Archive for the ‘leukemia’ Category

ASH: Nine Genes Drive CLL

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Posted 13 Dec 2011 — by James Street
Category Gene sequencing, genetic research, leukemia, leukemia (APL)
Visit us online at www.MedPageToday.com A | A | A | A
By Michael Smith, North American Correspondent, MedPage Today
December 12, 2011

SAN DIEGO — Using massively parallel genetic analysis, researchers have found nine genes that appear to be the drivers of chronic lymphocytic leukemia (CLL).

Five of the nine have not been previously associated with the disease, according to Catherine Wu, MD, of the Dana Farber Cancer Institute in Boston, and colleagues.

And one — splicing factor 3b, subunit 1 (or SF3B1) — was surprising, in that it implicates errors in RNA splicing in the pathogenesis of the disease, the researchers reported online in the New England Journal of Medicine and here at the American Society of Hematology meeting.

Taken together, the finding “defines the landscape” of mutations in chronic lymphocytic leukemia and highlights RNA splicing as a “critical cellular process” contributing to the disease, the researchers concluded.

Indeed, the link with mutations in genes involved in RNA splicing was “highly unexpected,” commented Benjamin Ebert, MD, PhD, of Brigham and Women’s Hospital in Boston, and Olivier Bernard, PhD, of INSERM’s Institut Gustave Roussy in Villejuif, France.

That said, they noted in an accompanying editorial, the finding “converges” with recent studies showing that SF3B1 mutations are common in myelodysplastic syndromes, and are found in more than half of patients with refractory anemia and ring sideroblasts.

And it “raises the intriguing possibility” that the splicing mechanism might be a therapeutic target in both chronic lymphocytic leukemia and myelodysplastic syndromes, they concluded.

The researchers sequenced DNA samples of leukemia cells from 91 patients with the disease, including three complete genomes and 88 “exomes” — the complete collection of coding regions of genes — and compared the results with sequences from normal tissue.

Nine genes were mutated at a rate significantly higher than the background mutation rate, they found — TP53, ATM, MYD88, and NOTCH1 were previously linked to CLL and SF3B1, FBXW7, DDX3X, MAPK1, and ZMYM3 “do not have established roles” in the disease.

SF3B1 was the second most commonly mutated gene, with alterations occurring in 14 of the 91 patients. TP53 was first, being mutated in 15 patients.

The three most common mutations — in TP53, SF3B1, and NOTCH1 — appeared at similar frequencies in a separate cohort of 101 patients as they did in the original 91, the researchers reported.

The mutations in SF3B1 were clustered in a relatively small region that is highly conserved in species ranging from yeasts to human, Wu and colleagues found, and in half the cases the mutation produced the same amino acid change.

Those findings suggest that the mutations cause specific functional changes, the researchers argued.

A Cox multivariable regression model, intended to look for factors contributing to an earlier initiation of treatment, showed that an SF3B1 mutation predicted an earlier need for therapy. The hazard ratio was 2.20, which was significant at P=0.03 and was independent of known predictive markers.

The researchers also found defects in RNA splicing in 13 patients with the mutated SF3B1 gene, but none in 17 patients with a wild-type gene.

The study was supported by the Broad Institute, the NIH, the National Cancer Institute, the Melton and Rosenbach Funds, the Blavatnik Family Foundation, the Howard Hughes Medical Institute, and the Damon Runyon Cancer Research Foundation.

Wu did not report any financial links with industry.

The editorial writers did not report any financial links with industry.

Primary source: New England Journal of Medicine
Source reference:
Wang L, et al “SF3B1 and other novel cancer genes in chronic lymphocytic leukemia” N Engl J Med 2011; DOI: 10.1056/NEJMoa1109016.

Additional source: New England Journal of Medicine
Source reference:
Ebert B, Bernard OA “Mutations in RNA splicing machinery in human cancers” N Engl J Med 2011; DOI: 10.1056/NEJMe1111584.

New Method That Reveals Complete Set of Aberrant Signaling Pathways That Give Rise to Cancers

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Posted 02 Dec 2011 — by James Street
Category Breast Cancer, Heat Shock Protein, HSP90, leukemia, Lymphoma, Molecular, PU-H71

From HealthNewsDigest.com

Cancer Issues
Dec 1, 2011 – 1:38:32 PM

 

(HealthNewsDigest.com) – NEW YORK (Dec. 1, 2011) — One major obstacle in the fight against cancer is that anticancer drugs often affect normal cells in addition to tumor cells, resulting in significant side effects. Yet research into development of less harmful treatments geared toward the targeting of specific cancer-causing mechanisms is hampered by lack of knowledge of the molecular pathways that drive cancers in individual patients.

“A major goal of cancer research is to replace chemotherapy with drugs that correct specific molecular pathways disrupted by cancer,” says Dr. Ari Melnick, one of the study’s lead investigators and director of the Raymond and Beverly Sackler Center for Biomedical and Physical Sciences and associate professor of medicine at Weill Cornell Medical College. “But looking for mutations isn’t always the way to find the most important factors that are keeping cancer cells alive.”

Through a collaboration among Weill Cornell Medical College, the Sloan-Kettering Institute at Memorial Sloan-Kettering Cancer Center and the National Cancer Institute (NCI), a team of scientists has now reported that a tumor-targeting compound called PU-H71 can reveal with great accuracy the set of altered pathways that contribute to malignancy. Because the drug specifically binds to abnormal protein complexes in cancer cells, it could lead to the development of more targeted and effective therapies that produce fewer side effects. These findings were recently published in the journal Nature Chemical Biology.

“The holy grail in the field was to develop some way to figure out what factors keep cancer cells alive, regardless of whether they have mutations,” says Dr. Melnick. “In this paper, we present a method to do just that.”

Through nearly a decade of research, PU-H71 was discovered and refined in the laboratory of Dr. Gabriela Chiosis, associate member of the Molecular Pharmacology and Chemistry Program at the Sloan-Kettering Institute and an associate attending chemist of Memorial Hospital, Memorial-Sloan Kettering Cancer Center. Dr. Chiosis, who is the senior investigator in this new study, reported initial findings about the drug five years ago. The compound was designed to inhibit heat shock protein 90 (Hsp90), which helps other proteins fold into the correct three-dimensional shape and function properly.

Hsp90 plays an essential role in the ability of cells to tolerate stress. The altered growth and metabolism of tumors induce a high degree of stress in these cells. To cope with this stress, tumor cells produce a special form of Hsp90 that is tuned to specially protect those proteins required for their growth and survival. Because this tumor/stress form of Hsp90 regulates many pathways that go awry in cancer, it is a more promising drug target than current targets that play a role in only a single pathway, Dr. Chiosis says. Importantly, PU-H71 specifically suppresses the cancer form of Hsp90 but has little effect on Hsp90 in normal cells.

Several years ago, Dr. Chiosis partnered with Dr. Melnick to examine the effectiveness of PU-H71 in treating breast cancer and lymphomas, and they have previously reported that the drug has dramatic antitumor effects without being toxic to animals. As a result of the drug’s success in fighting these two aggressive types of cancer, the research team received approval from the National Cancer Institute to carry out clinical trials. Patients are currently being recruited for the first trial, which will test the drug’s safety in treating a variety of tumor types, and subsequent clinical trials are being planned for patients with lymphomas, breast cancer, chemotherapy-resistant leukemia and other specific types of cancer.

In their new study Dr. Chiosis, Dr. Melnick, and collaborators demonstrated that because PU-H71 binds to tumor-Hsp90, and tumor-Hsp90 binds to proteins that are required for tumor survival, it is possible to use PU-H71 as a method to “fish out” entire networks of abnormal proteins in tumor cells in an unbiased fashion, which has not been possible up until now. Importantly, many or even most of the genes encoding proteins that maintain tumor cell survival are not mutated in tumors. Hence genetic screening would not be able to detect these networks, Dr. Melnick says. “The value of this method is that it’s the first time you can go and probe the functional proteome, or the whole set of proteins that are important to maintaining the tumor.” This strategy opens up new avenues for understanding in greater detail the molecular basis of cancer and identifying novel drug targets.

For example, in chronic myeloid leukemia cells, the PU-H71 drug preferentially binds to the Hsp90 complex containing Bcr-Abl, an abnormal protein that is overactive in these cells, rather than to Hsp90 associated with the normal protein Abl. Similar findings were observed in other tumor types, with PU-H71-Hsp90 complexes protecting only the tumor-associated proteins.

The researchers then used PU-H71 and proteomic analyses to identify all of the abnormal proteins bound to Hsp90 in chronic myeloid leukemia cells and built networks of these proteins using bioinformatics analyses. They found that these proteins are part of signaling pathways involved in cell death, growth and division. Bcr-Abl is known to use many of these pathways to propagate abnormal signaling in this type of cancer cell. The researchers experimentally confirmed that proteins from these pathways are crucial for cancer cell growth, division and survival, suggesting that their approach can be used to accurately identify Bcr-Abl-related protein networks. Moreover, the same experiments identified many proteins not previously known to drive chronic myeloid leukemia cells. One example of such a protein was CARM1, a regulator of gene expression, which the investigators showed maintains survival of these tumor cells.

Importantly, this PU-H71 cancer proteome method can also be used to identify networks of abnormal proteins in the cells from individual patients, paving the way to personalized therapies that target multiple pathways. “No two tumors are exactly alike, and we don’t really know what is driving cancer in one patient versus the other,” the researchers say. “If you can use this method to identify in a given individual the factors that are maintaining that patient’s particular cancer, then you could develop targeted drugs that hit these specific factors — in effect, designing personalized therapy for individual patients.”

Based on these findings, Dr. Melnick and Dr. Chiosis recently received a multi-investigator collaborative grant from the National Cancer Institute to use this new PU-H71 proteome method to identify the proteins that maintain the survival of lymphoma cells. This funding is an example of how collaboration between investigators and institutions can synergistically accelerate the pace of biomedical research.

Study collaborators include Kamalika Moulick, James Ahn, Anna Rodina, Erica Gomes DaGama, Eloisi Caldas-Lopes, Fabiana Perna, Ly Vu, Xinyang Zhao, Danuta Zatorska, Tony Taldone, Mary Alpaugh, Stephen Nimer, Peter Smith-Jones, Nagavarakishore Pillarsetty, Thomas Ku, Jason Lewis, Steven Larson, Ross Levine and Hediye Erdjument-Bromage of Memorial Sloan-Kettering Cancer Center in New York City; Hongliang Zong, Leandro Cerchietti, Katerina Hatzi, Steven Gross and Monica Guzman of Weill Cornell Medical College; and Kristin Beebe and Len Neckers of the National Cancer Institute in Bethesda, Md.

This work was supported in part by the National Cancer Institute, Leukemia and Lymphoma Society, the Breast Cancer Research Fund, the SPORE Pilot Award and Research and Therapeutics Program in Prostate Cancer, the Hirshberg Foundation for Pancreatic Cancer Research, the Byrne Fund and the V Foundation for Cancer Research.

The Raymond and Beverly Sackler Center for Biomedical and Physical Sciences

The Raymond and Beverly Sackler Center for Biomedical and Physical Sciences of Weill Cornell Medical College brings together a multidisciplinary team of scientists for the purpose of catalyzing major advances in medicine. By harnessing the combined power of experimental approaches rooted in the physical and biological sciences, Sackler Center investigators can best accelerate the pace of discovery and translate these findings for the benefit of patients with various medical conditions including but not limited to cancer.

Weill Cornell Medical College

Weill Cornell Medical College, Cornell University’s medical school located in New York City, is committed to excellence in research, teaching, patient care and the advancement of the art and science of medicine, locally, nationally and globally. Physicians and scientists of Weill Cornell Medical College are engaged in cutting-edge research from bench to bedside, aimed at unlocking mysteries of the human body in health and sickness and toward developing new treatments and prevention strategies. In its commitment to global health and education, Weill Cornell has a strong presence in places such as Qatar, Tanzania, Haiti, Brazil, Austria and Turkey. Through the historic Weill Cornell Medical College in Qatar, the Medical College is the first in the U.S. to offer its M.D. degree overseas. Weill Cornell is the birthplace of many medical advances — including the development of the Pap test for cervical cancer, the synthesis of penicillin, the first successful embryo-biopsy pregnancy and birth in the U.S., the first clinical trial of gene therapy for Parkinson’s disease, and most recently, the world’s first successful use of deep brain stimulation to treat a minimally conscious brain-injured patient. Weill Cornell Medical College is affiliated with NewYork-Presbyterian Hospital, where its faculty provides comprehensive patient care at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. The Medical College is also affiliated with the Methodist Hospital in Houston. For more information, visit weill.cornell.edu.

Cancer Cure

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Posted 13 Aug 2011 — by James Street
Category genetic research, Immune System, leukemia, leukemia (APL), Natural Killer Cells

August 13, 2011. 3:

Some of the most amazing progress cancer treatment happened this week at the University of Pennsylvania.

Doctors, by giving a single shot in the arm eliminated the most common type of Leukemia in 2 patients and it is 70% gone in a third. Some of these patients had ugly tumor growths up to 5 pounds. Doctors said these preliminary results “exceeded their wildest expectations”. One of the patients was told over a year ago he only had weeks left to live. It is so successful phase 2 trials have been fast tracked. This could lead to cures for other cancers.

Now many of you are asked countless times to donate to Cancer charities. But here is why you should. Read this below.

Both the National Cancer Institute and several pharmaceutical companies declined to pay for the research. Neither applicants nor funders discuss the reasons an application is turned down. But good guesses are the general shortage of funds and the concept tried in this experiment was too novel and, thus, too risky for consideration.

The researchers did manage to get a grant from the Alliance for Cancer Gene Therapy, a charity founded by Barbara and Edward Netter after their daughter-in-law died of cancer. The money was enough to finance the trials on the first three patients.

 Your generous donations make a HUGE impact in this fight. That’s also why I am a constant fundraiser for cancer research. I feel in a decade we can cure all cancers.

I will be cycling Vancouver to Seattle in the Ride to Conquer Cancer that made $11 Million for reasearch last year. That’s huge. My link is below . Please have a look and make a donation . I need to raise at least $2000 to participate.

It WILL make a difference.

I will write everyone that donates and tell them the difference they made!

http://www.conquercancer.ca/site/TR/Events/Vancouver2012?px=2838054&pg=personal&fr_id=1413

Gene therapy wipes out leukemia

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Posted 13 Aug 2011 — by James Street
Category genetic research, Immune System, leukemia, Natural Killer Cells

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Last Update:  13 August 2011 19:27  GMT                                                        Volume. 11221

Amazing potent tumor-killing agents helped three leukemia sufferers stay cancer-free, say US researchers.

The findings are the first to show how gene transfer therapy can create specialized T-cells, which guard the body from infection, that attack cancerous tumors in advanced cases of chronic lymphocytic leukemia (CLL).

The technique helped patients who had little hope of survival fend off their cancer and stay in remission, said the research published simultaneously in the New England Journal of Medicine and Science Translational Medicine.

Further studies are needed, but the advances offer hope to people who suffer from similar cancer types such as ovarian, lung, myeloma and melanoma.

“Within three weeks, the tumors had been blown away, in a way that was much more violent than we ever expected,” said senior author Carl June of the Abramson Cancer Center of the University of Pennsylvania.

“It worked much better than we thought it would.”

Scientists removed a sample of the patients’ T-cells and genetically modified them to attack all cells that express a certain kind of protein, CD19, which includes tumor cells.

They also engineered the T-cells to start triggering other T-cells to multiply as soon as they attached to a cancer cell, bringing on a faster death for the tumor but avoiding the side-effects of cancer drugs.

“We saw at least a 1,000-fold increase in the number of modified T-cells in each of the patients. Drugs don’t do that,” said June, describing the infused T-cells as “serial killers.”

“On average, each infused T-cell led to the killing of thousands of tumor cells — and overall, destroyed at least two pounds of tumor in each patient.”

One patient’s case, described in the New England Journal of Medicine, involved a 64-year-old man whose blood and marrow were “replete with tumor cells.”

He saw little change for the first two weeks after treatment, but then started experiencing nausea, chills and fever. Test showed he was undergoing a huge rise in T-cell count. By day 28, his blood showed no evidence of leukemia.

“Most of what I do is treat patients with no other options, with a very, very risky therapy with the intent to cure them,” said co-principal investigator David Porter.

“This approach has the potential to do the same thing, but in a safer manner.”

Bone marrow transplants are typically the only treatment for leukemia patients, but they carry a 20 percent risk of dying from the procedure and cure rates hover at around 50 percent.

It remains unknown how long the treatment may keep cancer at bay.

“The doctors have found evidence that months after infusion, the new cells had multiplied and were capable of continuing their seek-and-destroy mission against cancerous cells throughout the patients’ bodies,” said the study.

Chronic lymphocytic leukemia is the second most common type of adult leukemia after chronic myeloid leukemia, according to the National Cancer Institute.

The researchers intend to study similar approaches in children whose leukemia has resisted standard treatment.

They also want to see if the approach could target non-Hodgkin’s lymphoma and acute lymphocytic leukemia, mesothelioma cancer cells, ovarian and pancreatic cancer cells.

Cancer Docs Abuzz About New Leukemia Treatment

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Posted 12 Aug 2011 — by James Street
Category Cancer Types, Immune System, leukemia, leukemia (APL)

By MIKAELA CONLEY
Aug. 12, 2011

In preliminary research that’s been dubbed “remarkable,” “dramatic” and “sensational,” doctors made the most common type of leukemia disappear in two patients, and reduced cancer cells by 70 percent in a third.

Researchers at the University of Pennsylvania transformed patients’ own white blood cells into “serial killers” capable of annihilating cancer cells within the body. The two patients who experienced full recovery are still in remission more than a year later.

Right now, the only way to cure leukemia is through a bone marrow transplant, which carries several risks.

“[The serial killers] can kill one tumor cell and then go and kill another, and we found in all three of our patients that the T-cells killed at least a thousand tumor cells, and that’s the first time that has ever been shown anywhere near that kind of efficiency,” said Dr. Carl June, the lead author of the study, in a video released with the research.

“Previous attempts to engage the immune system in destroying cancer cells have often relied on ‘vaccination’ with tumor cells or tumor proteins,” Dr. Douglas Faller, director of Boston University School of Medicine Cancer Center, wrote in an email to ABCNews.com.

But in this case, researchers genetically altered and reprogrammed the killer cells of the immune system to recognize the leukemia tumor cells, Faller noted.

And for the million dollar question: What does this mean for the future of cancer treatment?

Gleevec for Leukemia Watch Video
Alternative Approaches For Leukemia? Watch Video
Balancing Positive Karma and Reality of Life Watch Video

“This is an evolving area of treatment that is pretty sophisticated,” said Dr. Steven Rosenberg, chief of the surgery branch at the National Cancer Institute. “Someone needs a fair amount of expertise in immunology and molecular biology, and there are very few groups that can do this around the world.”

In 2006, Rosenberg published the first study in which T-cell receptors were used for gene therapy, combined with chemotherapy, in 17 people who had advanced melanoma. Two patients from the trial remained disease-free several years after the study.

Since then, a tumor-specific approach to treatment has been used in clinical trials of patients who had breast, prostate, sarcoma and colon cancer.

“This study is probably the most clear-cut, well-studied and best-described of cases,” said Dr. Renier J Brentjens, a medical oncologist at Memorial Sloan-Kettering Cancer Center, who specializes in treating acute and chronic leukemia through immunology. “It’s very clear here that T-cells are responsible for this effect, and the effect is sustained.”

While the excitement among oncologists and the general public is apparent, experts cautioned that it was too early to tell whether this will become a mainstream cancer treatment. The final verdict is likely years away, experts said.

“[This] probably indicates that this kind of treatment is possible but hugely resource-intensive, and the longer term toxicities and efficacy are not at all clear,” said Dr. Bruce Chabner, clinical director at Massachusetts General Hospital Cancer Center. “It could be historic, but it will take several more years and many more cases before we know.”

“These are expensive trials, and it’s hard to get funding,” said Brentjens. “It might be a little easier now that these papers are published, but you still need a highly expert staff of well-trained specialists. It’s a pretty large operation.”

Even with the proper monetary resources, only a handful of facilities across the country are capable of making these cells.

Despite the financial and staffing hurdles, Brentjens remains optimistic.

It gets me up every morning knowing that this is the future,” said Brentjens. “This is very exciting, and I hope and pray that immunotherapy will one day replace the more toxic chemotherapy for treatment in cancer patients.”

Feverfew and Cancer

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Posted 14 Jul 2011 — by James Street
Category feverfew (parthenolide), leukemia

By Dr. Ralph Moss
from CancerDecisions.com

Many readers know the feverfew plant (Tanacetum parthenium), a member of the Chrysanthemum family, sometimes called bachelor’s buttons. This is a cheerful-looking perennial, with a profusion of white pompon-like blooms—like a shower of tiny daisies. Feverfew is often included in mixed bouquets and, to me, is the essence of summer.

Others know this plant as a source of herbal relief. One traditional usage, as a febrifuge (or fever-reducer) is apparent from its name. It is also a well-known folk remedy for migraine. I keep a feverfew product in my medicine chest, in anticipation of the summertime visits of a friend who is prone to these massive headaches (Pfaffenrath 2002; Murphy 1988).

Now scientists at the Univeristy of Rochester Medical Center have found that an extract of feverfew is effective against a type of human leukemia. Monica L. Guzman, PhD, and Craig T. Jordan, PhD, report that feverfew extracts kill malignant stem cells like no other single therapy they have tested. The active ingredient is derived from parthenolide, one of a class of sesquiterpene lactones found in the plant. The US National Cancer Institute is sufficiently excited by this work to have accepted it into the rapid access program, which aims to move experimental drugs from the laboratory to human clinical trials as quickly as possible.

“This research is a very important step in setting the stage for future development of a new therapy for leukemia,” said Dr. Jordan. “We have proof that we can kill leukemia stem cells with this type of agent, and that is good news.”

A Focus on Stem Cells

What is particularly exciting is that this feverfew extract is the first agent known to destroy myeloid leukemia at the level of the stem cells. Increasingly, cancer research is homing in on these primordial cells as the source of cancer. This is the level at which malignancy is born, and unless it is attacked at this level it can rarely be controlled, much less cured.

In the 19th century there were many intimations that primitive cells, called “embryonal rests,” were fundamentally connected with the development of cancer. A high point came over a century ago, when University of Edinburgh, Scotland, embryologist John Beard, DSc (1858-1924) put forward the theory that cancer was in fact caused by the malignant transformation of what he called pluripotent germ cells. It now seems almost certain that Beard was giving an early description of stem cells and their propensity to undergo malignant change. Beard’s idea was initially greeted with interest, but was later marginalized, and finally all but forgotten. However, his philosophy was kept alive through the work of a few maverick biologists, such as Ernst T. Krebs, Sr. and Jr., H.H. Beard, William D. Kelley, DDS, and others. Click here for information on Prof. John Beard.

In recent years, academic scientists have identified cancer stems cells in blood cancers as well as in brain and breast tumors. The work of Michael Clarke, MD, and his post-doctoral student, Mohammed Al-Hajj, PhD, at the University of Michigan, has been particularly influential. Clarke and Al-Hajj have shown that, contrary to what is generally assumed, not all tumor cells are equally capable of causing metastatic cancer. In fact, they found that in experimental breast tumors only a tiny fraction – less than one percent – of tumor cells are actually capable of causing metastasis. These highly malignant cells are identifiable as stem cells. Click here for information on Dr. Clarke’s work.l

Research in 2005 by JeanMarie Houghton, MD, PhD, of the University of Massachusetts, Worcester, showed that in certain stomach cancers the cells that initiate the malignancy originate not in the tissues of the stomach itself, but are actually stem cells that have migrated there from the bone marrow. The initiating event in this sequence is a low-grade infection in the stomach, typically caused by Helicobacter pylori. Bone marrow derived cells (BMDCs) are sent to the stomach in response to this infection, as part of the body’s attempt to heal itself. Once in the stomach, BMDCs assume the characteristics of the surrounding tissues, but under the influence of hormonal signals emitted by the inflamed tissue, they undergo malignant change. Click here and then here for information on Dr. Houghton’s work.

The latest University of Rochester findings on feverfew, while interesting from the point of view of pharmacology, are even more important in terms of basic science. They have deepened the scientific understanding of how stem cells are involved in the origin and progression of cancer.

Currently, other treatments for AML, including the recently approved drug Gleevec, are only moderately effective. That may be because they do not affect the malignant stem cells, so “you’re pulling the weed without getting to the root,” as Dr. Craig T. Jordan of the University of Rochester said. In laboratory experiments, the Rochester scientists have now shown that parthenolide is in fact more selective at stopping cancer through apoptosis (programmed cell death) than was the standard drug cytarabine (Ara-C).

There have been some prior experiments showing that feverfew compounds halt the growth of cancer cells. A phase I trial found that it was also relatively non-toxic, laying the groundwork for future studies of its effectiveness (Curry 2004).

Feverfew Available

According to a University of Rochester press release, a person with leukemia would not be able to take enough of the over-the-counter herbal remedy to halt the disease. It is not clear how this information has been established in the absence of clinical trials. In fact, patients with leukemia might want to discuss this information with their hematologist-oncologist.

Standardized feverfew products are widely available for the treatment of migraine and other conditions. Many brands describe their products as “high parthenolide.” One needs to read the labels carefully, however. I have found various products claiming to have 2, 5 or even 7 percent parthenolide by weight. Some of these come from obscure companies. One should definitely look for a product marketed by a reputable company which would have something substantial to lose by deceiving the public about the strength and purity of its product.

One such company is Nature’s Way. This company markets three separate feverfew products: feverfew leaves, feverfew extract and an even more concentrated product called MygraFew. This claims to have a standardized content of 2 percent parthenolide. Thus, a 30 milligram tablet contains 600 micrograms of parthenolide.

Cautions

The label cautions that feverfew is not recommended for use by pregnant or lactating women, or children under two years of age. Certain individuals may also experience oral discomfort or irritation when using the product. If irritation does occur, the manufacturer advises discontinuing the use of the product immediately. According to the website www.intelihealth.com:

Feverfew has been well tolerated in studies. The most common side effects are mouth inflammation or ulcers, including swelling of the lips, bleeding of the gums, and loss of taste. When stopped suddenly after being used for long periods of time, feverfew may cause rebound headaches, anxiety, sleep disturbances, muscle stiffness or pain. Some people may experience more rapid or pounding heart rates. Skin irritation or eczema may occur in those with feverfew allergies. Photosensitivity (sensitivity to sunlight or sunlamps) has been reported with other herbs in the Compositae plant family and may be possible with feverfew as well. Less common side effects may include stomach upset, such as indigestion, nausea, gas, constipation, diarrhea, bloating or heartburn.

It is not at all clear how often these adverse events occur. The website further cautions that feverfew may combine adversely with certain drugs:

In theory, feverfew may increase the risk of bleeding when used with anticoagulants (blood thinners) or anti-platelet drugs. Examples include warfarin (Coumadin), heparin and clopidogrel (Plavix). Feverfew may also increase the risk of bleeding when used with anti-inflammatory pain relievers, such as aspirin, ibuprofen (Motrin, Advil) and naproxen (Naprosyn, Aleve, Anaprox). However, it is possible that feverfew may increase the effectiveness of these pain relievers.

“Based on the results from some animal studies, it has been suggested that feverfew could worsen symptoms of depression or reduce the effectiveness of antidepressants such as fluoxetine (Prozac). Feverfew should be used with caution in individuals with a history of depression or other psychiatric illnesses.

The current research work on the use of feverfew in the treatment of AML is extremely good news. Apart from anything else, it strengthens the argument that what is at the root of cancer is not a transformed body (somatic) cell, but a special type of stem cell. This concept has the potential to revolutionize the understanding of cancer, and its treatment.

However, even with the help of NCI, it may be years before this flower derivative makes it to the market. One thing is certain. At around 20¢ per tablet, the cost is reasonable, and compares favorably with patented Gleevec, which, although better researched, costs around $100 per day.

National Debate

There is a major national debate in the US over stem cell research. The use of stem cells has been restricted by government decree.

The National Institutes of Health (NIH) in principle is in favor of stem cell research. An NIH news release states:

“Research involving human pluripotent stem cells…promises new treatments and possible cures for many debilitating diseases and injuries. The NIH believes the potential medical benefits of human pluripotent stem cell technology are compelling and worthy of pursuit in accordance with appropriate ethical standards.”

Yet there is a curious lack of support for stem cell research, at least at NCI. For instance, when I searched the NCI’s financial year 2006 budget proposal I could find only one glancing reference to stem cells in that entire document.

I could also find no references whatsoever to stem cells in Andrew C. von Eschenbach’s “A vision for the National Cancer Program in the United States.” This is the statement in which the NCI director put forward his views on how to eliminate the death and suffering due to cancer by the year 2015. “A new era is now within our grasp,” he stated, “a time when no one suffers or dies as a result of cancer.” It is hard to imagine how the NCI intends to accomplish this without a serious involvement in the most important and exciting research initiative of our time.

CancerDecisions.com is directed by Ralph W. Moss, Ph.D. Dr. Moss is the author of eleven acclaimed books including Antioxidants Against Cancer, Herbs Against Cancer, Questioning Chemotherapy, and Cancer Therapy. He consults for thousands of clients through his Moss Reports service. The Moss Reports specializes in educating cancer patients about the most promising alternative treatments for their condition.

Editor’s note: Click here to sign up for Dr. Moss’s excellent newsletter.

References:

Curry EA 3rd, Murry DJ, Yoder C, et al. Phase I dose escalation trial of feverfew with standardized doses of parthenolide in patients with cancer. Invest New Drugs. 2004;22:299-305

von Eschenbach AC. A vision for the National Cancer Program in the United States. Nat Rev Cancer. 2004;4:820-8. Retrieved February 22, 2004.

Guzman ML, Rossi RM, Karnischky L, et al. The sesquiterpene lactone parthenolide induces apoptosis of human acute myelogenous leukemia stem and progenitor cells. Blood. 2005 Feb 1; [Epub ahead of print]

Murphy JJ, Heptinstall S, Mitchell JR. Randomised double-blind placebo-controlled trial of feverfew in migraine prevention. Lancet. 1988;2:189-92

Pfaffenrath V, Diener HC, Fischer M, et al. The efficacy and safety of Tanacetum parthenium (feverfew) in migraine prophylaxis–a double-blind, multicentre, randomized placebo-controlled dose-response study. Cephalalgia. 2002;22:523-32