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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

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A potential new way to make a good anti-leukemia drug even better
By Dross at 2008-10-21 01:10

A recently identified cancer-causing protein makes the anti-leukemiaterm drug imatinib, less effective. By blocking the protein, an international team of researchers was able to slow the spread of leukemia cells in culture. The study, which will appear online on October 20 in the Journal of Experimental Medicine, suggests that the most effective treatment for leukemia may rely on a combination of targeted drugs, rather than a single miracle drug.

Imatinib is currently the most popular therapy for chronic myeloid leukemia (CML). CML is a type of blood cancer that is most common among middle-aged adults and accounts for 15-20% of all cases of adult leukemia in the western world. Accumulation of cancer cells in the patient's blood causes infections, anemia, and other potentially life-threatening complications.

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Early Phase II results show bosutinib safe, effective for CML
By Dross at 2007-12-12 09:58

ATLANTA - A new drug for chronic myelogenous leukemiaterm works for patients who have developed resistance to frontline therapy and causes fewer side effectsterm than other medications in its class, a research team led by scientists at The University of Texas M. D. Anderson Cancer Center reports at the 49th annual meeting of the American Society of Hematology.

"Bosutinib has shown good efficacy and very little toxicity compared to other tyrosine kinase inhibitors at this stage of the clinical trial," says lead researcher Jorge Cortes, M.D., professor in M. D. Anderson's Department of Leukemia.

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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).

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New role for microRNA in chronic leukemia
By Dross at 2007-12-09 02:16



            COLUMBUS, Ohio – Scientists here have found that mini-molecules called microRNA may play a critical role in the progression of chronic myeloid leukemia (CML) from its more treatable chronic phase to a life-threatening phase, called blastterm crisis.

Furthermore, they discovered an entirely new function for these molecules. The researchers show that microRNAs can sometimes directly control a protein’s function – not just whether or not the protein is made by the cell, as has been believed.

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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.

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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.

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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.  

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Phase I Trial of Rigel' Aurora Kinase Inhibitor Begins
By HCat at 2007-02-15 02:04

    Announced February 13th on Rigel's site, the second of several phase I studies to evaluate the safety and initial efficacy of the candidate R763 in different types of cancers is starting. The trials will tests the inhibitor in solid tumors, hematological malignancies, and in combination with standard therapies.

    Merck Serono licensed development and commercialization rights to R763 and Rigel's Aurora kinase program in October 2005. Aurora kinases are a family of kinases (proteins that put phosphate groups on other proteins) that regulate mitosis (cellular division). It is thought that these kinases are deregulated in cancer, and culture cell studies have shown Aurora kinases have anti-tumor effects.

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News: ChemGenex Recieves Patent Protection on Production of Leukemia Candidate. Genetic Engineering News - Biotechnology from Be
| |
By Dross at 2007-02-03 03:55

-Press Release 


ChemGenex Pharmaceuticalspatent related to the manufacture of its leukemiaterm candidate received approval. The patent covers the semisynthetic production of homoharringtonine (Ceflatonin) and its analogs and the use of these compounds in a treatment of leukemia. The patent provides ChemGenex and its partner, Stragen Pharma, with a proprietary position until 2019 in the U.S. Ceflatonin is a potent inducer of apoptosis in myeloid cells and inhibits angiogenesis.


In Phase II studies, it demonstrated clinical activity in patients with chronic myeloid leukemia (CML), both as a single agent and in combination with other chemotherapeutic drugs, according to ChemGenex. The company is developing Ceflatonin for the treatment of CML, and pilot studies are underway in myelodysplastic syndrome (MDS) and in acute myeloid leukemia (AML). "In addition to the strong regulatory position obtained through patents and orphan drug status in major jurisdictions, the Ceflatonin clinical development program is progressing very well,%u201D points out Greg Collier, Ph.D., CEO and managing director. "We now have 11 centers in the U.S.A. and Europe recruiting patients for our registration-directed trial of Ceflatonin in chronic myeloid leukemia patients with the T315I mutation who have failed Gleevec therapy."

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Reasons Why Cancer Drug Discovery is so Difficult
By HCat at 2007-01-31 23:56

    In the perspective article in Nature Reviews Drug Discovery, the authors discuss the challenges facing drug discovery as intricate and numerous. They present a broad picture of drug discovery as three parts pertaining to targets, drugs, and patients. Targets for drug discovery are broken down into two classes, each of which is either essential or non-essential. Essential targets for drug discovery are targets that have essential function within all cells or a specific cell type. That means that the cell has to have this function operating or it will die. Non-essential targets are targets whose function can be lost and the cell will still survive. This concept can also be applied in terms of tissues as a target such as in breast tissue which is considered a non-essential tissue for life. Drugs that inhibit or block essential functions are likely to have narrow therapeutic windows. That is the drugs beneficial dose range is likely to be small before it becomes toxic such as 5-FUterm. 5-FU relies on the principle that cancer cells should be faster growing since they are growing out of control. 5-FU inhibits DNA synthesis, an essential function. Slow growing cells are not as affected as fast growing cells from 5-FU. This therapeutic windowterm is narrow and the consequences or side effectsterm of the narrow window is that 5-FU affects some of the naturally fast growing cells in the body, which is why hair loss is a common side-effect in 5-FU treatment.

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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.

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New drug therapy to combat GVHD in stem-cell patients shows significant reduction in deaths
By Dross at 2007-01-24 07:26


Gastrointestinal graft-vs.-host disease is a common and potentially deadly side effect for patients who undergo an allogeneic stem-cell transplant to treat certain blood cancers. Now, new research from Fred Hutchinson Cancer Research Center shows that adding a widely used topical corticosteroid to the standard treatment for GVHD kept the disease in remission and significantly reduces deaths one year after therapy.


A reformulation of beclomethasone dipropionate (BDP) into two different pills specifically releasing the drug into the stomach and mid-small intestine prevented relapse of gastrointestinal GVHD and allowed those patients to be on a shorter treatment course of high-dose prednisone. Mortality was reduced by 46 percent a year following the start of treatment in a multi-center Phase III clinical trial, according to findings published today in the online edition of the journal Blood.

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Phase 1 study of low-dose prolonged exposure schedules of the hypomethylating agent 5-aza-2'-deoxycytidine (decitabine) in hemat
By admin at 2006-12-28 09:46

New Results from Kantarjian. Dosing levels for use of decitabine are still an ongoing question. Here Kantrajian et al. present new results from a phase one study of lowered but prolonged doses versus the standard 15mg/m2 for five days. Their results show a greater efficacy at the current 15mg/m2 dose.

[via Phase 1 study of low-dose prolonged exposure schedules of the hypomethylating agent 5-aza-2'-deoxycytidine (decitabine) in hematopoietic malignancies -- Issa et al. 103 (5): 1635 -- Blood]:

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Five-year study shows Imatinib's excellent survival rate
By admin at 2006-12-08 23:30

[via Five-year study shows Imatinib's excellent survival rate]:

A 5-year follow-up of patients with chronic myeloid leukemiaterm ( CML ) who began continuous treatment with Imatinib ( Glicev / Gleevec ) reports that the drug can induce durable hematologic and cytogenetic responses in a high proportion of patients. When the drug first was developed by Brian J. Druker, at the Oregon Health & Science University Cancer Institute, the overall survival rate for patients with chronic myelogenous leukemia taking this new experimental drug was unknown. " We've completely changed the outlook for patients with this disease. Before Imatinib, patients were fortunate if they lived five years. Now, we've given patients a hopeful future," said Druker, the principal investigator for the study. Today, after five years, the overall survival of 553 subjects randomized to receive Imatinib as their initial therapy is nearly 90 percent, 95 percent if only deaths related to chronic myelogenous leukemia are considered. Just 5 percent of subjects discontinued Imatinib because of side effectsterm. The results are published in the New England Journal of Medicine ( NEJM ). This study also shows that the risk of relapse has trended downward during the past three years. In the study's fifth year, less than 1 percent of patients progressed from the chronic phase to more advanced phases of the disease. " This trend, coupled with the low risk of relapse, means that the possibility of long-term survival with chronic myelogenous leukemia is increasingly likely," Druker said. The five-year study was conducted at 117 centers in 16 countries. Imatinib is a signal transduction inhibitor that interferes with the enzymes that trigger the growth of cancerous cells. Imatinib acts on CML cells by inhibiting the disease-causing enzyme BCR-ABL that tells cells to grow and divide. Imatinib has also been approved for people with advanced gastrointestinal stromal tumors, dermatofibrosarcoma protuberans, Philadelphia chromosome-positive acute lymphoblastic leukemia, certain forms of myeloproliferative disorders, hypereosinophilic syndrome, and aggressive systemic mastocytosis. Source: Oregon Health & Science University, 2006

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