Posted by rob on October 25, 2005 under Uncategorized | 
D’Antonio J
Clin J Oncol Nurs. 2005 Oct ; 9(5): 535-8
Chronic myelogenous leukemia (CML) represents about 14% of all leukemias and occurs with a frequency of about 1 in 100,000. It is rare in children. Symptoms include fatigue, weight loss, sweating, and abdominal discomfort from an enlarged spleen. The white blood cell count can range from 100-600 ul. CML has three phases: the chronic phase, accelerated phase, and blast phase. Most patients are diagnosed during the chronic phase. Ionizing radiation has been implicated in some cases of CML, but in most individuals no cause is known. The Philadelphia chromosome, an acquired genetic mutation represented by a translocation of chromosome 22 and chromosome 9, drives the leukemic changes in CML. Imatinib mesylate, a tyrosine kinase inhibitor, was approved in 2002 for the treatment of all phases of CML. Because of its effectiveness, imatinib has become the treatment of choice for most patients with CML. Stem cell transplantation also is an option for eligible patients. It is the only curative treatment for CML. Two drugs under study for patients who cannot tolerate or who become resistant to imatinib are BMS-354825 and AMN107. Oncology nurses who are knowledgeable about new therapies for CML can be effective resources for their patients.
Chronic myelogenous leukemia.
Posted by rob on under Uncategorized |
Wu D, Nair-Gill E, Sher DA, Parker LL, Campbell JM, Siddiqui M, Stock W, Kron SJ
Anal Biochem. 2005 Sep 22;
There is a current and increasing demand for simple, robust, nonradioactive assays of protein tyrosine kinase activity with applications for clinical diagnosis and high-throughput screening of potential molecularly targeted therapeutic agents. One significant challenge is to detect and measure the activity of specific kinases with key roles in cell signaling as an approach to distinguish normal cells from cancer cells and as a means of evaluating targeted drug efficacy and resistance in cancer cells. Here, we describe a method in which kinase substrates fused to glutathione-S-transferase and immobilized on glutathione agarose beads are phosphorylated, eluted, and then assayed to detect kinase activity. The activity of recombinant, purified c-Abl kinase or Bcr-Abl kinase in whole cell extracts can be detected with equivalent specificity, sensitivity, and reproducibility. Similarly, inhibition of recombinant c-Abl or Bcr-Abl in cells or cell extracts by imatinib mesylate and other Bcr-Abl targeted kinase inhibitors is readily assayed. This simple kinase assay is sufficiently straightforward and robust for use in clinical laboratories and is potentially adaptable to high-throughput assay formats.
Assaying Bcr-Abl kinase activity and inhibition in whole cell extracts by phosphorylation of substrates immobilized on agarose beads.
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Onitilo AA, Kio EA, Singh AK, Lazarchick J
Leuk Lymphoma. 2005 Nov ; 46(11): 1667-70
We report a 50-year-old patient with idiopathic hypereosinophilic syndrome with trisomy 8 who experienced a complete and durable hematological and cytogenetic remission with low-dose imatinib therapy. He also had a significant reversal of cardiac dysfunction with a reduction in cardiac hypertrophy, resolution of pericardial effusion and mitral and tricuspid regurgitation. He remained in remission 3 years after therapy.
Cytogenetic remission with imatinib therapy in hypereosinophilic syndrome with trisomy 8 and resolution of severe cardiac dysfunction.
Posted by rob on under Uncategorized |
Khoury HJ, Loberiza FR, Ringden O, Barrett AJ, Bolwell BJ, Cahn JY, Champlin RE, Gale RP, Hale GA, Urbano-Ispizua A, Martino R, McCarthy PL, Tiberghien P, Verdonck LF, Horowitz MM
Blood. 2005 Oct 20;
Granulocyte-colony-stimulating factor (G-CSF) is often administered after hematopoietic cell transplantation (HCT) to accelerate neutrophil recovery, but it is unclear what impact G-CSF has on long-term transplant outcomes. We analyzed within the database of the Center for International Blood and Marrow Transplant Research, the impact of giving posttransplant G-CSF on the outcomes of allogeneic HCT for acute myelogenous leukemia and chronic myelogenous leukemia in 2,719 patients transplanted between 1995 and 2000. These included 1,435 recipients of HLA-identical sibling bone marrow (BM), 609 recipients of HLA-identical peripheral blood stem cells (PBSC), and 675 recipients of unrelated donor BM transplants. Outcomes were compared between patients receiving or not receiving G-CSF within 7 days of HCT according to graft type. Median follow-up was >30 mo (range, 2-87 mo). G-CSF shortened the post-transplant neutropenic period, but did not affect days +30 and +100 treatment-related mortality (TRM). Probabilities of acute and chronic graft-versus-host disease (GVHD), leukemia-free (LFS) and overall survival were similar whether or not G-CSF was given. Multivariate analyses confirmed that giving G-CSF did not affect the risk of GVHD, TRM, LFS, or survival. In conclusion, results of this study found no long-term benefit or disadvantage of giving G-CSF posttransplant to promote hematopoietic recovery.
Impact of posttransplant G-CSF on outcomes of allogeneic hematopoietic stem cell transplantation.
