Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In three cases of acute nonlymphocytic leukemia we observed a translocation (8;16)(p11;p13); in one case it was the sole karyotypic change and in the other two cases it was associated with other structural anomalies. All three cases were nonhyperleukocytic myelomonocytic leukemias with erythrophagocytosis by some blast cells and cytochemistry results consistent with leukemic proliferation of a common monocytic-granulocytic precursor. The importance of this translocation is discussed, and the implication of band 16p13 in myelomonocytic leukemia is stressed.
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PMID:Three cases of translocation (8;16)(p11;p13) observed in acute myelomonocytic leukemia: a new specific subgroup? 347 40

The translocation t(8;16) (p11;p13) was found as the sole deviation from the normal karyotype in three patients with acute monocytic leukaemia. The bone marrow morphology was strikingly similar in the two cases where smears were available for re-evaluation: the leukaemic cells showed signs of differentiation, and active erythrophagocytosis was a particularly conspicuous feature. We suggest that t(8;16) (p11;p13) represents a new consistent abnormality in acute monocytic leukaemia, specifically associated with the differentiated subtype (M5b) and with pronounced phagocytic activity by the leukaemic monocytes.
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PMID:A new specific chromosomal rearrangement, t(8;16) (p11;p13), in acute monocytic leukaemia. 347 50

A 51-year-old man presented with a T-cell leukemia of large granular lymphocytes and rapidly developed a nephrotic syndrome due to presumptive minimal-change glomerulopathy. The E-rosette+, Ia+ cells demonstrated cytotoxic activity similar to that of natural killer lymphocytes but lacked other T-subset markers, except that one third of them bore Fc(IgG) receptors. Cytogenetic analysis revealed loss of chromosome 10 and the translocation (1;10)(p11;q11) in all metaphases. Regression of the leukemia after chemotherapy was accompanied by a dramatic resolution of the nephrotic syndrome, suggesting that the activated granular lymphocytes induced the renal lesion. The close association of a clonal T-lymphoproliferative disorder with minimal-change nephrotic syndrome lends further support to current views implicating activated T cells or their products in the pathogenesis of this glomerulopathy.
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PMID:Nephrotic syndrome associated with a clonal T-cell leukemia of large granular lymphocytes with cytotoxic function. 348 48

A 17-year old caucasian male presented with B-cell acute leukemia which proved aggressive and refractory to treatment. Cytogenic investigation showed a single clone with a complex karyotype 49,XY,del(2)(p13),+4,del(4)(p11),-6,+i(6)(p),+7,+8, t(8;14), (q24;q32),del(17)(p11). This includes the Burkitt's translocation and a deletion at the site of the immunoglobulin kappa light chain gene. Clonal evolution included tetraploidy, duplication of the derived chromosomes and, terminally, trisomy 1q. Immunological investigation revealed a monoclonal population of B-cell blasts, expressing the kappa light chain, and with an extremely rare combination of SIg and TdT positivity. Immunoglobulin gene rearrangement confirmed monoclonalility. Tetraploidy of the clone and del(17)(p11) have been previously described only in a cell line or at end stage disease in B-ALL. It is suggested that the chromosomal abnormalities present at diagnosis were directly related to the refractory nature of this leukemia.
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PMID:Multiple chromosome abnormalities in a drug resistant TdT positive B-cell leukemia. 349 93

A translocation, t(11;19)(q23;p11), is reported in a child with T-cell leukemia. Our case indicates that the t(11;19) may not be restricted to the monocytic leukemias, as earlier reported, but may occur in other malignancies.
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PMID:t(11;19)(q23;p11) in a child with acute T-cell leukemia. 385 77

Preleukaemia has been identified as a clonal haemopathy in which progression to acute leukaemia involves conservation of the preleukaemic karyotype in the blast cells or the development of new abnormalities superimposed on the original clone. In this report, a case of childhood preleukaemia is presented in which two cytogenetically distinct clones developed over 2 years in a dysplastic marrow that was initially karyotypically normal. One clone with 47 chromosomes (47,XY,+21), disappeared without therapy. Predominance of the cytogenetically abnormal clone, 45,XY,-12,-17,t(12;17)(p11;q11) was associated with the development of acute myelogenous leukaemia and myelofibrosis. The development of independent clonal abnormalities in the unstable preleukaemic marrow may occur more commonly than has been previously recognized. Implications of the progression of the karyotypic abnormalities are discussed.
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PMID:Sequential development of distinct clonal chromosome abnormalities in a patient with preleukaemia. 385 52

A balanced translocation t(8;9) (p11;q34) was present in the peripheral blood, bone marrow, and spleen cells of a patient with Ph negative chronic myeloid leukaemia. Subsequent transformation into acute leukaemia was associated with the emergence of trisomy 8 and der(8)(8qter----cen----8p11::9q34----9qter). This is the third reported case of t(8;9) (p11;q34) and raises the question of the role of c-abl in the pathogenesis of this myeloproliferative disorder.
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PMID:Reciprocal translocation between chromosomes 8 and 9 in atypical chronic myeloid leukaemia. 386 76

No consistent chromosome abnormalities have been reported so far in T-cell lymphoma-leukemia. We report here two children suffering from T-cell acute lymphoblastic leukemia (ALL) with t(11;14)(q13;p11). Even though the breakpoints we claim are different from those in a recent report, we believe that their cases and ours have the same abnormality and that patients with this abnormality constitute a distinct subgroup of T-cell ALL positive for sheep erythrocyte receptor (E+) in children.
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PMID:11;14 translocation in childhood T-cell acute lymphoblastic leukemia. 392 32

Four patients with chromosome #12 rearrangement at the p11 level are described. One had acute promyelocytic leukemia, one had myelofibrosis evoluting to acute undifferentiated leukemia, one had acute nonlymphoid leukemia (ANLL) secondary to Hodgkin's disease, and another had acute leukemia recurring after allogeneic bone marrow transplantation. This chromosome abnormality was always associated with other karyotypic aberrations, probably as a secondary event. Possible correlations with recent findings in oncogene research are discussed.
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PMID:Chromosome 12 rearrangement with breakage at the p11 level in hematologic disorders: report of four cases. 397 22

Four cases with myeloproliferative syndromes or acute nonlymphocytic leukemia associated with t(1;7)(p11;p11) are presented. In each case, as in all cases published in the literature, the karyotypes of the affected cells contained two normal chromosomes #1, but only one chromosome #7, with the result that the basic karyotype was 46, -7, +t(1;7). This chromosome change is not geographically restricted, and appears to characterize a group of patients with myeloproliferative disorders and acute nonlymphocytic leukemia, including myeloproliferative syndromes, in whom exposure to previous chemotherapy, x-rays, or drugs is in the background history. The t(1;7) in secondary leukemia and myeloproliferative syndromes serves to duplicate the long arm of a chromosome #1 and to rescue the short arm of a chromosome #7.
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PMID:Translocation (1;7)(p11;p11): a new myeloproliferative hematologic entity. 405 81


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