacy group.
But Stossel and his colleagues said the new rules stifle invention. They believe the impact of small gifts and meals on doctors is negligible compared with the benefit of collaboration.
“I’ve been in medicine 40 years, and medicine is incomparably better than when I started out,’’ Stossel said. “I don’t think anyone can challenge the fact that it’s because of the tools we’ve gotten from industry.’’ Stossel is a former member of Cambridge-based Biogen Idec’s scientific advisory board. He said he now does occasional consulting to companies on conflict-of-interest policies. The conference was funded by attendees’ fees, though participants who work for drug and device companies are charged more, he said.
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` NEW DRUG KILLS MOTHER CANCER CELLS
Scientists have developed a drug for the cancer disease which destroys the lethal cells that give birth to the cancer tumors. It has already been successful in dealing with BREAST CANCER and it has offered a hope to people who are suffering from cancer in their BOWEL, SKIN or PROSTATE. The drug works by killing the cancer stem cells that help cancer tumors to grow and spread the disease to entire body of the patient. Unlike all other cancer cells, the ‘mother’ stem cells are not effectively abolished by chemotherapy and radiotherapy, as a result of which the cancer may returns after the treatment.
In the laboratory tests, Salinomycin, a new drug, was hundred times more efficient in destroying the stem cells as compared to powerful Taxol, the chemo treatment. When the drug injections were given to mice suffering from breast cancer, it also resulted in slowing down of the tumor growth. According to a journal Cell report, stem cells that were treated with Salinomycin were less capable of starting tumor in animals than the cells which were treated with Taxol.
The researchers from the US believe that a good number of drugs with similar capabilities can be developed in the period of next few years and that the treatment for cancer is only about 10 years away from reaching the market.
The new drug can be combined with the standard therapies so that the cancer stem cells that are left behind after the traditional methods of treatment can be mopped away from the body. Thus the chances of the return of cancer will be abolished It can also stop the cancer cells from spreading to other parts of the body.
Metastasis is a very common cause of deaths of 155,000 cancer patients every year.
Piyush Gupta, from the Broad Institute of Massachusetts Institute of Technology and Harvard, commented that until now, it was not clear whether it's possible to find compounds that can selectively kill cancer stem cells.. This research seems to indicate how targeted cancer stem cells are affected biologically. It also suggests an approach to find novel therapies to treat cancer which are applicable to any solid tumors maintained by the cancer stem cells.
In the beginning, the researchers found a way to create cancer stem cells in the laboratory in large numbers. Then 16,000 chemicals were tested on the cells to check whether or not any of them and which of them proved to be toxic. A lot of work remains to identify how Salinomycin works whether it can be effective for human tumors. Professor Colin Goding, an expert of stem cells at the Oxford University, cautioned that there could be danger that the drug might kill wrong type of cells also inside the body.
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One of the drawbacks of getting information from the Internet is that you're often unsure of the background - more importantly, the qualifications of the people passing you the news. In the case of the next story about a new cancer study, I've worked a story with Nicholas Wade, and I found that anything with his name on it is well-researched and accurate (plus, he's such a good writer...):
NEW CANCER TREATMENT SHOWS PROMISE IN TESTING By Nicholas Wade
A new method of attacking cancer cells, developed by researchers in Australia, has proved surprisingly effective in animal tests. The method is intended to sidestep two major drawbacks of standard chemotherapy: the treatment’s lack of specificity and the fact that cancer cells often develop resistance.
In one striking use of the method, reported online Sunday (no date given) in Nature Biotechnology, mice were implanted with a human uterine tumor that was highly aggressive and resistant to many drugs. All of the treated animals were free of tumor cells after 70 days of treatment; the untreated mice were dead after a month.
The lead researchers, Jennifer A. MacDiarmid and Himanshu Brahmbhatt, say their company, EnGeneIC of suburban Sydney, has achieved a similar outcome in dogs with advanced brain cancer. “We have been treating more than 20 dogs and have spectacular results,” Dr. Brahmbhatt said. “Pretty much every dog has responded and some are in remission.” These experiments have not yet been published.
Cancer experts who were not involved with the research say that the new method is of great interest, but that many treatments that work well in laboratory mice turn out to be ineffective in patients.
Bert Vogelstein, a leading cancer researcher at Johns Hopkins University, called the method “a creative and promising line of research,” but noted the general odds against success. “Unfortunately our track record shows that far less than 1 percent of our promising approaches actually make the grade in patients,” he said.
The EnGeneIC researchers said they had conducted successful safety tests in a large number of monkeys and will start safety trials in patients with all kinds of solid tumors in three Melbourne hospitals next month. They said they had discussed licensing their technology with large pharmaceutical companies and others.
Stephen H. Friend, head of cancer research at Merck until early this year, said he had been following EnGeneIC’s work for more than a year, and praised the company for trying a method that others had written off without trying. “I consider the approach is remarkable and more than intriguing,” said Dr. Friend, who is now at Sage Bionetworks in Seattle. But he warned that cancer cells are very versatile and can “evolve around any pressure you put on them,” so that no single approach is likely to afford a cure.
The EnGeneIC method uses minicells to deliver a variety of agents to tumor cells, including both anticancer toxins and mechanisms for suppressing the genes that make tumors resistant to toxins. The minicells are generated from mutant bacteria which, each time they divide, pinch off small bubbles of cell membrane. The minicells can be loaded with chemicals and coated with antibodies that direct them toward tumor cells.
No tumor cell, so far as is known, produces a specific surface molecule for toxins to act on. But 80 percent of solid tumors have their cell surfaces studded with extra-large amounts of the receptor for a particular hormone, known as epidermal growth factor.
The minicells can be coated with an antibody that recognizes this receptor, so they are more likely to attach themselves to tumors than to the normal cells of the body. The tumor cells engulf and destroy the minicells, a standard defense against bacteria, and in doing so are exposed to whatever cargo the minicells carry.
What also helps direct the minicells toward tumors, the EnGeneIC researchers say, is that the blood vessels around tumors tend to be leaky, and the minicells are small enough to leave the circulation at the leak sites.
The minicells do not seem to be highly provocative to the immune system, even though they are made of bacterial cell membrane. The reason may be that the provocative parts of the membrane are masked by antibodies with which the minicells are coated, Dr. Brahmbhatt said.
In the experiments reported, EnGeneIC treated cancer-ridden mice with two waves of minicells. The first wave contained an agent that suppressed an important gene for toxin resistance. The gene makes a protein that pumps toxin out of cells, and is a major cause of the resistance that tumors often develop toward chemotherapeutic agents. After the toxin-expelling gene had been knocked down in the tumor cells, the EnGeneIC researchers injected a second wave of minicells, each loaded with half a million molecules of doxorubicin, a toxin used in chemotherapy.
The two-wave treatment arrested tumor growth in mice implanted with either human COLON or human BREAST TUMORS, and enabled mice with drug-resistant human uterine tumors to eliminate the tumors altogether.
“The technology looks very good,” said Bruce Stillman, president of the Cold Spring Harbor Laboratory on Long Island. It provides a general method of delivering chemicals to tumors, he said, especially those that are usually degraded in the bloodstream. Dr. Stillman, who has advised EnGeneIC and is a co-author of its report, said the minicells could be particularly helpful for delivering silencing RNAs, a promising new class of drug that is rapidly destroyed in the body unless protected.
Though the minicells can be varied to attack different receptors and to import any gene of interest on elements called plasmids, the method still has several hurdles to jump.
`Robert M. Hoffman, of the University of California, San Diego, said that the minicells were “good strategy and good science” but that the researchers had implanted the human tumors under the mice’s skin, a position from which they do not usually spread through the body. So the experiments do not answer the question of whether minicells can attack metastasized cancer, he said.
Dr. Hoffman, who is president of AntiCancer Inc., has obtained striking remissions with metastasized cancers in mice by treating them with salmonella bacteria. The bacteria have been engineered to lack two kinds of amino acid, which makes them unable to grow in normal tissues. In cancer cells, however, where the missing amino acids are in more plentiful supply, the bacteria are highly virulent and kill the cells.
The idea of treating cancer with bacteria goes back to the 19th century, when physicians noticed that cancer patients who became infected sometimes enjoyed a remission. Both Dr. Hoffman’s method and the minicells, in different ways, revisit these old observations. Both may face special scrutiny from regulators concerned at the prospect of putting bacteria into people.
Dr. Hoffman said his studies with the defective bacteria were going well and that his company might be ready to start a safety test in patients in two years if it can find a good partner. Use of bacteria in cancer “is an old story but there is definitely a lot of promise there,” he said.
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SEE YOU NEXT MONTH....
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And if you have any thoughts of how this newsletter could be improved, please email me directly, at firstname.lastname@example.org