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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a 3 1/2 year cytogenetic study of 107 leukemia patients diagnosed in childhood and adloescence, 8 presented with chronic myelogenous leukemia (CML). Seven of the 8 had chromosomal abnormalities. Six had the Ph1 chromosome; 5 had the usual 9;22 translocation. Two patients had involvement with chromosome 15; one had a 9;15 translocation in Ph1 positive cells during remission while a second had a 1;15 translocation during blastic crisis. The 2 patients who did not have a Ph1 chromosome survived 13 and 30 months, respectively, considerably less time than the 4+ year survival in most of those with Ph1 positive CML.
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PMID:Cytogenetic studies of chronic myelocytic leukemia in children and adolescents. 28 50

Leukemia accounts for 15-20% of the secondary malignancies among survivors of Wilms' tumor. We report three patients who developed leukemia after the successful treatment of Wilms' tumor, each of whom demonstrates the importance of close long-term medical surveillance. The first patient developed Philadelphia chromosome positive chronic myelogenous leukemia (CML) 6 years after the diagnosis of Wilms' tumor. This is the second report of CML occurring after Wilms' tumor. The other two patients developed acute nonlymphocytic leukemia (ANLL) 3 and 18 years after successful treatment of Wilms' tumor. In one patient, the clinical manifestations were subtle, and in the other the latency period was the longest reported for secondary leukemia following Wilms' tumor. We conclude that survivors of childhood cancer require frequent medical surveillance even in their adult years.
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PMID:Secondary leukemia following successful treatment of Wilms' tumor. 254 63

Despite the major breakthrough in the knowledge of the molecular events underlying the t(9;22) translocation, still no consistent data have been found on the evolution of Ph1 positive CML from the chronic to the accelerated or blastic phase of the disease. In most patients in fact the bcr/abl rearrangements are identical both in chronic phase and in blast crisis, and overall differences in chronic phase duration, related to different location of breakpoints inside the bcr region, were found to be marginal. We approached this problem by studying the molecular features of the bcr/abl abnormality in rare CML patients with very long, atypical chronic phase. The three patients studied, whose chronic phase duration is 17, 19, and 21 years, respectively, have typical genomic bcr rearrangements, and two of them show, hybridizing Northern blots to c-abl, the 8.5 kb mRNA, as that typically present in CML. It seems that genomic alterations within bcr and abl cannot account, alone, for the duration of the chronic phase of Ph1 positive CML and those quantitative and/or qualitative alterations of the p210 bcr/abl protein, unluckily awkward to prove, might be responsible for the atypical clinical features of these CML long survivors.
Leukemia 1989 Jul
PMID:Philadelphia-positive chronic myelogenous leukemia with typical bcr/abl molecular features and atypical, prolonged survival. 273 55

A rare type of rapidly fatal childhood leukemia, generally called juvenile chronic myelogenous leukemia, is characterized by absence of the Philadelphia chromosome and a predominantly monocytic proliferation, among other features. Unlike Philadelphia chromosome positive chronic myelogenous leukemia, this disease is neither chronic nor principally a disorder of granulocytic cell lines. A case is presented, with several clinical and laboratory parameters useful in establishing the correct diagnosis, and a change in terminology to "rapidly progressive juvenile myelomonocytic leukemia" is proposed.
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PMID:Rapidly progressive myelomonocytic leukemia (juvenile CML). 347 55

The prognostic value of several clinical and hematologic features, recorded at diagnosis, in chronic phase Ph1 positive chronic myelocytic leukemia (CML), was analyzed in 135 patients using life-table analysis. About one third of patients were atomic bomb survivors and they had been examined twice a year before the diagnosis of CML. In general, features representing tumor cell burden, i.e., leukocyte count, spleen sizes, and absolute differential cell counts of all granulocyte series cells except myeloblasts affected survival significantly, while sex, age, hemoglobin, platelets and features representing quality of leukemia, i.e. neutrophils alkaline phosphatase score, percent Ph1 positive cells in bone marrow, and percent differentials of all granulocyte series cells except promyelocytes and segmented neutrophils were all insignificant. Multivariate life-table analysis was also performed using age, sex, hemoglobin, platelets, and leukocyte count as predictor variables. The result was that leukocyte was the single most important factor in this analysis and annual death rates between low risk (risk ratio less than 0.8) and high risk (risk ratio greater than 1.4) differed considerably up to four years from diagnosis, indicating our formula to calculate risk ratio is valid as a grading parameter of chronic phase Ph1 positive CML within four years from diagnosis.
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PMID:Factors influencing survival in Philadelphia chromosome positive chronic myelocytic leukemia. 695 55

Bone marrow and peripheral blood samples from 36 patients with Philadelphia chromosome positive chronic myelogenous leukemia (Ph+ CML) (30 in chronic phase, four in accelerated phase, and two in blastic crisis) were tested with two CD56 monoclonal antibodies (My31 and Eric 1) using the Facscan flow cytometer. Two- and three-color fluorescence experiments indicated that CD13+/CD33+ myeloid cells from 19 out of the 36 patients were positive for CD56 in 12-77% of the cells. In contrast, no CD56 positivity was documented in myeloid cells from bone marrow (BM) of healthy donors. Immunocytochemical staining (APAAP technique) of CML peripheral blood (PB) and BM slides showed that CD56 expression was detectable from the myelocyte stage with the strongest staining in the metamyelocyte stage. Neutrophils were negative both by flow cytometry and APAAP analysis. In individual CML patients, an increasing number of CD56+ cells were recovered with progressively higher density cuts (1.065-1.077 g/ml), supporting the concept that the antigen level tends to increase during myeloid differentiation. Furthermore, 19% of CML patients coexpressed CD56 and CD34 antigens in 10-45% of the CD34+ cells. The myeloid nature of CD56+/CD34+ CML cells has been ascertained by granulocyte-macrophage colony-forming unit (CFU-GM) assays on CD56+ cells sorted on FACS. Furthermore, in six out of eight CML patients in whom we performed a comparative BM and PB analysis, we found that the CD56 expression was brighter and the number of positive cells significantly higher in the peripheral blood myeloid cells as compared to their BM counterpart. In short-term liquid cultures, low doses (50 U/ml) of alpha interferon down-regulated the CD56 expression in CML cells, accompanied by a significant reduction of the Ph positivity. In conclusion, the expression of CD56 on CML myeloid elements seems to represent an aberrant phenomenon which could affect the cell homing mechanisms and, probably, the pattern of tumor cell dissemination. In patients with CD56+ CML, its detection could be further used as a means of monitoring patients undergoing bone marrow transplantation, since its reappearance is associated with early relapse of the disease.
Leukemia 1993 Oct
PMID:Abnormal expression of N-CAM (CD56) adhesion molecule on myeloid and progenitor cells from chronic myeloid leukemia. 769 92

We report a patient with Philadelphia chromosome (Ph1)-positive chronic myelogenous leukemia (CML) which transformed into blast crisis bearing the immunophenotypic features similar to those of the myeloid/natural killer (NK) cell precursor leukemia we proposed previously. Using a CD45 blast gating method, the myeloperoxidase-negative blasts were positive for CD7, CD13, CD33, CD34, CD56, and HLA-DR, but no other lymphoid antigens. Southern blot analysis showed germ line T cell receptor beta and delta genes and immunoglobulin heavy and light chain genes. Although NK cell blastic transformation with Ph1 positive CML has been reported in a single patient, this is, to our knowledge, the first report of CML blast crisis of myeloid/NK cell precursor origin.
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PMID:Blast crisis of chronic myelogenous leukemia exhibiting immunophenotypic features of a myeloid/natural killer cell precursor. 1007 56