In contrast to JCML, PB from six adults with Philadelphia (Ph1) chromosome-positive chronic myelogenous leukemia (Ph1 + CML) yielded CSA-dependent CFU-C colonies which were composed of granulocytes, macrophages, or both, as well as exuberant growth of BFU-E colonies.
A mutation within NRAS codon 12 could thus be demonstrated in a patient with idiopathic myelofibrosis and in another with chronic myelomonocytic leukemia.
The presence of the Xmn I site 5' to the G gamma-globin gene (at-158 base pairs from the G gamma-globin gene cap site) was observed only in 1 typical JCML patient with elevated %G gamma.
The presence of the Xmn I site 5' to the G gamma-globin gene (at-158 base pairs from the G gamma-globin gene cap site) was observed only in 1 typical JCML patient with elevated %G gamma.
Karyotypes of different cellular populations made after separation of bone marrow cells on a gradient of Percoll were evaluated in seven patients affected by chronic myelomonocytic leukemia diagnosed according to FAB criteria.
Although FRA16B was detected only in PBLs from two healthy subjects who had been previously treated for non-Hodgkin's lymphoma (NHL), both cell types displayed FRA16B in a patient with chronic myelomonocytic leukemia (CMMoL).
We therefore analyzed samples obtained from 57 patients with a variety of hematologic malignancies (21, acute myelogenous leukemia; 14, acute lymphoblastic leukemia; 12, Philadelphia chromosome-positive chronic myelogenous leukemia [blast phase] or acute leukemia; 5, chronic lymphocytic leukemia; and 5, chronic myelomonocytic leukemia) for expression of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) transcripts on Northern blots.
We therefore analyzed samples obtained from 57 patients with a variety of hematologic malignancies (21, acute myelogenous leukemia; 14, acute lymphoblastic leukemia; 12, Philadelphia chromosome-positive chronic myelogenous leukemia [blast phase] or acute leukemia; 5, chronic lymphocytic leukemia; and 5, chronic myelomonocytic leukemia) for expression of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) transcripts on Northern blots.
We studied 71 children, including 28 with bone marrow monosomy 7 syndrome (Mo7), 35with juvenile chronic myelogenous leukemia (JCML), three with other forms of preleukemia, and five with acute myelogenous leukemia (AML), for activating mutations of KRAS and NRAS.