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acute myeloid leukemia
Tiny RNA shown to cause multiple types of leukemia
By Dross at 2010-11-30 05:09


CAMBRIDGE, Mass. (November 29, 2010) – Whitehead Institute researchers have shown in mouse models that overexpression of the microRNA 125b (miR-125b) can independently cause leukemiaterm and accelerate the disease's progression. Their results are published in this week's online edition of the Proceedings of the National Academy of Sciences (PNAS).

read more | 2405 reads

Mutations Predict Quick Recurrence Of Acute Leukemia
By Dross at 2008-08-18 21:28



The presence of mutations in a particular gene may forecast the quick return of acute leukemiaterm in some people with the disease, a new study shows.

            Researchers at The Ohio State University Comprehensive Cancer Center examined the prognostic importance of mutations in a gene called Wilms tumor 1 (WT1). The study involved 196 patients under age 60 with acute myeloid leukemia (AML) whose leukemic cells had normal-looking chromosomes, a characteristic present in nearly half of adult AML cases.

read more | 2874 reads

Ambit Biosciences Begins Dosing Patients in Phase I Clinical Trial of Lead Kinase Inhibitor AC220
By Dross at 2007-04-10 22:44

Ambit Biosciences today announced that the first patients have been dosed in its Phase I clinical trial to evaluate AC220 in the treatment of acute myeloid leukemiaterm (AML).


The Phase I trial is a multi-center, open-label, sequential dose-escalation study that will enroll 20-40 patients with relapsed or refractory AML. AC220 will be administered daily via oral solution, beginning at 12 mg for 14 days and then increasing until the maximum tolerated dose is established. In addition to evaluating the safety, tolerability and pharmacokinetics of AC220, the study will measure pharmacodynamics of the investigational drug by monitoring FLT3 receptor phosphorylation and peripheral blood blastterm counts.

read more | 2667 reads

Callisto Pharmaceuticals Starts Phase I Clinical Trial with L-Annamycin in Pediatric Relapsed and Refractory Acute Leukemia
By HCat at 2007-03-11 23:27

    Callisto Pharmaceuticals, Inc. opened a phase I clinical trial testing L-Annamycin in children and young adults on February 22nd and announced dosing on March 8th. The trial will test the drug in pediatric patiens with refractory or relapsed acute lymphocytic leukemiaterm (ALL) or acute myelogenous leukemia (AML). Patients with relapsed or refractory acute leukemia who have prior treatment with approved chemotherapeutics generally have a poor prognosis at this point in the disease and are in need of new agents.

read more | 2659 reads

CDX2 -- A protein that promotes leukemia
By Dross at 2007-03-10 01:34

Researchers from Harvard Medical School, Boston, have found that most individuals with acute myeloid leukemiaterm (AML) inappropriately express a protein known as CDX2 in their leukemic cells. CDX2 regulates the expression of a number of genes that encode members of the HOX family of proteins, which might provide a new set of targets for the treatment of individuals with AML.


In the study, which appears online on March 8 in advance of publication in the April print issue of the Journal of Clinical Investigation, Stefan Fröhling and colleagues show that the gene encoding CDX2 is expressed in 90% of the patients with AML that they analyzed. Moreover, reducing the amount of CDX2 in human AML cell lines decreased their ability to proliferate, indicating that CDX2 has a causal role in the pathogenesis of AML. Further evidence of this was provided by the observation that mouse hematopoietic cells engineered to express CDX2 were induced to proliferate and were able to cause full-blown AML when transplanted into mice. Expression of CDX2 in the mouse hematopoietic cells induced altered expression of a number of genes that encode HOX family of proteins, leading the authors to conclude that aberrant expression of CDX2 drives the dysregulated HOX gene expression observed in most individuals with AML.

read more | 2052 reads

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]:

read more | 2620 reads

Downregulation of VEGF-A, STAT5 and AKT in acute myeloid leukemia blasts of patients treated with SU5416.
By admin at 2006-12-20 03:55

[via Entrez PubMed]:

Interesting article re a tyrosine kinase inhibitor Sugen is developing. I love to see real translational research, using patients' cells in trials and doing molecular assays for effects. In this case the researchers are demonstrating down regulation of VEGFterm messenger RNA levels, which is an assumption of down regulation in the final protein product.

In acute myeloid leukemiaterm (AML), autocrine or paracrine activation of receptor tyrosine kinases such as c-kit and FLT3 contributes to proliferation and apoptosis resistance of leukemic blasts. This provided the rationale for a multicenter clinical trial in patients with refractory AML with SU5416, a small molecule kinase inhibitor which blocks phosphorylation of c-kit, FLT3, VEGFR-1, VEGFR-2 (KDR) and VEGFR-3. The levels of VEGF mRNA expression were investigated in peripheral blood leukemic blasts taken from AML patients before and during treatment with SU5416. Rapid down regulation of VEGF was observed in AML blasts from 72% (13 of 18) of patients analysed. Patients initially expressing high VEGF-levels had a stronger downregulation and a higher clinical response rate (mean 865-fold, n = 10, P = 0,01) than patients initially expressing low VEGF-levels (mean four-fold, n = 8). These results suggest that abnormal high VEGF expression is downregulated by SU5416 treatment, and furthermore that decreases in VEGF mRNA levels may provide an early marker of therapeutic response with anti-angiogenic therapy. Additionally, protein expression of STAT5 and AKT was assessed by western blotting in these patient samples, as well as in the leukemia cell line, M-07e, treated in vitro with SU5416 as a model system. In the AML patient samples, parallel downregulation of both STAT5 and AKT was observed in several cases (STAT5 in four of 15; AKT in three of six examined patients). These effects were confirmed with the cell line M-07e after incubation with SU5416 in vitro using concentrations that are achievable in patients. In summary, our data show suppression of the expression of VEGF and key signal transduction intermediates in AML blasts during treatment with SU5416.

read more | 2554 reads

Acute myeloid leukemia is propagated by a leukemic stem cell with lymphoid characteristics in a mo
By admin at 2006-12-14 02:17

[via ScienceDirect - Cancer Cell : Acute myeloid leukemia is propagated by a leukemic stem cell with lymphoid characteristics in a mouse model of CALM/AF10-positive leukemia]:A challenge for the development of therapies selectively targeting leukemic stem cells in acute myeloid leukemia (AML) is their similarity to normal hematopoietic stem cells (HSCs). Here we demonstrate that the leukemia-propagating cell in murine CALM/AF10-positive AML differs from normal HSCs by B220 surface expression and immunoglobulin heavy chain rearrangement. Furthermore, depletion of B220 cells in leukemic transplants impaired development of leukemia in recipients. As in the murine model, human CALM/AF10-positive AML was characterized by CD45RA (B220)-positive, IG DH-JH rearranged leukemic cells. These data demonstrate in a murine leukemia model that AML can be propagated by a transformed progenitor with lymphoid characteristics, which can be targeted by antibodies that do not crossreact with normal HSCs.

read more | 1799 reads

Efficacy and safety of thalidomide in patients with acute myeloid leukemia
By admin at 2006-12-05 03:36

[via leukemia-research : Message: Re: [leukemia-research] Digest Number 62]:

Martin B. Steins, Teresa Padre, Ralf Bieker, Sandra Ruiz, Martin Kropff, Joachim Kienast, Torsten Kessler, Thomas Buechner, Wolfgang E. Berdel, and Rolf M. Mesters From the Department of Medicine/Hematology and Oncology, University of Muenster, Germany.


Emerging data suggest an involvement of angiogenesis in the pathophysiology of acute myeloid leukemiaterm (AML). Thus, antiangiogenic therapy could constitute a novel strategy for the treatment of AML. To test this hypothesis, a phase I/II dose-escalating trial was performed to study the safety and efficacy of thalidomide, a putative inhibitor of angiogenesis, in 20 patients with AML. Thirteen patients were assessable for both toxicity and response, tolerating a maximum dose of 200 to 400 mg daily for at least 1 month. Seven patients had to be prematurely withdrawn from drug administration owing to progressive disease and death (3 patients), personal decision (2 patients), or inability to tolerate thalidomide (2 patients).

read more | 2484 reads

Acute Myeloid Leukemia
By admin at 2006-12-03 07:59

What Is Acute Myeloid Leukemiaterm?


Acute myeloid leukemia (AML), also known as acute myelocytic leukemia or acute myelogenous leukemia, is a cancer that begins in cells that normally develop into blood cells. The disease is characterized by the proliferation of immature cells termed "blasts." These blasts eventually overrun the marrow to the detriment of normal cells and the patient dies. When the number of abnormal blasts reaches 20% or greater the term "Leukemia" is used.

read more | 59974 reads

Acute Myelogenous Leukemia
By admin at 2006-11-09 01:35

A phase II study of the farnesyltransferase inhibitor tipifarnib in poor-risk and elderly patients with previously untreated acute myelogenous leukemia.

Outcomes for older adults with acute myelogenous leukemia (AML) are poor due to both disease and host-related factors. In this phase 2 study, we tested the oral farnesyltransferase inhibitor tipifarnib in 158 older adults with previously untreated, poor-risk AML. The median age was 74 years, and a majority of patients had antecedent myelodysplastic syndrome. Complete remission was achieved in 22 patients (14%); partial remission or hematologic improvement occurred in 15 patients, for an overall response rate of 23%. The median duration of CR was 7.3 months and the median survival of complete responders was 18 months. Adverse karyotype, age >/=75, and poor performance status correlated negatively with survival. Early death in the absence of progressive disease was rare, and drug-related non-hematologic serious adverse events were observed in 74 patients (47%). Inhibition of farnesylation of the surrogate protein HDJ-2 occurred in the large majority of marrow samples tested. Baseline levels of phosphorylated mitogen-activated protein kinase and AKT did not correlate with clinical response. Tipifarnib is active and well tolerated in older adults with poor-risk AML, and may impart a survival advantage in those patients who experience a clinical response.

read more | 3110 reads

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