Sentences with phrase «in chronic myelogenous leukemia»

An exciting development in rational anticancer drug design is Gleevac, a drug that acts on a protein unique to the defective white blood cells in chronic myelogenous leukemia and on a related protein in a rare form of gastrointestinal cancer.

New treatment strategies to overcome drug resistance in chronic myelogenous leukemia and other cancers will come from the detailed structure of the enzyme Abl.

In 1972, she identified a genetic glitch in chronic myelogenous leukemia cells — a swap of genes she called chromosomal translocation — that resulted in the uncontrolled cell growth of cancer.

Her research has recently shown that a signaling pathway dubbed «hedgehog» is important not only for normal development of stem cells but also for the growth of cancer cells in chronic myelogenous leukemia.

Not exact matches

A research group in Japan and in Korea has found a novel nutrient uptake process that maintains the activity of murine chronic myelogenous leukemia (CML) stem cells.

The most prominent example so far is the drug sti571, known as Gleevec, which in a recent clinical trial put an amazing 53 out of 54 patients with chronic myelogenous leukemia into remission.

In both acute and chronic myelogenous leukemia, immature white blood cells in the bone marrow multiply out of controIn both acute and chronic myelogenous leukemia, immature white blood cells in the bone marrow multiply out of controin the bone marrow multiply out of control.

Chronic myelogenous leukemia (CML) is a human disease associated with a consistent chromosomal translocation that results in sequences from the c - abl locus on chromosome 9 being fused to sequences in a breakpoint cluster region (bcr) on chromosome 22.

Such fusions have been implicated in other cancers, notably chronic myelogenous leukemia (CML).

City of Hope researchers may have discovered a more effective treatment for patients with chronic myelogenous leukemia (CML) according to a study published today in Nature Medicine.

These mutant kinases are attractive therapeutic targets, as demonstrated by the efficacy of imatinib in BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowIn addition, activating mutations in the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin the FLT3 receptor tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin acute myeloid leukemia (AML), and specific inhibitors of the FMS - like tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknown.

We used direct sequence analysis to determine if the JAK2V617F mutation was present in acute myeloid leukemia (AML), chronic myelomonocytic leukemia (CMML) / atypical chronic myelogenous leukemia (aCML), myelodysplastic syndrome (MDS), B - lineage acute lymphoblastic leukemia (ALL), T - cell ALL, and chronic lymphocytic leukemia (CLL).

ONC201 demonstrated (GI50 1 - 8 µM) dose - and time - dependent efficacy in acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), chronic myelogenous leukemia (CML), chronic lymphocytic leukemia (CLL), diffuse large B - cell lymphoma (DLBCL), mantle cell lymphoma (MCL), Burkitt's lymphoma, anaplastic large cell lymphoma (ALCL), cutaneous T - cell lymphoma (CTCL), Hodgkin's lymphoma (nodular sclerosis) and multiple myeloma (MM) cell lines including cells resistant to standard of care (dexamethasone in MM) and primary samples.