Sentences with phrase «in acute myelogenous leukemia»

Antineoplastic mechanisms of niclosamide in acute myelogenous leukemia stem cells: inactivation of the NF - kappaB pathway and generation of reactive oxygen species.

[3]-RRB- However, the presence of the Philadelphia (Ph) chromosome is not sufficiently specific to diagnose CML, since it is also found in acute lymphoblastic leukemia [4](aka ALL, 25 — 30 % of adult cases and 2 — 10 % of pediatric cases) and occasionally in acute myelogenous leukemia (AML).

Dominique Bonnet and John E. Dick report the first conclusive evidence for cancer stem cells, identified in acute myelogenous leukemia (AML).

Not exact matches

It is activated in 50 to 80 percent of patients with acute myelogenous leukemia (AML), and in some, but not all cases, is associated with genetic mutations.

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.

A Phase I Study of DS - 3201B in Subjects with Acute Myelogenous Leukemia (AML) or Acute Lymphocytic Leukemia (ALL)

There was scant experimental evidence for this hypothesis until 1994, when John Dick and colleagues demonstrated that leukemia - initiating stem cells (LSCs) present in the blood of leukemia patients may induce acute myelogenous leukemia (AML) when transplanted into severe combined immunodeficient mice (2).

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.

A 64 - year - old male with history of Acute Myelogenous Leukemia (AML) status post bone marrow transplant (BMT) in complete remission presented with dyspnea when laying on his right side which resolved when supine or in the left lateral decubitus position.