Articles about new chemotherapy drugs, treatment methods etc.

*Researchers At Vanderbilt-Ingram Cancer Center Study Exercise To Curb 'chemo Brain'
*DNA Vaccine Improves Chemotherapeutic Drug Uptake In Colon And Breast Cancer
*Almost 1 / 3 Of Colon Cancer Patients Stop Chemotherapy, Leading To Double The Death Rate
*Predicting Chemotherapy Success
*New Device Could Cut Chemotherapy Deaths
*Arthritis Drug Might Reduce Fatigue In Cancer Patients
*Inhibiting Cell Process May Give Cancer Drug A Boost
*Protecting Against Serious Chemotherapy Side Effect
*Takeda And BioNumerik Announce Results Of Tavocept(TM) Phase III Trials Focused On Neuropathy Indication
*Hope For A More Effective And Less Toxic Cancer Drug
*Sutent, One Of The New 'Targeted' Cancer Drugs
*Longer Anthracycline Therapy Reduces Heart Failure In Adult Cancer Patients
*Chemotherapy Temporarily Affects The Structures Of The Human Brain
*Par Pharmaceutical Receives Approval For Ondansetron Orally Disintegrating Tablets
*Mechanism By Which Cells Resist Chemotherapy Found By Researchers
*Advanced Cancer Patients Could Benefit From Personalized Healthy Diets
*No Carrier Necessary: This Drug Delivers Itself
*CoGenesys Expands Clinical Programs With Initiation Of Phase 1-2a Trial Of Neugranin In Cancer Patients
*Antioxidants May Aid Chemotherapy Patients

Researchers At Vanderbilt-Ingram Cancer Center Study Exercise To Curb 'chemo Brain'

29 Mar 2006

Researchers at the Vanderbilt-Ingram Cancer Center are studying whether exercise can help curb memory and cognitive problems experienced by many cancer survivors following chemotherapy, with the help of funding from the Foundation established by well-known cancer survivor and athlete, Lance Armstrong.

The funding will allow Charles Matthews, Ph.D., and Laurel Brown, Ph.D., in the Departments of Medicine and Psychiatry, and a team of researchers at Vanderbilt-Ingram, to take a closer look at the chemotherapy side effect commonly referred to as "chemo brain" or "chemo fog," and determine whether starting a walking exercise program can help patients with these problems.

"A substantial number of cancer survivors who receive chemotherapy report mild to moderate cognitive impairment that persists following treatment. These impairments have been reported across a range of cancer types and chemotherapy agents," said Brown.

Participants will be asked to make three visits to Vanderbilt University Medical Center during this six-month study, and will be placed into either a walking exercise group or a control group. Study members in the exercise group will receive a personalized walking program that they can do at home, counseling to help them reach their exercise goals, and techniques to help with memory problems. People enrolled in the control group will immediately receive counseling and techniques to help with memory problems, but will only be given the exercise program at the end of the six-month study period. All participants will be asked to complete measures of memory and cognitive function, physical activity and fitness, questionnaires, and to provide urine and blood samples. Anyone 18 and older who has received chemotherapy in the last five years, experienced persistent memory or cognitive problems since chemotherapy, does not already exercise regularly, and has no history of brain cancer, heart disease, or a serious medical condition that could be worsened by exercise, is eligible for the study.

Matthews said exercise at levels most adults can perform -- such as brisk walking for 30 to 45 minutes, four to five days a week -- has been shown to improve cognitive function in older adults. "A wealth of research now indicates that exercise participation preserves cognition function as we age. In addition, sedentary older adults without cancer who completed six months of exercise have been shown to improve their cognitive function. We want to see if exercise might help cancer survivors in the same way," said Matthews.

Matthews said the exercise intervention study is the first of its kind for cancer survivors. "To our knowledge this study would be the first to examine the influence of regular exercise on cancer survivors who experienced cognitive difficulties following chemotherapy."

Matthews and his research team hope to identify new tactics to help cancer survivors coping with "chemo brain" and provide substantial information to lead the way for further studies that address quality of life issues faced by cancer survivors.

Vanderbilt was one of 21 institutions across the country and in Rome, Italy, to receive cancer survivorship and testicular cancer research grants from the Lance Armstrong Foundation.

DNA Vaccine Improves Chemotherapeutic Drug Uptake In Colon And Breast Cancer

25 Jun 2006

After the genetic events that initiate malignancy have occurred, tumor progression critically involves interactions between the malignant cells and the normal cells in the tumor environment. An example of such cells are tumor-associated fibroblasts that make collagen type I, which play a role in the poor uptake by tumors of some chemotherapeutic drugs.

In a study appearing online in June in advance of print publication in the July issue of the Journal of Clinical Investigation, Ralph Reisfeld and colleagues from The Scripps Research Institute, California, show that by specifically targeting and killing tumor-associated fibroblasts with an orally delivered DNA-based vaccine, they can significantly suppress the growth and spread of multidrug-resistant colon and breast carcinomas in mice. By disrupting collagen type I expression the authors were able to significantly increase tumor uptake of chemotherapeutic drugs, resulting in tumor rejection and a 3-fold prolongation of lifespan of these mice. This novel technique opens up new and exciting avenues for the improvement of cancer chemotherapy.

Almost 1 / 3 Of Colon Cancer Patients Stop Chemotherapy, Leading To Double The Death Rate

02 May 2006

New research from Columbia University Medical Center has found that as many as 30 percent of patients with stage III colon cancer who were prescribed six months of chemotherapy with a combination of 5-fluorouracil and leucovorin stopped their treatment prematurely. Stopping chemotherapy for colon cancer prematurely was shown to be equivalent to receiving no treatment at all. The findings add to the arsenal of reasons why colon cancer patients, and all cancer patients, need to complete their chemotherapy regimens whenever possible.

Previous studies have shown that not completing chemotherapy regimens for breast cancer is associated with shorter survival. This is the first study to look at a link between mortality rates from colon cancer and treatment adherence.

"The intuitive thinking is that if you complete most of a treatment regimen, you should get most of the treatment benefit. But these findings are significant because they indicate that completing treatment is as critical for colon cancer as it is for breast cancer - and we need to do better to ensure that patients who can, complete treatment as intended," said Alfred I. Neugut, M.D., Ph.D., who led the study along with Dawn L. Hershman, M.D., M.S.

The study will be published in the May 20, 2006 issue of the Journal of Clinical Oncology (published online April 2006).

The research team used the Surveillance, Epidemiology, and End Results (SEER)-Medicare database to identify stage III colon cancer patients who were at least 65 years of age or older, and who received one to seven months of fluorouracil (FU)-based adjuvant chemotherapy treatment.

Among the 1,579 patients who survived eight months or longer, the 1,091 (69.1 percent) who underwent five to seven months of treatment survived nearly twice as long as the 488 (30.9 percent) who received only one to four months of treatment. Patients who were older, unmarried and had comorbid conditions, were more likely to receive less than five months of treatment.

Dr. Neugut is the Myron M. Studner Professor of Cancer Research in Medicine at Columbia University Medical Center. He is also professor of epidemiology at Columbia University's Mailman School of Public Health, as well as head of Cancer Prevention and Control for the Herbert Irving Comprehensive Cancer Center, and co-director of the Cancer Prevention Center of New York Presbyterian Hospital/Columbia.

Dr. Neugut sees patients as an attending physician in medical oncology at New York-Presbyterian Hospital/Columbia and Harlem Hospital Center, an affiliate institution of Columbia University Medical Center.

Dr. Hershman, co-lead author, is assistant professor of medicine and epidemiology at the Columbia University College of Physicians and Surgeons in the Division of Medical Oncology. She is co-director of the Breast Program for the Herbert Irving Comprehensive Cancer Center at Columbia University Medical Center and New York-Presbyterian Hospital/Columbia. Dr. Hershman is an assistant attending physician in medical oncology at New York-Presbyterian Hospital/Columbia specializing in breast cancer.

Additional members of the Columbia University Medical Center research team included: Matthew Matasar, M.D., former instructor in clinical medicine; Xiaoyan Wang, M.A., staff associate in epidemiology, Mailman School; Russell McBride, doctoral student in epidemiology, Mailman School; Judith S. Jacobson, DrPH, assistant professor of clinical epidemiology, Mailman School; Wei-Yann Tsai, Ph.D., professor of biostatistics, Mailman School; and, Victor R. Grann, M.D., MPH, clinical professor of medicine and epidemiology and health policy and management at the College of Physicians & Surgeons and Mailman School of Public Health.

The same research team recently published (Journal of Clinical Oncology, Sept. 20, 2005 issue) the first study to link treatment completion issues with race and poor survival rates. The 2005 study found that black women with early stage breast cancer were more likely than their counterparts of other races to abandon chemotherapy before completing their full course of treatment. The findings shed new light on why breast black cancer patients experience lower survival rates than other women, despite a lower incidence.

Predicting Chemotherapy Success

28 Apr 2006

Chemotherapy drugs, given intravenously, are the mainstay of the fight against cancer. But doctors know that sometimes these drugs effect a complete cure, while other times they can be nearly ineffective. How to turn some of those failures into successes? A team of scientists at the Weizmann Institute, headed by Prof. Hadassa Degani of the Biological Regulation Department, has come up with a non-invasive, magnetic resonance imaging- (MRI-) based method for predicting possible problems. The findings of their studies on animals, which appeared in the journal Cancer Research, may, in the future, influence treatment regimes for millions of cancer patients.

Intravenous infusions rely on the bloodstream to carry drugs to where they are needed. Normally, a material such as a chemotherapy drug crosses into a tissue on the principle of concentration equalization - the material diffuses from an area of high concentration to one of low concentration until the concentrations become equal all around. However, in some cancers, even though the material "wants" to spread out evenly, fluids inside the tumor may be exerting pressure to prevent this. When the internal pressure created by these fluids rises above a certain level, it acts as a barrier that keeps drugs and other materials from entering the tumor.

The method the Institute scientists developed can measure, with a non-invasive MRI scan, whether the fluid pressure in cancer tissues is at levels that could render chemotherapy ineffective. Their research, which led to the method, was done with MRI equipment similar to that found in hospitals and clinics. A contrast agent often employed in MRI was used as a stand-in for chemotherapy drugs, and this material was injected into special mice with different cancerous growths. The team created computer algorithms (instructions for computers) that allowed them to verify the connection between the amount of material that found its way into the growth and the pressure of the fluids inside the tumor tissue. The Weizmann Institute team's research, as well as that of other research groups, shows that this relationship can differ from one animal to the next, from one human to the next, and even from one tissue to the next in the same animal.

Prof. Degani says that, ideally, the fluid pressure inside tumor tissues would be checked using the MRI method she and her team developed before a patient begins chemotherapy. If the pressure is discovered to be high, it might be possible to reduce it by various means, such as drugs similar to those for lowering blood pressure. The method, if it proves successful in clinical trials, might have the potential to significantly increase the success rate of chemotherapy.

New Device Could Cut Chemotherapy Deaths

01 Apr 2006

A new method of delivering chemotherapy to cancer patients without incurring side effects such as hair loss and vomiting is being developed.

The method, produced at the University of Bath, involves using tiny fibres and beads soaked in the chemotherapy drug which are then implanted into the cancerous area in the patient's body.

These fibres are bio-degradable and compatible with body tissue, which means they would not be rejected by the patient's body. They gradually turn from solid to liquid, releasing a regular flow of the chemotherapy chemical into the cancer site, and a much lower dose to the rest of the body.

This is a more localised way of killing cancer cells than the current method of injecting the chemical into a cancer sufferer's vein so that it is carried around the body.

As well as reducing the side-effects, the new drug delivery vehicle, known as Fibrasorb, could also cut the numbers of patients who die from the effects of chemotherapy because they need such high doses to tackle their cancer.

The method, developed by Dr Semali Perera, of the University's Department of Chemical Engineering, over the past few years, has successfully gone through preliminary laboratory trials. The first clinical trials on volunteer patients with ovarian cancer in Avon, Somerset and Wiltshire could begin in the next few years and, if successful, the technology could be put into general use.

The research team at Bath is collaborating closely with the Avon, Somerset and Wiltshire Cancer Centre and the oncology team at the Royal United Hospital for the design and development of these drug delivery vehicles. This team includes Dr Ed Gilby, one of the most experienced consultant oncologists, surgeons Mr Nicholas Johnson and Mr Kenneth Jaaback (correct), clinical trials experts and specialist nurses such as Tracie Miles.

?Side effects from chemotherapy can be very unpleasant and sometimes fatal,? said Dr Perera.

?The new fibres and beads could cut out some side-effects entirely, including nausea and vomiting, and could reduce the number of people who die each year.

?Although the first study will be on patients with ovarian cancer, soon we hope that other cancer sufferers with solid tumours will benefit.

?Give that around one in eight people worldwide die of cancer, this could be a vitally important step in the treatment of this disease.

?We have now assembled an extremely experienced team to develop the Fibrasorb technology."

The Fibrasorb technology is a flexible fully resorbable device that can be formulated as a bead, a fibre or mesh, or as a tube inserted into the body into which leads outside the body and through which drugs can be fed.

For the pre-clinical studies, funded by the Department of Health, Dr Perera will be working closely with Dr Vasanta Subramanian a lecturer in the University's Department of Biology & Biochemistry. Dr Subramanian is a cell and molecular biologist with extensive research experience in gastrointestinal cancers and stem cells in the gastrointestinal tract.

Dr Perera has also been working with the University's Department of Pharmacy & Pharmacology to make the fibres more sterile so they cannot be attacked by harmful bacteria.

She said that other researchers had worked on using tiny beads as a way of delivering drugs locally, but the new system showed greater promise because it could achieve better control when delivering the drug.

A patent application has been filed on the drug delivery system, and drug companies across the world are expected to express great interest in the new technology. Dr Perera has been working closely with David Coleman and Jennie Solb? from the University's Research Innovation Services department, to develop this technology.

The University of Bath is one of the UK's leading universities, with an international reputation for quality research and teaching. In 16 subject areas the University of Bath is rated in the top ten in the country. View a full list of the University's press releases:

Arthritis Drug Might Reduce Fatigue In Cancer Patients

02 May 2006

Researchers here have found evidence that combining a drug typically used to treat rheumatoid arthritis with chemotherapy might help reduce fatigue and muscle wasting that often afflicts cancer patients.

The findings of the preliminary study with 24 patients are reported in the April issue of the Journal of Clinical Oncology.

"Even though this was a small study, we found that we could deliver more chemotherapy when combined with the drug etanercept," said lead author Miguel A. Villalona-Calero, an associate professor of hematology and oncology and of pharmacology at Ohio State.

"This shows promise in helping reduce fatigue in cancer patients while increasing their ability to tolerate higher doses of chemotherapy on a more frequent basis," said Villalona-Calero, who is also researcher at The Ohio State University Comprehensive Cancer Center - Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC - James).

Patients' fatigue - the state of overwhelming and sustained exhaustion that is not relieved by rest - often hinders physicians' ability to deliver chemotherapy to them on schedule because of their weakened state.

The fatigue and muscle wasting that are associated with cancer are largely caused when immune cells release a substance known as tumor necrosis factor (TNF). Although TNF historically has been studied for its anticancer properties, recent studies indicate that TNF probably promotes tumor growth instead of hindering it.

The drug etanercept is a decoy receptor that blocks interaction with TNF. The researchers hypothesized that the drug might therefore work like a sponge to "soak up" TNF and lower the amount of the substance in the body, which would decrease tumor growth and help reduce fatigue.

They tested the idea in patients who were being treated with the chemotherapy drug docetaxel.

Initially, 12 patients with a variety of advanced solid malignancies that were resistant to conventional treatment, or for which no effective treatment existed, were randomly assigned to two groups, one receiving docetaxel, and one receiving docetaxel along with etanercept. Subsequently, an additional 12 patients who were later added to the study received higher doses of docetaxel combined with etanercept.

Patients were evaluated and answered weekly questionnaires about their perceived fatigue and weakness. Although only a limited group of patients received docetaxel without etanercept, the questionnaires showed that they have increased fatigue compared to the patients who received etanercept.

Researchers concluded that the addition of etanercept is safe and had no impact on the concentration of the chemotherapy drugs in the body. The finding that patients could tolerate higher doses of the chemotherapy drug suggests that the use of drugs to block TNF might improve the effectiveness of cancer therapies, Villalona-Calero said.

Others involved in the study were J. Paul Monk, Michael A. Caligiuri, Larry J. Schaaf, Gregory W. Otterson, Denis Guttridge, Chris Rhoades, Manisha Shah, Gary Phillips and Tamara Criswell, all of the Ohio State cancer program.

Inhibiting Cell Process May Give Cancer Drug A Boost

06 May 2006

A molecule that interferes with the internal scaffolding that shapes the cell may kill cancer cells, retard the growth of tumors and give a boost to a common chemotherapy drug, according to findings appearing in the May issue of the European Journal of Cancer.

Although tumor growth depends on the rapid cell division and mobility of cancer cells -- processes highly dependent on the cytoskeleton -- the cytoskeleton has not been a target in treating cancer, said Primal de Lanerolle, professor of physiology and biophysics at the University of Illinois at Chicago and principal author of the study.

The researchers found that ML-7, which inhibits an enzyme called myosin light chain kinase, which is important to the structure and dynamics of the cytoskeleton, induces cell suicide, or apoptosis, in cultured breast and prostate cancer cell lines. In addition, treatment with ML-7 in combination with etoposide, a chemotherapy drug used to treat solid tumors, enhanced the ability of etoposide to kill cancer cells.

In animal models, ML-7 retarded growth of breast cancer and Prostate Cancer tumors. The combination of ML-7 and etoposide reduced tumor growth by 88.5 percent for the breast cancer tumors and by 79.1 percent in the prostate cancer tumors compared to controls.

Like many chemotherapy drugs, etoposide can have adverse side effects.

"Reducing the dose of the drug without losing effectiveness would have important clinical benefits," said de Lanerolle. "ML-7 seemed to be tolerated very well, without any overt toxic side effects of its own."

The study suggests an entirely new target for cancer therapies, de Lanerolle said. "Our study supports the idea that the cytoskeleton is important in determining whether cells live or die, and that destabilizing the cytoskeleton may be a good way to induce apoptosis in cancer cells."

Researchers now must test ML-7 for toxicity and perform further preliminary animal experiments before human trials could be planned. Only a tiny fraction of promising candidate drugs enter clinical trials, and few of those are approved.

Protecting Against Serious Chemotherapy Side Effect

16 Jul 2006

Every year, Over one million cancer patients in the u.s. receive chemotherapy. One serious side effect of chemotherapy is neutropenia, a shortage of infection-fighting white blood cells. Complications associated with neutropenia can delay a patient's chemotherapy or keep them from getting a full dose.

Dr. Michael rader, assistant professor columbia university medical center:

"With sufficient white blood cells, patients have a better chance of adhering to their chemotherapy schedule, giving them the best chance for successful treatment. Using Neulasta, a medication that increases white blood cell count, from the start of chemotherapy can help protect patients from neutropenia."

Neulasta helps protect patients against chemotherapy related Complications and significantly reduces the risk of infection and incidence of hospitalization related to neutropenia.

Rare cases of splenic rupture and allergic reactions, including Anaphylaxis, have been reported in postmarketing experience. Rarely, these allergic reactions recurred within days after discontinuing anti-allergic treatment. For more information, visit or speak to your healthcare professional.

Takeda And BioNumerik Announce Results Of Tavocept(TM) Phase III Trials Focused On Neuropathy Indication

01 Aug 2006

Takeda Pharmaceutical Company Limited ("Takeda," Osaka, Japan) and BioNumerik Pharmaceuticals, Inc. (BioNumerik, San Antonio, Texas) today announced the results of two Phase III Trials for Tavocept(TM). Tavocept is an investigational new drug with potential for oncology and non-oncology indications that was originated and developed by BioNumerik.

The initial development focus for Tavocept has been as an investigational new drug to prevent or mitigate the peripheral nerve damage, or neuropathy, that is known to be associated with certain commonly used classes of chemotherapy drugs, such as taxane and platinum agents. Data was recently unblinded by BioNumerik from two placebo controlled Tavocept Phase III clinical trials consisting of (1) a Phase III trial of weekly administration of paclitaxel (a widely used taxane drug) to patients with metastatic breast cancer enrolled from the United States, Russia, and Ukraine (the "Weekly Paclitaxel Breast Cancer Trial"); and (2) a Phase III trial involving administration of paclitaxel and cisplatin (a widely used platinum drug) every 3 weeks to patients with non-small cell lung cancer from Eastern and Western Europe (the "European Lung Cancer Trial"). Both of these trials were aimed at evaluating Tavocept's potential for a neuropathy related treatment indication.

Each of the Phase III trials was designed as a randomized double-blind placebo controlled trial with each patient to be randomly assigned to receive either Tavocept or placebo in conjunction with chemotherapy. The primary endpoints for the Weekly Paclitaxel Breast Cancer Trial and the European Lung Cancer Trial were: (1) the total incidence of severe neuropathy caused by the administration of chemotherapy in combination with Tavocept or placebo; and (2) the difference in rates of tumor shrinkage in patients receiving chemotherapy in combination with Tavocept or placebo, in order to determine whether Tavocept has an impact on the anti-tumor effect of chemotherapy.

Based on review and analysis of the results, the trials did not meet their primary endpoints and they were inconclusive in terms of demonstrating a statistically significant effect of Tavocept in reducing the incidence of severe neuropathy caused by the administration of paclitaxel and/or cisplatin. In addition, neither of the trials demonstrated a statistically significant finding in terms of objective tumor response rate or tumor protection as assessed in accordance with the predefined statistical analysis plans for the trials, or by an independent radiological review committee.

In commenting on the data, Frederick H. Hausheer, M.D., Chairman and Chief Executive Officer of BioNumerik stated, "Many patients suffer from chemotherapy induced neuropathy and there is no FDA-approved treatment to prevent or reduce neuropathy caused by taxane and platinum chemotherapy drugs. Although we did not see the results that we hoped to observe in these Phase III trials, we believe there is evidence of potential clinical activity of Tavocept that supports consideration of possible further Tavocept development aimed at addressing the large unmet medical need for neuroprotective agents. Certain trends and subgroup analyses for the trials indicate that Tavocept may have potential for reducing chemotherapy-induced neuropathy that merits consideration of further clinical testing. In addition, the way that neuropathy was measured and the countries where the trials were conducted may also have impacted the results."

Subgroup analysis by country from the Weekly Paclitaxel Breast Cancer Trial revealed a notable finding in favor of Tavocept in the reduction of patient-reported severe neuropathy (as measured by Patient Neurotoxicity Questionnaire (PNQ) grades D or E) for patients enrolled only from U.S. sites. In this subpopulation comprising patients enrolled only from U.S. sites, the incidence of patient-reported severe neuropathy confirmed for at least 4 weeks (PNQ grades D or E) was 3.2% in the Tavocept group as compared to 20.0% in the placebo group. This observation represents an 84% lower incidence of severe neuropathy in favor of Tavocept. The Patient Neurotoxicity Questionnaire (or PNQ) is a patient-based neuropathy measurement tool that was used to measure neuropathy in the Tavocept Phase III trials. The National Cancer Institute Common Toxicity Criteria ("NCI-CTC"), a physician-based neuropathy measurement tool, showed a consistent trend with that of the PNQ in terms of comparing the overall severe neuropathy reported in the Tavocept and placebo arms for patients from U.S. sites in the Weekly Paclitaxel Breast Cancer Trial. However, it is also important to note that only about 8% of the total number of patients treated in the Weekly Paclitaxel Breast Cancer Trial were treated at U.S. clinical sites.

"An important factor supporting possible future Tavocept development for a neuropathy indication is the subgroup analysis for patients enrolled only at clinical sites located in the United States who participated in the Weekly Paclitaxel Breast Cancer Trial," said Hausheer. "We also observed some encouraging trends in the Weekly Paclitaxel Breast Cancer Trial that indicate potential activity of Tavocept in reducing moderate to severe neuropathy. These are some of the first Phase III trials conducted to assess the potential reduction of chemotherapy induced neuropathy. We believe there may be modifications in the trial endpoints in the future as well as changes in the procedures for assessing neuropathy in order to clinically assess patients at risk for this complication and to address some of the technical challenges we have observed in these trials to date. While we are encouraged by some of the observations in these trials, it is clear that additional clinical testing will be required to support development of Tavocept for a neuropathy indication."

Takeda has notified BioNumerik that, given the additional time necessary to conduct additional clinical testing for a Tavocept neuropathy indication, one possible alternative is termination of the existing Tavocept License and Development Alliance Agreement between Takeda and BioNumerik for the United States and Canada. Takeda and BioNumerik are continuing to discuss the data from the trials as well as considerations regarding the alliance agreement and the future development of Tavocept.

About Tavocept:

Tavocept is an investigational new drug with potential for oncology and non-oncology indications that was originated and developed by BioNumerik. Tavocept has potential applicability in multiple therapeutic areas including diabetic neuropathy, protection against toxicity from radiation therapy, lymphedema and other potential medical indications. In addition to chemotherapy induced neuropathy, BioNumerik is evaluating further Tavocept development possibilities in these areas.

Hope For A More Effective And Less Toxic Cancer Drug

20 Nov 2006

Detailed evaluation conducted at WEHI into a possible new cancer drug suggests that it may prove to be more effective and less toxic than current chemotherapeutic drugs.

Dr David Huang, Dr Andrew Roberts, Prof Jerry Adams and their teams from WEHI's cancer research divisions have been assessing the potential of a new compound, ABT-737, that was developed by US-based healthcare company, Abbott.

Under normal circumstances, human cells have a limited lifespan. They die when they are damaged, worn out or no longer needed by the body. When they die, these cells are replaced by new ones. The body depends on a normal and healthy process called programmed cell death - or apoptosis - to ensure that unwanted cells die on cue. If this process fails, then the damaged cells live on and multiply indefinitely and uncontrollably. This uncontrolled multiplication of rogue cells can lead to cancer.

Conventional chemotherapeutic drugs target and attempt to kill rapidly dividing cancer cells. This is sometimes successful in halting the disease, but these drugs inevitably damage many normal tissues. Hence, even when the chemotherapy works, the side effects for the patient can be very serious.

ABT-737 is a drug with a different strategy for attacking cancer. Rather than attempting to poison the rogue cells, the new drug attempts to reactivate the healthy and normal cell death program that failed to kill the unwanted cells on cue.

WEHI's leading researcher with the assessment project, Dr David Huang, explains, "Normally, the cell death machinery is switched on when damaged cells need to be removed. The failure of the machinery to be turned on when it should can lead to cancer. ABT-737 is a 'switch flicker' that kicks the cell death machinery into action. Much more remains to be done to assess the drug's safety and effectiveness in patients, but early results from the laboratory are promising. Our hope is that the new drug will prove to be more effective while having fewer side effects."

The findings of the scientific assessment team are published in the 13 November 2006 issue of the prestigious international journal Cancer Cell.

Sutent, One Of The New 'Targeted' Cancer Drugs

25 Nov 2006

The new "smart" drugs are a really exciting element of cancer medicine. One of the new molecularly-targeted cancer drugs is Sutent. It is a "multi-targeted kinase inhibitor." A drug that inhibits several proteins involved in triggering replication in cancer cells. Basically, inhibits various kinases, a type of enzyme that transfers phosphate groups from high-energy donor molecules to specific target molecules.

Sutent (sunitinib) is an inhibitor of multiple protein kinases, platelet-derived growth factor (PDGFR), vascular endothelial growth factor receptors (VEGFR), stem cell factor receptor (KIT), FMS-like tyrosine kinase (Flt3), colony stimulating factor (CSF-1R), and the neurotrophic factor receptor (RET). Because these proteins are involved in both tumor proliferation and angiogenesis, Sutent has both anti-tumor as well as anti-angiogenic properties. In addition, because Sutent inhibits multiple kinases, it possesses activity against multiple types of tumors.

Sutent can be used as a second-line drug for tumors that are non-responsive to Gleevec. The proto-oncogene KIT, a tyrosine kinase that is inhibited by Gleevec, is overexpressed in a majority of GISTs. Some patients have suffered relapses due to acquired point mutations in KIT, which prevents Gleevec from binding to the protein. Similar mutations have been characterized in EGFR from Iressa-resistant lung cancer patients.

The largest group of kinases are Protein kinases, which act on and modify the activity of specific proteins. So people will try and get some sort of gene-based test to measure the expression-mutation of these kinases. But something more elemental is going on. Does the drug even enter the cell? Once entered, does it immediately get metabolized or pumped out, or does it accumulate?

On the EGFRx? Assay, Sutent is conveniently pigmented, brilliant yellow. Easy to see which cells have taken it up. In photomicrographs (two magnifications), it is fairly easy to see that some clones of tumor cells don't accumulate the drug. These cells won't get killed by it. But you wouldn't pick this up with an assay which only measured the kinases themselves. The EGFRx? Assay measures the net effect of everthing which goes on (Whole Cell Profiling). Are the cells ultimately killed, or aren't they?

Normal chemotherapy kills both cancer cells and healthy normal cells (mainly rapidly-dividing cells). Oncologists try to minimize damage to normal cells and to enhance the cell-killing effect on cancer cells. Too often, this delicate balance is not achieved.

??Targeted therapy drugs interfere with specific molecules (receptors and enzymes inside and outside a cancer cell). By focusing on these molecular and cellular changes, targeted cancer drugs go after the "target" in these cells, rather than just all cells. Because of this, "targeted" drugs may be more effective than current treatments, and may be less harmful to normal cells.

??Whole cell profiling can discriminate between the activity of different "targeted" drugs and identify situations in which it is advantageous to combine the "targeted" drugs with other types of cancer drugs. Because these new "smart" drugs will work for "some" but not "all" cancer patients who receive them, whole cell profiling can accurately identify patients who would benefit from treatment with molecularly-targeted anti-cancer therapies.

??Not only is this an important predictive test that is available, but it is also a unique tool that can help to identify newer and better drugs, evaluate promising drug combinations, and serve as a "gold standard" correlative model with which to develop new DNA, RNA, and protein-based tests that better predict for drug activity.

This kind of technique exists, and might be very valuable, especially when active chemoagents are limited in a particular disease; it makes more sense than ever to test the tumor first. Afterall, cutting-edge techniques can often provide superior results over tried-and-true methods that have been around for many years.

The EGFRx? Assay is the only assay that involves direct "visualization" of the cancer cells at endpoint. This allows for accurate assessment of drug activity, discriminates tumor from non-tumor cells, and provides a permanent archival record, which improves quality, serves as control, and assesses dose response in vitro.

Longer Anthracycline Therapy Reduces Heart Failure In Adult Cancer Patients

27 Nov 2006

Stretching out a dose of chemotherapy over six or more hours may reduce the risk of heart problems caused by certain commonly used cancer drugs, according to a new review of recent research.

Anthracycline drugs like daunorubicin and doxorubicin are used to treat many types of solid tumors and blood cancers such as leukemias in adults and children.

Anthracycline therapy can be very successful at controlling cancer, but heart damage caused by anthracycline treatment "is a considerable and serious problem," said Dr. Elvira van Dalen of the Emma Children's Hospital in the Netherlands.

She and her colleagues found that the rates of heart failure among adult patients receiving anthracycline therapy were significantly lower when the patients had an infusion of the drug that lasted six or more hours, compared to shorter infusions times.

In five studies involving 557 patients, the longer treatment cut the risk of heart failure by nearly 75 percent compared to the risk in patients who received the short treatment.

van Dalen said the prolonged dose of six hours or more "might be justified" if a patient is at high risk of heart damage or needs a high cumulative dose of the chemotherapy.

The review appears in the latest issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.

In some of the studies, the prolonged dose also reduced the risk of less severe problems such as weakened heart function. Patients had the same chance of survival and tumor shrinkage whether they received the long or short therapies, the Cochrane researchers found.

"It should be emphasized that the majority of the patients included in these studies were adults with advanced solid tumors," van Dalen and colleagues said, noting that there are few good studies about the length of anthracycline treatment in children.

Among the children in the study, there was no difference in heart damage between the long and short treatments "and no information on survival and tumor shrinkage was available," van Dalen said.

Recent studies have shown that the toxic heart effects of anthracycline therapy can have lasting effects on children's health. Dr. Stephen Lipshulz, a pediatric cancer specialist at the University of Miami, said childhood cancer survivors "may be at significant risk of serious cardiovascular problems at a much younger age," than researchers believed a few years ago.

Lipshulz's work suggests many childhood cancer survivors suffer from enlarged hearts and prematurely hardened arteries, due at least in part from their chemotherapy. "It's alarming that we've found such dramatic heart damage and blood vessel risk in some survivors who are just 10 or 15 years from treatment," he said.

Chemotherapy Temporarily Affects The Structures Of The Human Brain

03 Dec 2006

Researchers have linked chemotherapy with short-term structural changes in cognitive areas of the brain, according to a new study. Published in the January 1, 2007 issue of CANCER, a peer-reviewed journal of the American Cancer Society, the study reveals that within 12 months of receiving adjuvant chemotherapy, significant regions of the brain associated with memory, analysis and other cognitive functions were significantly smaller in breast cancer patients who received chemotherapy than those who did not. Within four years after treatment, however, there were no differences in these same regions of the brain.

While the development of chemotherapy has had substantial and beneficial impact on cancer survival rates, it is also linked to significant short- and long-term adverse effects. Gastrointestinal complaints, immunosuppression, and painful mucositis, for example, are the immediate risks of the treatment.

Patients receiving chemotherapy have also long complained of problems with memory, problem-solving and other cognitive abilities. Although chemotherapy was thought not to affect brain cells due to the blood-brain barrier, recent clinical studies have confirmed declines in cognitive functions in patients receiving chemotherapy. Animal studies have shown physical changes in the brain and in neurons caused by chemotherapy drugs. In human studies, however, the little data that is available is only available through imaging and is not consistent in the long-term. In addition, lack of controls in studies makes it difficult discern cancer- versus drug-effects.

Led by Masatoshi Inagaki, M.D., Ph.D., of the Breast Cancer Survivors' Brain MRI Database Group in Japan, researchers used MRI to take high-resolution images and measure volumes in specific areas of the brain of breast cancer patients who received chemotherapy and those who did not one-year after surgery and three-years after surgery. In addition, they compared brains of cancer survivors one-year after surgery and three-years after surgery with healthy subjects.

They found that at one-year, patients treated with chemotherapy had smaller volumes in cognitively sensitive areas, such as the prefrontal, parahippocampal and cingulate gyri, and precuneus regions. However, at three-years post-surgery there was no volume differences. That there were no differences between cancer patients and healthy controls at any time point demonstrates that there is no observable cancer-effect in cognitive deficits.

The authors write that this study suggests that regional brain changes are observable within 12 months and correlate with receiving chemotherapy rather than a secondary effect of the cancer, although it cannot be concluded because of several limitations caused by the study design. However, these structural changes to the central nervous system were not sustained for patients three years after chemotherapy. The authors conclude that "these results lead to the idea that adjuvant chemotherapy could have a temporary effect on brain structure."

Par Pharmaceutical Receives Approval For Ondansetron Orally Disintegrating Tablets

29 Dec 2006

Par Pharmaceutical Companies, Inc. (NYSE: PRX) today announced that it has received final approval from the U.S. Food and Drug Administration (FDA) for its Abbreviated New Drug Application (ANDA) for ondansetron orally disintegrating tablets (ODT) in 4 mg and 8 mg strengths. Par has been awarded 180 days of marketing exclusivity for being the first to file an ANDA containing a paragraph IV certification for the product, which will be marketed by PLIVA, Inc., the U.S. subsidiary of PLIVA d.d., which is a subsidiary of Barr Pharmaceuticals, Inc. of Woodcliff Lake, New Jersey.

Ondansetron ODT is the generic version of GlaxoSmithKline's Zofran ODT(R). The product is used for the prevention of nausea and vomiting associated with highly emetogenic cancer chemotherapy and with initial and repeat courses of moderately emetogenic cancer chemotherapy, certain radiotherapies, and the prevention of postoperative nausea and/or vomiting. Annual U.S. sales of Zofran ODT(R) are approximately $300 million, according to IMS Health.

Under the terms of an agreement between the two companies, Barr will have exclusive rights to market, sell and distribute ondansetron ODT in the U.S. The product will be manufactured by Par, and the companies will split profits from the sales of the product.

Par Pharmaceutical Companies, Inc. develops, manufactures and markets generic drug and innovative branded pharmaceuticals for specialty markets. For press release and other company information, visit

Certain statements in this press release constitute "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. To the extent any statements made in this news release contain information that is not historical, these statements are essentially forward- looking and are subject to risks and uncertainties, including the difficulty of predicting FDA filings and approvals, acceptance and demand for new pharmaceutical products, the impact of competitive products and pricing, new product development and launch, reliance on key strategic alliances, uncertainty of patent litigation filed against us, availability of raw materials, the regulatory environment, fluctuations in operating results and other risks and uncertainties detailed from time to time in the Company's filings with the Securities and Exchange Commission, such as the Company's Form 10-K, Form 10-Q, and Form 8-K reports.

Par Pharmaceutical Companies, Inc.

Mechanism By Which Cells Resist Chemotherapy Found By Researchers

07 Mar 2007

In his paper, to be published in The EMBO Journal, Dr Surrall?s describes how proteins of the Fanconi/BRCA pathway recognise the presence of genetic mutations in order to repair them. The researchers also found that alteration of this mechanism makes tumour cells much more sensitive to certain drugs. This discovery will make it possible to develop strategies to make tumours more vulnerable to chemotherapy.

One of the main mechanisms responsible for repairing mutations in humans is the cancer-suppressing Fanconi anaemia/BRCA pathway. This mechanism makes it possible for the cells to identify genetic mutations in order to correct them.

If this mechanism does not function correctly, it leads to Fanconi anaemia, a rare genetic disorder characterised by progressive bone-marrow failure, various congenital malformations and a very high risk of cancer.

Furthermore, the proteins of this pathway are largely responsible for the resistance of tumours to many antitumour agents such as cisplatin and other chemotherapeutic agents that kill tumour cells by producing DNA interstrand crosslinks. That is, they identify cellular alterations induced by chemotherapy and correct them, "accidentally" helping the tumour.

Many tumours have molecular anomalies in this pathway. These defects mean the tumours can be treated efficiently using certain antitumour agents. There are at least 13 genes involved in the pathway. Three of these (BRCA2, BRIP1 and PALB2) are responsible for the high proportion of hereditary breast cancers (between 5 and 10% of all breast cancers).

Understanding how this DNA repair pathway works is of great interest to biomedicine, not only for Fanconi anaemia patients, but also for the general cancer population, since it determines the the efficacy of chemotherapy in treating many tumours. However, the involvement of 13 genes in the same pathway makes the study more complexed.

A team of researchers from the UAB's Mutagenesis Group, led by Doctor Jordi Surral?s, has identified one of the important unresolved questions regarding this pathway: how the Fanconi anaemia proteins detect the presence of mutations so they can repair them.

The researchers have found that the mutations block the DNA replication process, a process that is necessary, especially in tumour tissues, for the cells to be able to divide and proliferate. By blocking the replication process, the mutations activate a type of enzyme, the ATR kinase, which phosphorylates (introduces phosphate groups into) histone H2AX, a protein present in the chromatin that surrounds the damaged DNA. The phosphorylated histone H2AX indicates the location of the genetic damage to the Fanconi proteins and places them in exactly the right place to repair the DNA.

The researchers have shown that one of the 13 Fanconi proteins, the FANCD2, binds directly to the phosphorylated histone H2AX. The BRCA1 protein also plays a part in this process and, alongside the BRCA2, it is involved in most hereditary breast cancers. So these proteins cooperate in repairing the genetic damage, preserving the stability of the chromosomes and preventing the onset of tumours.

This research will have many implications on biomedicine. The increase in knowledge on this pathway will make it possible to design strategies for the chemosensitisation of tumour cells. Dr Jordi Surall?s's team has also observed that many breast cancer cell lines are between two to three times more sensitive to chemotherapy if they have partially inhibited the Fanconi FANCD2 gene expression.

Advanced Cancer Patients Could Benefit From Personalized Healthy Diets

14 Mar 2007

It is well known that cancer patients undergoing chemotherapy and radiation therapy often experience nausea and loss of appetite. But until now, few researchers have looked into why this happens and what can be done to ensure that cancer patients maintain a healthy diet during treatment.

Researchers at the University of Alberta studying the effects of chemotherapy and radiation therapy on the senses report that most advanced cancer patients experience unique and persistent taste and smell abnormalities, believed to be a key factor in malnutrition and poor quality of life. The condition, known as chemosensory dysfunction, is believed to last long after patients have finished active chemotherapy or radiation therapy.

Taste distortion, heightened sensitivity to odours and a persistent bad taste in the mouth were the most common symptoms described by participants in the recent study conducted by Dr. Wendy Wismer and Dr. Vickie Baracos. However, Wismer says that every patient with chemosensory dysfunction has unique symptoms, and a diet tailored to her needs would likely improve quality of life.

"With taste and smell, and even with food consumption, we tend to draw broad conclusions and make sweeping recommendations," she says. For example, individuals with severe chemosensory dysfunction will often end up on a diet of soup or oral nutritional supplements such as Boost because their heightened or distorted senses make it difficult to eat much else.

"We're looking at how an altered sense of taste and smell affects the food you select. We argue that altered chemosensory perception is unique to the individual. In the same way that people need unique corrective lenses for their eyesight, patients need unique solutions for chemosensory distortion," Wismer explains.

Wismer and Baracos studied 66 patients with advanced cancer receiving palliative care and asked them to evaluate their own taste and smell functions using a validated questionnaire and three-day food diaries to assess their dietary intake. The vast majority - 86 per cent of participants - reported some level of chemosensory abnormality. While this study focused on advanced cancer patients, Wismer believes the findings are relevant to any patient who has received chemotherapy or radiation therapy.

Further research will look at appropriate strategies to alleviate chemosensory dysfunction and explore how matching foods to an individual's unique chemosensory profile might help to prevent high rates of weight loss and malnutrition and improve quality of life.

No Carrier Necessary: This Drug Delivers Itself

17 Mar 2007

The problem of efficiently delivering drugs, especially those that are hydrophobic or water-repellant, to tumors or other disease sites has long challenged scientists to develop innovative delivery systems that keep these drugs intact until reaching their targets.

Now scientists in the University at Buffalo's Institute for Lasers, Photonics and Biophotonics and Roswell Park Cancer Institute have developed an innovative solution in which the delivery system is the drug itself.

They describe for the first time in Molecular Pharmaceutics a drug delivery system that consists of nanocrystals of a hydrophobic drug.

The system involves the use of nanocrystals measuring about 100 nanometers of pure HPPH, (2-devinyl-2-(1'-hexyloxyethyl) pyropheophorbide), a photosensitizer currently in Phase I/II human clinical trials at RPCI for treating various types of cancer.

The UB researchers found that the nanocrystals of HPPH were taken up by tumors in vivo, with efficacy comparable to conventional, surfactant-based delivery systems.

A patent has been filed on this work.

"In this case, the drug itself acts as its own carrier," said Haridas Pudavar, Ph.D., UB research assistant professor of chemistry and a co-author.

The nanocrystals present a major advantage over methods of delivery involving other carriers, according to Paras Prasad, Ph.D., SUNY Distinguished Professor in the Department of Chemistry in UB's College of Arts and Sciences, executive director of the institute and a co-author.

Because other delivery systems, especially those containing surfactants, commonly used with HPPH and many other drugs, may add to the toxicity in the body, they have been considered imperfect solutions.

"Unlike formulations that require separate delivery systems, once this drug is approved, no additional approvals will be needed," said Prasad.

"Our published data in animal models demonstrate no difference in drug activity with the nanocrystal formulation," said Ravindra Pandey, Ph.D., Distinguished Professor of Biophysical Sciences at RPCI and a co-author on the paper.

"This is a case where the easiest formulation works the best," added Indrajit Roy, Ph.D., UB research assistant professor of chemistry and another co-author.

The researchers found that because HPPH is amphiphillic, i.e., partially soluble in water and oil, nanocrystals of it will self-assemble, that is, in solution the molecules aggregate, but not into such big clusters that they settle to the bottom.

"It's a controlled formation of a colloidally stable suspension of nanosized crystals," explained Tymish Ohulchanskyy, Ph.D., UB senior research scientist and a co-author.

The researchers originally were investigating nanocrystals as a delivery method for hydrophobic dyes in bioimaging applications, another promising use for nanocrystals that they continue to pursue.

Further in vivo studies with HPPH nanocrystals are being conducted by scientists at UB and RPCI, including Pandey and Allan R. Oseroff, M.D., Ph.D., chair of the department of dermatology at RPCI and in UB's School of Medicine and Biomedical Sciences.

The UB/RPCI team is exploring the use of the same technique for delivering other hydrophobic drugs, including those used in chemotherapy.

CoGenesys Expands Clinical Programs With Initiation Of Phase 1-2a Trial Of Neugranin In Cancer Patients

29 Mar 2007

CoGenesys, Inc. announced today that the Company has initiated a Phase 1-2a study in Europe of Neugranin(TM), a long-acting form of Granulocyte Colony Stimulating Factor (G-CSF). Neugranin is designed to reduce infections associated with neutropenia, a reduction in the number of white blood cells which is the most common side effect associated with the administration of chemotherapy in cancer patients.

CoGenesys' Phase 1-2a study is a randomized, multicenter, double-blind, controlled safety, tolerability, and evaluation for effect trial in more than 60 patients with breast cancer. In the first phase of the study, subjects will receive a subcutaneous dose of Neugranin prior to receiving myelosuppressive chemotherapy (Doxorubicin/Docetaxel). In the second phase, patients will receive their chemotherapy prior to dosing, and a positive control group will receive Neulasta(R), a pegylated form of G-CSF. Evaluations will include safety and tolerability, pharmacokinetic profiles, and, additionally, in the second phase, signals for effect.

Martha A. Reitman, M.D., CoGenesys' Senior Vice President, Medical Affairs, stated, "The Phase 1-2a study builds on previous preclinical research demonstrating that our long-acting form of G-CSF will likely have a therapeutic profile comparable to that of Neulasta(R), the current market leader for the treatment of patients with neutropenia. In designing the trial, we have benefited from the fact that G-CSF is a well-characterized compound which has been studied in a number of patient populations, and we expect the program to advance rapidly through clinical development. We also believe that Neugranin will have a competitive cost-of-goods profile and therefore may represent an affordable treatment alternative to current therapy."

Steven C. Mayer, CoGenesys' Chief Executive Officer, commented, "We are pleased to announce the initiation of clinical trials for the second product candidate from our diverse pipeline of improved, long-acting biopharmaceuticals. The first study initiated in October 2006 with patient enrollment for our Phase 1-2 testing of Cardeva(TM), a long-acting form of B-type natriuretic peptide (BNP) which is being developed for the treatment of patients with heart failure. We also expect to initiate clinical trials of our third product candidate, a long-acting basal insulin, during summer 2007. In all of these trials, our strategy has been to identify important therapeutic areas and pursue strongly validated therapeutic modalities which can substantially benefit from our proprietary albumin-fusion technology."

Fighting Infections in Cancer Patients

Serious infections and hospitalization can result from neutropenia, and the presence of neutropenia-associated fever often necessitates the reduction of the dose of chemotherapy in patients or can cause a delay in the administration of the next cycle of chemotherapy. Treatment and prevention of neutropenia is a particular concern in a number of cancers, such as breast cancer or non-Hodgkin's lymphoma, in which the importance of dose maintenance for treatment success has been well-established.

The worldwide market for colony stimulating factors is expected to reach $5 billion by 2010. Three products have been approved for marketing in the United States: Amgen's Neupogen(R) and Neulasta(R), and Schering AG's Leukine(R). Neulasta(R) is the only long-acting G-CSF product presently approved in the world. Neulasta alone generated $2.7 billion in sales in 2006. CoGenesys believes that Neugranin has the potential to be the second long-acting G-CSF product to enter this very large market.

Antioxidants May Aid Chemotherapy Patients

27 Apr 2007

There is no evidence that antioxidant supplements interfere with the therapeutic effects of chemotherapy agents, according to a recent systematic review of the use of antioxidants during chemotherapy, available in the May, 2007 issue of the peer-reviewed journal Cancer Treatment Reviews. In fact, they may help increase survival rates, tumor response, and the patient's ability to tolerate treatment. This conclusion has important implications for patients whose oncologists discourage the use of antioxidant supplements during treatment. Until now, their concern has been that these supplements may counteract the tumor-shrinking abilities of the chemotherapy.

"This review demonstrates that there is no scientific support for the blanket objection to using antioxidants during chemotherapy. In addition, it also appears that these supplements may help mitigate the side effects of chemotherapy," said Keith I. Block, MD, lead author of the study and Medical Director of the Block Center for Integrative Cancer Treatment. "This is significant because it increases the likelihood that patients will be able to complete their treatment."

Co-author Dr. Robert Newman, Professor of Cancer Medicine at M. D. Anderson Cancer Center said, "This study, along with the evolving understanding of antioxidant-chemotherapy interactions, suggests that the previously held beliefs about interference do not pertain to clinical treatment."

The analysis, titled "Impact of Antioxidant Supplementation on Chemotherapeutic Efficacy: A Systematic Review of the Evidence from Randomized Controlled Trials," evaluated 845 articles from five scientific databases that examined the effects of taking natural antioxidant supplements concurrent with chemotherapy.

Out of the 845 studies that were analyzed, 19 met all evaluation criteria. These included the use of randomized trials with a control group, and the reporting of treatment response (tumor shrinkage) and survival data. The 1,554 patients represented had a variety of cancer types, and most had advanced or relapsed disease. Some of the antioxidants used in the trials included glutathione, vitamin A, vitamin C, vitamin E, ellagic acid, selenium and beta carotene.

Among the findings:

All of the studies that included survival data showed similar or better survival rates for the antioxidant group than the control group.

-- None of the trials supported the theory that antioxidant supplements diminish the effectiveness of chemotherapy treatments.

-- All but one of the studies that reported treatment response showed similar or better response in the antioxidant group than in the control group.

-- 15 of 17 trials that assessed chemotherapy toxicities, including diarrhea, weight loss, nerve damage and low blood counts, concluded that the antioxidant group suffered similar or lower rates of these side effects than the control group.

The authors noted that reducing side effects may help patients avoid having to cut back on their chemotherapy dosing, interrupt scheduled treatments, or abandon treatment altogether. This in turn, is likely to favorably impact treatment outcomes. A recent study of a group of colon cancer patients indicated that those who completed their full prescribed schedules of chemotherapy had survival rates nearly double those of patients who abandoned their chemotherapy treatment prematurely.

This new study encourages further exploration of the potential importance of antioxidant supplements as a means of improving cancer survival.

Block Center for Integrative Cancer Treatment

Valid XHTML :: Valid CSS: :: Powered by WikkaWiki