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Leading leukemia experts: High leukemia treatment costs may be harming patients
By Dross at 2013-04-26 00:29

 The increasing cost of treatments for chronic myeloid leukemiaterm (CML) in the United States has reached unsustainably high levels and may be leaving many patients under- or untreated because they cannot afford care, according to a Blood Forum article supported by nearly 120 CML experts from more than 15 countries on five continents and pu

read more | 4168 reads

Antivascular activity of lapatinib and bevacizumab in primary microcluster cultures of breast cancer and other human neoplasms
By gdpawel at 2008-09-12 04:09

Antivascular activity of lapatinib and bevacizumabtermterm in primary microcluster cultures of breast cancer and other human neoplasms

Sub-category: New Systemic Agents - New drugs and targets (includes anti-angiogenics) - Other

Category: Treatment

Meeting: 2008 Breast Cancer Symposium

Abstract No: 166

Author(s): L. Weisenthal, D. J. Lee, N. Patel



The following tyrosine kinase inhibitors (TKI) have been shown to have antivascular (AV) activity: sunitinibterm (Su), sorafenibterm (So), gefitinib (G), erlotinib (E), and imatinib (I). To date, AV activity has not been reported for lapatinib (LAP).

read more | 1 comment | 4299 reads

Leukemia drug could save lives of stroke patients
By Dross at 2008-06-23 05:10

(New York, June 22). The drug tPA is the most effective treatment currently available for stroke patients, but its safety is limited to use within the first three hours following the onset of symptoms. After that, tPA may cause dangerous bleeding in the brain. However, in a study published today in Nature Medicine, investigators from the Stockholm Branch of the Ludwig Institute for Cancer Research (LICR) and the University of Michigan Medical School show that these problems might be overcome if tPA is combined with the leukemiaterm drug, imatinib (Gleevec®). The results demonstrate that imatinib greatly reduces the risk of tPA-associated bleeding in mice, even when tPA was given as late as five hours after the stroke had begun. The LICR team, in collaboration with the Karolinska University Hospital in Stockholm, is now planning a clinical trial with imatinib in stroke patients.

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Leukemia Therapy With Imatinib During Pregnancy May Cause Infant Abnormalities
By Dross at 2008-03-06 05:05

While doctors already face many challenges in treating patients with cancer, treating pregnant women with the disease, in particular, can be quite difficult as studies suggest that certain therapies can harm developing fetuses. According to the results of a study prepublished today online in Blood, the official journal of the American Society of Hematology, expectant women treated with imatinib, a commonly used therapy for chronic myeloid leukemiaterm (CML), may be at moderate risk of developing fetal abnormalities.

Imatinib was introduced for the treatment of CML in 1998 and has become a primary therapy for most patients, turning the previously fatal disease into a mostly chronic condition in the last decade. The drug's label warns that women of child-bearing age should avoid pregnancy while taking the drug based on earlier studies that suggested it may penetrate the placenta and cause damage to developing cells.

read more | 2647 reads

Another 'smart' cancer drug can have toxic effects on the heart
By Dross at 2007-12-14 21:51

Another FDA-approved targeted cancer drug, sunitinibterm (SutentTM, Pfizer), may be associated with cardiac toxicity, report researchers at Children’s Hospital Boston, Dana-Farber Cancer Institute (Boston), and Thomas Jefferson University (Philadelphia). Their collaborative study, led by Ming Hui Chen, MD, MMSc, a cardiologist at Children’s who specializes in the cardiac health of cancer patients, appears in the December 15 issue of The Lancet, accompanied by an editorial.

Sunitinib is one of several new “smart” cancer drugs called tyrosine kinase inhibitors that targets specific signaling molecules inside cancer cells that aid cancer spread. Another “targeted” cancer therapy, imatinib (GleevecTM, Novartis Pharmaceuticals), was reported last year in Nature Medicine to be associated with heart failure in patients with chronic myelogenous leukemiaterm.

read more | 2 comments | 2547 reads

Gleevec, the targeted cancer pill, still proving effective
By Dross at 2007-12-11 00:01

PORTLAND, Ore. – Gleevec, the targeted cancer pill that has saved more than 100,000 lives, now is saving more children with a dire leukemiaterm, as well as preventing disease progression with long term use in adults with chronic myeloid leukemia.

“Data at this weekend’s meeting continues to show how much Gleevec has completely changed the outlook for so many, many patients facing cancer,” said Brian Druker, M.D., director of the OHSU Cancer Institute.

At the plenary session of the annual meeting of the American Society of Hematology researchers delivered news that Gleevec has been shown to improve outcomes for children with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL).

read more | 4 comments | 2332 reads

Leukemia drug proves safe and effective over the long term
By Dross at 2007-11-08 22:18

(WASHINGTON, November 7, 2007) – The drug imatinib mesylate, more commonly known as Gleevec®, proves safe and effective over the long term in patients with an advanced form of chronic myeloid leukemiaterm (CML), according to a study prepublished online in Blood, the official journal of the American Society of Hematology.

A team of researchers from the U.S. and Europe, including the drug’s creator, Brian Druker, MD, followed 454 patients with chronic-phase CML taking imatinib for more than six years. Prior to enrollment, all study participants had experienced either treatment failure or intolerance with interferon alpha, which was the standard of care for CML at the time the study was initiated.

read more | 1974 reads

Study finds heart failure is rare among leukemia patients on imatinib
By Dross at 2007-09-08 00:52

HOUSTON - Congestive heart failure rarely occurs among leukemiaterm patients who take imatinib, researchers at The University of Texas M. D. Anderson Cancer Center found after an exhaustive review of the detailed medical histories of 1,276 patients who enrolled in clinical trials for the drug.

Researchers found 22 patients, or 1.7 percent, had symptoms that could have been caused by heart failure. Of those, 18 had previous medical conditions that could also cause heart failure, such as type II diabetes, hypertension, irregular heartbeat or coronary artery disease. Six had congestive heart failure before entering treatment. The results were reported in the Aug. 15 edition of the journal Blood.

read more | 1713 reads

Bosutinib: A New Kinase Inhibitior for Treatment of Philadelphia Chromosome Positive Leukemia
By Dross at 2007-06-13 01:47

Researchers involved in an international study have reported that Bosutinib (SKI606) is a new active kinase inhibitor for the treatment of patients with Philadelphia chromosome positive chronic myeloid leukemiaterm (CML) or acute lymphoid leukemia (ALL). The details of this study were presented at the 2007 meeting of the American Society of Clinical Oncology in June.

Over the past 2 years nilotinib and Sprycel® have emerged as potent kinase inhibitors active in patients with Philadelphia chromosome positive CML or ALL (See related news). Bosutinib, a 7-alkoxy-4-[(2,4-dichloro-5-methoxyphenyl)amino]-3-quinolinecarbonitrile, is a potent inhibitor of Src kinase activity. At ASCO 2007 the results of treating 69 patients with chronic phase of CML or ALL who had relapsed or were resistant to Gleevec with bosutinib were presented. This is the first clinical report evaluating bosutinib. The first part of the study established that the appropriate dose was 500 mg/day. The phase II part of the study included 51 patients. Nineteen patients had no prior exposure to Gleevec, nilotinib or Sprycel. The major cytogenetic response rate for these 19 patients was 52%. In 9 patients with advanced leukemia, 4 had a complete hematological response and 2 had a major cytogenetic response. Bossutinib was also found to be effective in patients with defined Gleevec-resistant mutations. These authors concluded that bosutinib was active across a range of mutations. Side effectsterm included diarrhea, nausea, vomiting and abdominal pain. Grade3/4 toxicities occurred in 5% of patients with chronic phase of CML. Dose reductions were made in 17 of the 69 patients studied.  

read more | 2169 reads

Gleevec decreases cancer recurrence for patients with primary gastrointestinal stromal tumor
By Dross at 2007-04-13 23:38

Preliminary results from a large, randomized, placebo-controlled clinical trial for patients with primary gastrointestinal stromal tumor (GIST), a type of tumor usually found in the stomach or small intestine, showed that patients who received imatinib mesylate (Gleevec ®) after complete removal of their tumor were significantly less likely to have a recurrence of their cancer compared to those who did not receive imatinib. The clinical trial was sponsored by the National Cancer Institute (NCI), part of the National Institutes of Health (NIH), and conducted by a network of researchers led by the American College of Surgeons Oncology Group (ACOSOG).

read more | 2 comments | 3736 reads

Simple 2-gene test sorts out similar gastrointestinal cancers
By Dross at 2007-02-13 21:54

    A powerful two-gene test distinguishes between a pair of nearly identical gastrointestinal cancers that require radically different courses of treatment, researchers report this week in the online Early Edition of the Proceedings of the National Academy of Sciences. "This simple and accurate test has the potential to be relatively quickly implemented in the clinic to benefit patients by guiding appropriate treatment," says senior author Wei Zhang, Ph.D., professor in the Department of Pathology at The University of Texas M. D. Anderson Cancer Center. The analytical technique employed to tell gastrointestinal stromal tumor (GIST) from leiomyosarcoma (LMS) with near perfect accuracy will have wider application in more individualized diagnosis and treatment of other types of cancer, study co-authors from M. D. Anderson and the Institute for Systems Biology in Seattle conclude.

read more | 1339 reads

A visual picture of why Gleevec stops working
By Dross at 2007-02-09 03:17


See up close on an atomic scale how the mutation of one amino acid can render a drug like Gleevec useless. What is presented here is a crystal structure of the mutated protein CML patients have in a complex with the drug VX-680 which has been shown to inhibit the T315I mutation that no drug has yet been able to fight. Most interestingly is that the authors removed live cells from a patient harboring the mutation and tested the drug against these cells in a dish.The drug worked to kill the cells, but no word as to whether they could then give the drug to the patient. Probably not, as then the MD would be liable for murder before going through Phase I trials to determine the maximum tolerated dose. The drug showed inhibition at 10uM, whereas Gleevec is routinely given up to 5uM. The reading may be difficult, but that is what the forums are for, ask a question.

read more | 2627 reads

Why Her-2 has not been a magic bullet in Breast Cancer
By Dross at 2007-02-05 21:00

The success of the ABL-kinase inhibitor Gleevec in the treatment of BCR–ABL-driven leukaemiaterm (CML) raised hopes that drugs that target key kinases underlying other cancers, such as members of the human epidermal growth factor receptor (HER) family, might be similarly efficacious. However, several small-molecule inhibitors of HER family kinases have shown limited efficacy in HER2-driven breast cancers, despite effective inhibition of kinase activity. Writing in Nature, Sergina and colleagues now provide an explanation for this phenomenon: failure to completely inhibit the kinase activity of HER2 allows oncogenic signalling through the kinase-inactive family member HER3 to continue.

read more | 4 comments | 2097 reads

Disorderly protein brings order to cell division
By Dross at 2007-01-27 04:42


The secret to the ability of a molecule critical for cell division to throw off the protein yoke that restrains its activity is the yoke itself. disorderly molecule that seems to have a mind of its own, say investigators at St. Jude Children's Research Hospital, Innsbruck Medical University (Austria) and Max Planck Institute (Martinsried, Germany).


The researchers showed that the disorderly protein yoke, called p27, participates in its own destruction by swinging the end of its long arm up into a key side pocket of the cell division molecule called CDK2. After the end of p27 slips into the pocket, CDK2 marks p27 for destruction by tagging it with a molecule called phosphate. The tag signals the cell's protein destruction machinery to dispose of p27, freeing CDK2 to trigger cell division. The finding is important because it explains how CDK2 normally shrugs off p27. Once free of p27, CDK2 can participate in a specific step of cell division. The findings also explain how some abnormal enzymes cause this to occur prematurely, putting cell division into overdrive state that produces cancer. A report on the work appears in the January 25 issue of the journal Cell. The long p27 molecule drapes itself like an arm over the shoulders and down the side of CDK2, the researchers explained. The upper arm of p27 binds tightly to the shoulders of CDK2; as the arm drops over the shoulders, the "elbow" of p27 inserts itself into a side "pocket" of the molecule. Meanwhile, the long, floppy forearm and hand of p27 hangs freely below CDK2.

read more | 1595 reads

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