Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with chronic myelogenous leukemia (CML) had a Philadelphia chromosome (Ph') [t(9q+;22q-)] in all cells and trisomy C in 13% of cells (later determined to be trisomy 8) at the time of diagnosis. After 21 months of intermittent treatment with busulfan, the acute phase developed with the appearance of an additional abnormality (trisomy ? 19). During a complete remission and reconversion to the chronic phase, trisomies 8 and ? 19 DISAPPEARed, although the Ph' remained. Following a period of marked thrombocytosis, a second relapse occurred with the reappearance of both marker chromosomes.
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PMID:Chromosome changes in a patient achieving complete remission in the acute phase of chronic myelogenous leukemia. 28 90

A female patient with chronic myeloid leukemia in acute phase was found to have trisomy 11 in her bone marrow cells. The contemporary existence of different clones suggests the following clonal evolution: 46,XX leads to 46,XX,Ph' leads to 47,XX,Ph', +11 leads to 48,XX,Ph', +11, +Ph'. It is suggested, that the cytogenetic events leading to trisomy C in advanced cases of chronic myeloid leukemia are of a different character than those which often results in trisomy C in other myeloid disorders.
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PMID:Trisomy 11 in acute phase of chronic myeloid leukemia. 80 63

The chromosome banding pattern was analyzed in bone-marrow cells and/or spleen cells of 10 patients in the blastic phase of chronic myeloid leukemia (CML). It was obvious from the karyotype analysis that the chromosome aberrations occurring addition to the Philadelphia chromosome (Ph1) were strictly non-random. An extra Ph1, trisomy 8 and/or trisomy for the long arm of chromosome 17 were observed in all cases. This consistent pattern of chromosome involvement in CML was confirmed in 57 cases from the literature studied with banding techniques. In 88% of the total number of cases with further changes at least one of the three main chromosomal aberrations was found ("major route" of karyotypic evolution).
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PMID:Non-random karyotypic evolution in chronic myeloid leukemia. 106 18

We encountered a karyotypic abnormality, i.e. a trisomy of part of or the whole long arm of chromosome No. 1, in 4 patients with leukemia; 3 with acute myeloblastic, leukemia (AML) and 1 with chronic myelocytic leukemia (CML) in the blastic phase. Q- and G-banding techniques revealed that in two patients with AML and in the one with CML, this karyotypic abnormality was not an initial one and was apparently associated with clinical progression of the disease. This chromosome change is a common karyotypic abnormality in blood disorders, especially in AML, and possibly bears a relationship to selective growth advantages of the leukemia cells.
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PMID:Trisomy of the long arm of chromosome No. 1 in human leukemia. 125 46

The karyotypes of 98 patients between the ages of 8 and 81 years with acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), myelodysplastic syndromes (MDS), and chronic myeloid leukemia (CML) are presented. Although the well-described cytogenetic abnormalities associated with particular FAB subtypes in the West were observed, certain important local differences were noted. In ALL, hyperdiploidy was rarely observed, whereas the Philadelphia chromosome was observed in 50% of abnormal karyotypes. In AML, the t(8;21) was infrequently observed in M2 case, whereas trisomy 4 and 6, rarely reported elsewhere, formed 12% of the abnormal cases. In MDS, the incidence of -5/5q- and/or -7/7q- was 83% of cases with aberrant cytogenetic findings. Neither i(17q) nor an extra Ph was seen in 26 cases of CML including 9 cases of accelerated phase/blast crisis. In addition, previously unreported cytogenetic abnormalities occurring as single cases are presented. These findings are discussed in the context of geographical heterogeneity of chromosomal abnormalities in leukemia and emphasize the importance of continued epidemiologic studies of cytogenetics in hematologic malignancies.
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PMID:Cytogenetic analysis of hematologic malignancies in Hong Kong. A study of 98 cases. 139 2

Generally, malignant hematologic disorders have been believed to be of monoclonal origin. However, cytogenetically unrelated clones have been reported in some disorders including one case of acute leukemia (AL), one of acute lymphoblastic leukemia (ALL), one of acute myeloblastic leukemia (AMMoL), and five of myelodysplastic syndromes (MDS). The most frequent chromosome abnormality was trisomy 8 (75%), followed by trisomy 21 (37.5%, including tetrasomy 21) and trisomy 11 (25%). Two patients showed both trisomy 8 and 11, one also had trisomy 21 (triclonal). One patient showed two cytogenetically distinctive clones in which one was 47,XY,+8, related to myeloid cells, and the other had a del(6q) and del(9p), suggesting lymphoid cells. One patient we report and 5 from the literature had two unrelated clones with trisomy 8 and deletion of the long arm of chromosome 5 (5q-); all had MDS. Review of our records showed that 11 patients with both trisomy 8 and 5q- in the same abnormal karyotype (not biclonal) had AL, i.e., 10 of acute nonlymphocytic leukemia (ANNL) and one of chronic myelogenous leukemia (CML) in blastic crisis. These findings suggest that cytogenetically unrelated clones may indicate hematopoietic biclonality.
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PMID:Cytogenetic biclonality in malignant hematologic disorders. 152 Dec 30

A 36-year-old woman was referred to our hospital because of splenomegaly in February 1989. The leukocyte count was 55,500/microliter without hiatus leukemicus. The leukocyte alkaline phosphatase score was low (29). The bone marrow showed myeloid hyperplasia (24.8% myeloblasts) but no dysplastic change. The karyotype of the bone marrow cells was 46, XX and a diagnosis of Ph1 (-) CML was made. Treatment with VCR, 6MP and prednisolone made 7-month duration chronic phase, but the abnormal karyotype.[46, XX, i(17q)] gradually increased to 100% of bone marrow cells. The patient died in June 1990. The evidence that not only a BCR rearrangement but also messages of BCR/ABL fusion gene were negative made us able to differentiate this case from Ph1(-), BCR(+) CML. The addition of an i(17q) results in partial monosomy of 17q (17q13;p53 gene) and partial trisomy of 17q (17q11.2-12;G-CSF gene). We examined the rearrangement of p53 gene and G-CSF-dependent tumor cell growth in vitro, demonstrating one allelic loss of p53 gene and independent cell growth on G-CSF respectively. It is thought that in Ph1 (-), BCR (-) CML as well as in Ph1 (+) CML, an i(17q) is related to the progression but not to the initiation of these leukemias. However the precise mechanism, including p53 gene inactivation by point mutation, is still to be elucidated.
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PMID:[i(17q) appearing in acute phase in Ph1-negative, BCR-negative CML]. 163 23

In this report, we describe a patient with Philadelphia chromosome-negative chronic myelogenous leukemia (CML) with breakpoint cluster region gene rearrangement who developed T-cell lymphoblastic lymphoma. The occurrence of T-cell lymphoblastic lymphoma coincided with the appearance in the bone marrow of the cytogenetic abnormality, trisomy 22q11.2----22qter. This is the first report of high-grade T-cell lymphoma in a patient with documented CML.
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PMID:Occurrence of high-grade T-cell lymphoma in a patient with Philadelphia chromosome-negative chronic myelogenous leukemia with breakpoint cluster region rearrangement: case report and review of the literature. 843 86

A patient with a megakaryocytosis associated with a Philadelphia chromosome-positive chronic myeloid leukemia (CML) was found to have a trisomy of chromosome five. To our knowledge, this is the first case of trisomy 5 associated with a Ph + CML, particularly one with a megakaryocytosis. The trisomy 5 may be associated with the resistance to cytostatic drugs found in this patient.
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PMID:Trisomy 5 in Ph+ chronic myeloid leukemia in association with megakaryocytosis. 163 9

Cytogenetic analyses were performed on 12 adult patients with abnormal megakaryoblastic proliferation which was detected by ultrastructural cytochemical study (platelet peroxidase) and platelet-megakaryocytes-specific monoclonal antibodies (TP-80, Plt1, AN51, and KOR-77). The patients consisted of two patients with myelodysplastic syndromes (MDS), three with acute megakaryoblastic leukemia (AMKL), six with megakaryoblastic transformation in Philadelphia-positive chronic myelogenous leukemia (CML-meg-BC), and one case of chronic myeloproliferative disorder (CMPD). Among them, an inversion of the long arm of chromosome 3 [inv(3)(q21q26)] was found in one AMKL patient with a normal platelet count. Chromosome change at band 3q26 was also found in one MDS patient without thrombocythemia. Furthermore, the long arm of chromosome 13, where rearrangements in myelofibrosis are clustered (13q12----q22) was seen in one MDS patient. Trisomoy of chromosome 19 was found in one AMKL patient and three CML-meg-BC patients. These findings indicate that cytogenetic abnormalities involving 3q26, 13q, and trisomy 19 are associated with hematologic neoplasia with megakaryocytic lineage in adult patients, although these abnormalities were not related to the survival of the patients. During the period of this study, two acute myelogenous leukemia patients (AML-M2 and AML-M5b) with chromosome rearrangements at band 3q21 and thrombocythemia were found, indicating that chromosome abnormality at band 3q21 is related to quantitative platelet dysfunction, whereas that at 3q26 is related to hematologic malignancies with a proliferation of megakaryocytic lineage.
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PMID:Cytogenetic findings in adult acute leukemia and myeloproliferative disorders with an involvement of megakaryocyte lineage. 229 63


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