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Query: UMLS:C0023473 (chronic myeloid leukemia)
18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of chronic myelogenous leukemia (CML) with a Philadelphia (Ph) chromosome. During the transformation phase of the disease, a del(7)(p11p15) and a +Ph were identified as additional chromosomal anomalies. We believe that loss of the segment 7p11-->p15 may play an important role in the progression of the disease.
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PMID:Deletion (7)(p11p15) in a patient with Philadelphia-positive chronic myelogenous leukemia. 148 63

We report two patients with a myelodysplastic syndrome and the Philadelphia (Ph) chromosome. The first patient was a 73-year-old man who was diagnosed as having a chronic myelomonocytic leukemia in combination with features suggestive of a myeloproliferative syndrome. Chromosomal analysis showed a normal karyotype in the majority of cells, mixed with metaphases containing a standard Ph translocation, t(9;22)(q34;q11), as well as a translocation between chromosome 4 and 6: t(4;6)(p15;p12). Southern blot analysis showed breakpoint cluster region rearrangement as observed in classic chronic myeloid leukemia. The second patient was a 63-year-old man with a myelodysplastic syndrome, type refractory anemia. Cytogenetic study of bone marrow cells at the time of diagnosis revealed a normal karyotype: 46,XY. The initial myelodysplastic syndrome evolved to a myeloproliferative phase with progressive leukocytosis and thrombocytosis. During the terminal phase the Ph chromosome was discovered in 100% of the examined cells. We discuss the correlation between MDS and myeloproliferative diseases, the de novo acquisition of the Ph chromosome during the course of a myelodysplastic syndrome, and review the literature.
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PMID:Cytogenetic and molecular studies of the Philadelphia translocation in myelodysplastic syndromes. Report of two cases and review of the literature. 158 81

The standard t(9;22)(q34;q11) found in Philadelphia (Ph) chromosome positive chronic myeloid leukemia (CML) involves a highly restricted (5.8 kb) chromosome 22 breakpoint cluster region (bcr), which results in the formation of a chimeric gene comprising exons from the 5' end of bcr and protooncogene c-abl coding sequences from chromosome 9. In a survey of 21 patients with hematologic and clinical features of CML we detected rearrangement of the chromosome 22 bcr by gene probe analysis in all cases, including 16 with a standard t(9;22), two with variant Ph translocations [t(10;22)(q26;q11);t(11;22)(p15;q11)], one with a complex Ph translocation [t(9;11;22)(q34;q13;q11)], one with a complex translocation and a masked Ph[t(9;14;22) (q34;q24;q11)], and one Ph-negative case with a t(1;9)(p32;q34). These observations further substantiate the suggestion that, despite karyotypic heterogeneity, a common underlying molecular lesion, the bcr-abl gene chimera, is involved in the disease pathogenesis of CML.
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PMID:Chromosome 22 breakpoints in variant Philadelphia translocations and Philadelphia-negative chronic myeloid leukemia. 264 33

A patient whose leukaemic cells carried the rare t(7;11)(p15;p15) was diagnosed as having acute myelomonocytic leukaemia (AML-M4), and supports the association of this specific translocation with forms of acute myeloid leukaemia showing differentiation. Blast phase chronic myeloid leukaemia was excluded by lack of involvement of the ABL and BCR genes. Chromosome in situ hybridization studies showed that both the HRAS1 and INS genes were present on the terminal part of chromosome 11p which was translocated to chromosome 7p. Neither HRAS1 nor INS were structurally rearranged. Field inversion gel electrophoresis showed that a 400 kb fragment encompassing HRAS1 was structurally entire in leukaemic DNA. Because the INS gene, which was also translocated, is probably located proximal to HRAS1 on chromosome 11p, it is unlikely that HRAS1 was near the chromosome 11 breakpoint or involved in this leukaemia.
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PMID:HRAS1 and INS genes are relocated but not structurally altered as a result of the t(7;11)(p15;p15) in a clone from a patient with acute myeloid leukaemia (M4). 271 71

Out of 105 Philadelphia (Ph) positive chronic myeloid leukemia patients analyzed, six (5.7%) carried a variant Ph translocation, namely t(6;9;9;10;22)(q24;p13;q34;p15;q11); t(9;13;22)(q34;q21;q11);der(2)(2pter----2q31::9q21---- 9q34::22q11----22qter) and der(9)t(2;9) (9pter----9q21::2q31----2qter);t(7;9;22)(q11;q34 ;q11), 14q + ;t(7;9;22)(q35;q34;q11), and t(9;11;22) (q34;q13;q11), respectively. Five of these patients were analyzed with Southern blotting. Three of them showed an atypical molecular pattern; namely, the patient with t(9;13;22) showed no rearrangement in the breakpoint cluster region (bcr), the patient with t(7;9;22)(q35;q34;q11) showed a 3' deletion, and the patient with t(7;9;22), 14q + showed a bcr rearrangement 3' to the exon 4 of the M-BCR. Chromosome in situ hybridization studies demonstrated that in patient one, a two-step translocation occurred: the first step moved the 3' bcr from chromosome 22 to chromosome 9, and the second moved the terminal part of 22q, carrying the c-sis protooncogene, to 10p. Variant Ph translocations appear to be associated with atypical molecular breakpoints.
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PMID:Cytogenetic and molecular studies in patients with chronic myeloid leukemia and variant Philadelphia translocations. 279 Jul 54

Two cases of childhood myelodysplastic syndrome with chromosome abnormalities involving band 11p15 are described. The first case, with inv(11)(p15q23), had a complex clinical course; the initial diagnosis was aplastic anemia, then refractory anemia with excess of blasts in transformation (RAEB-t), and finally, before death, chronic myelomonocytic leukemia with hematologic features similar to those of chronic myelogenous leukemia (CML). The second case, with t(4;11)(p13;p15), progressed from RAEB to acute myelogenous leukemia (M2). In the literature, we found 12 patients with nonlymphocytic leukemia and chromosome abnormalities involving band 11p15, including seven cases with t(7;11)(p13-p15;p15); four cases (including the present case 1) showed CML-like hematologic features. It is suggested that translocations involving 11p15 are a nonrandom chromosome abnormality in nonlymphocytic leukemia.
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PMID:Childhood myelodysplastic syndromes with 11p15 translocation. 329 71

A reciprocal translocation involving the short arms of chromosomes #7 and #11, t(7;11)(p15;p15), was found in two patients with myeloid leukemia, one with acute myelogenous leukemia (AML-M2) and the other with Philadelphia chromosome-positive chronic myelocytic leukemia (CML) in blastic phase. In both cases, a minor fraction of leukemic blasts in the bone marrow had Auer rods in the cytoplasm. In situ chromosome hybridization showed that the c-Ha-ras-1 oncogene localized to the breakpoint (p15) of chromosome #11 is translocated to the rearranged chromosome #7 in the AML case, whereas, it remained on the conserved region of the rearranged chromosome #11 in the CML case. The significance of the t(7;11) abnormality in myeloid leukemia is discussed.
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PMID:Localization of c-Ha-ras-1 oncogene in the t(7p-;11p+) abnormality of two cases with myeloid leukemia. 331 81

Three cases with chromosome changes involving bands 7p14 or 7p15 and 11p15 are described: one was a Japanese female with an acute myelomonocytic leukemia, the second was a white female with a 10-year history of paroxysmal nocturnal hemoglobinuria who developed a myelodysplastic syndrome, and the third was a patient with Ph-negative atypical chronic myelogenous leukemia with trisomy 8 and a chromosome change involving bands 7p14 and 11p15. These cases possibly indicate that the t(7;11)(p14 or p15;p15) change may characterize a subset of human nonlymphocytic neoplasia.
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PMID:Translocation between chromosomes 7 and 11 in nonlymphocytic neoplasia. 347 6

A reciprocal translocation involving the short arms of chromosomes 7 and 11, t(7;11)(p15;p15), was found in nine patients including eight with acute myelogenous leukemia (AML) and one with Philadelphia (Ph1) chromosome-positive chronic myelogenous leukemia (CML) in blastic crisis. Although a similar chromosome rearrangement has previously been reported in five patients, including three with AML and two with CML, the 7p breakpoint in some of these cases was slightly different from that detected in our patients. Notable cytogenetic and clinicohematologic findings in our patients and those reported in the literature were as follows: (a) t(7;11) occurred in myeloid leukemia, predominantly AML with subtype M2, and occasionally in other AML subtypes and in CML with or without Ph1 chromosome; (b) t(7;11) frequently occurred as the sole chromosome abnormality; (c) most patients showed a low neutrophil alkaline phosphatase score; and (d) Auer rods were present in leukemic cells of most cases including Ph1-positive CML. Our findings suggest that a t(7;11)-associated leukemia constitutes a subgroup of myeloid malignancy involving maturing leukemic cells.
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PMID:Reciprocal translocation involving the short arms of chromosomes 7 and 11, t(7p-;11p+), associated with myeloid leukemia with maturation. 347 4

A Ph1 chromosome-negative chronic myelogenous leukemia (CML) with t(7;11)(p15;p15) in a 6-year-old girl is reported. Three cases of 7;11 translocation have been reported so far. The patients concerned were between 37 and 72 years of age; 2 of them had CML and the other had acute myelomonocytic leukemia. Data from these 4 cases suggest that the 7;11 chromosome translocation may be related to a subgroup of Ph1-negative CML, specifically to one that may easily proceed to blast phase, or to "subacute" myelogenous leukemia. The present case demonstrates that CML with this chromosome abnormality is not restricted to adults but also affects children. The t(1;11)(q21 or 23;p15) reported in another case with Ph1-negative CML may be a variant of this translocation.
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PMID:Possible association of a new translocation, t(7;11)(p15;p15), with Ph1 chromosome-negative chronic myelogenous leukemia. 386 54


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