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

We performed a cytogenetic study on 16 murine mature B-cell lymphomas and 10 T-cell lymphomas, using G-banding techniques. All tumors, with the exception of 3 spontaneous B-cell tumors, were induced by various slowly transforming murine leukemia viruses (MuLV). Metaphases were obtained from primary (10 B-cell tumors) and first or second transplant generation lymphomas (6 B-cell and 10 T-cell tumors), all of which were well characterized with respect to phenotypic, histologic and genotypic features. In the T-cell tumors we found relatively simple karyotypic abnormalities, including various numerical aberrations, such as trisomy 15, in line with many earlier reports. However, the majority of B-cell tumors showed a great variety of both structural and numerical chromosomal anomalies. Three B-cell lymphomas had an apparently normal karyotype. No single cytogenetic abnormality occurred commonly in the B-cell lymphomas, but some structural abnormalities were found in more than one stemline, in particular, ins (II) (A1; A2) in 3 tumors, and deletions involving the D-region of chromosome 14 in 3 other lymphomas. These cytogenetic results clearly indicate that the pathogenic mechanisms involved in MuLV-induced (long latency) B-cell lymphomagenesis and (short latency) T-cell lymphomagenesis differ considerably.
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PMID:Distinct chromosomal abnormalities in murine leukemia virus-induced T- and B-cell lymphomas. 254 44

The Philadelphia (Ph) chromosome in leukemia is invariably derived from chromosome #22. A break occurs in the long (q) arm of chromosome #22 and, in every case observed until now, all of the material from that breakpoint through the telomere of chromosome #22 has been reciprocally translocated to another chromosome, most often chromosome #9. With the t(9;22) translocation, the oncogene c-sis moves from chromosome #22 onto 9q and the oncogene c-abl moves reciprocally from chromosome #9 onto 22q. We report a new mechanism for the genesis of the Ph chromosome in chronic myelocytic leukemia (CML) involving interstitial deletion of chromosome #22 with insertion of the deleted material into another chromosome: 46,XX,dir ins(11;22)(q13;q11q13). The distal portion of chromosome #22, including the telomere, appeared to have been retained in the Ph chromosome. There was no visible involvement of chromosome #9. This insertional deletion is of potential importance in evaluating the roles of oncogenes such as c-abl and c-sis in the Ph rearrangement in the origin of leukemia.
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PMID:The Philadelphia (Ph) chromosome in leukemia. I. A new mechanism due to interstitial deletion and insertion in chronic myelocytic leukemia. 298 Nov 54

By in situ chromosomal hybridization, the GM-CSF and FMS genes were localized to human chromosome 5 at bands q23 to q31, and at band 5q33, respectively. These genes encode proteins involved in the regulation of hematopoiesis, and are located within a chromosome region frequently deleted in patients with neoplastic myeloid disorders. Both genes were deleted in the 5q-chromosome from bone marrow cells of two patients with refractory anemia and a del(5)(q15q33.3). The GM-CSF gene alone was deleted in a third patient with acute nonlymphocytic leukemia (ANLL) who has a smaller deletion, del(5)(q22q33.1). Leukemia cells from a fourth patient who has ANLL and does not have a del(5q), but who has a rearranged chromosome 5 that is missing bands q31.3 to q33.1 [ins(21;5)(q22;q31.3q33.1)] were used to sublocalize these genes; both genes were present on the rearranged chromosome 5. Thus, the deletion of one or both of these genes may be important in the pathogenesis of myelodysplastic syndromes or of ANLL.
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PMID:Evidence for the involvement of GM-CSF and FMS in the deletion (5q) in myeloid disorders. 348 37

Fourteen patients with acute nonlymphocytic leukemia (ANLL) or dysmyelopoietic syndromes were found to have abnormalities involving the long arm of chromosome 3. In eight patients, the structural rearrangements involved both bands 3q21 and 3q26 and included t(3;3) (four patients), inv(3) (three patients), and ins(5;3) (one patient). Before treatment, seven of these eight patients had platelet counts above 100,000 per microliter, five had normal or elevated platelet counts, and four had significantly elevated platelet counts (600,000 to 1,731,000 per microliter). In each of the eight cases, normal or elevated platelet counts were associated with marked abnormalities of megakaryocytopoiesis, including increased numbers of megakaryocytes and numerous micromegakaryocytes. Classification within the French-American-British system was difficult in most of these cases; however, the leukemia in five of the eight patients with abnormalities of chromosome 3 that involved both bands 3q21 and 3q26 was classified as M4. The remaining six of the 14 patients had translocations between chromosome 3 and another chromosome. None involved both bands 3q21 and 3q26, and a break in either q21 or q26 was noted in only two patients. One of the six, who had ANLL (M4) with a normal platelet count, had a 3;5 translocation which involved band 3q25. These data suggest that in patients with ANLL, abnormalities of chromosome 3 which simultaneously involve bands 3q21 and 3q26 are associated with unusually high platelet counts.
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PMID:Rearrangements of chromosome 3 involving bands 3q21 and 3q26 are associated with normal or elevated platelet counts in acute nonlymphocytic leukemia. 406 25

When leukemic blood or marrow specimens from 148 adults with newly diagnosed acute nonlymphocytic leukemia (ANLL) were studied with chromosome banding techniques, 79 were found to have clonal abnormalities. Among 130 treated patients, the 53 with initially normal karyotypes had a significantly longer survival rate than the 16 in whom no normal metaphases were observed (p = 0.02). The 55 patients with both normal and abnormal metaphase cells had an intermediate survival. Once a complete remission had been attained, however, there was no significant difference in median survival between those patients with entirely normal karyotypes and those with abnormal karyotypes. Among the various FAB morphologic subsets of ANLL, the differences in complete remission rate and overall survival between the various cytogenetic subsets were greatest in acute myelogenous leukemia (AML, M1 + M2). The presence of an abnormal clone was a more important predictor of clinical outcome (p = 0.02) than the presence of normal stem cell clones. Aneuploidy alone (hyperdiploidy or hypodiploidy) was not of predictive value, indicating that the use of banding techniques to identify structural rearrangements in pseudodiploid cells was essential. Clonal chromosomal abnormalities were nonrandom and acquired, and specific abnormalities were closely associated with specific clinical-pathologic subsets of ANLL. All 13 patients with acute promyelocytic leukemia and adequate cytogenetic specimens had t(15;17); this translocation was not found in any other subset of ANLL. Six patients with AML (M2) had t(8;21) or a variant of this rearrangement. Seven patients had inv(16)(p13q22) associated with acute myelomonocytic leukemia (AMMoL, M4) and abnormal marrow eosinophils. Two patients had ins(3;3) and thrombocytosis. Four patients had a translocation involving 11q, but none of these had acute monocytic leukemia (AMoL, M5); no patient had del(11q).
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PMID:The predictive value of initial cytogenetic studies in 148 adults with acute nonlymphocytic leukemia: a 12-year study (1970-1982). 662 22

Variants of the t(15;17)(q22;q12-q21) chromosomal rearrangement associated with acute promyelocytic leukemia (APL) have been previously described and they frequently involve either chromosome 15 and/or 17. Previously we reported a rare variant t(11;17). We now describe two patients with myelodysplastic syndrome (MDS) that transformed to APL-like leukemia. Both had trisomy 11 at the diagnosis of APL-like leukemia. Following treatment for APL, patient 1 reverted to MDS and showed a normal karyotype. When leukemia recurred, his bone marrow karyotype was 47,XY,t(4;11), +11,der(22)t(1;22). Both patients were treated with all-trans retinoic acid (ATRA) for APL for 5 weeks, but failed to respond. The karyotype of patient 1 after ATRA treatment was 46,XY,t(4;11); the trisomy 11 had been lost and the bone marrow was replaced with immature myeloblasts without promyelocytes. In patient 2, the karyotype remained the same as at diagnosis, i.e., 47,X,-Y,dir ins(4;7),del(5), +6,del(7), +8, + 11,-18. Molecular analysis by reverse transcriptase PCR analysis showed the presence of wild type retinoic acid receptor alpha (RARA) and the absence of the PML-RARA chimeric gene associated with t(15;17). Additional analysis of PLZF, a new zinc finger gene associated with t(11;17), also showed the absence of this hybrid gene. These data support the concept that APL is a heterogeneous disorder and that variants with chromosome 11 rearrangement exist that do not respond to ATRA.
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PMID:Myelodysplastic syndrome transforming to acute promyelocytic-like leukemia with trisomy and rearrangement of chromosome 11. 751 69

We describe two new human leukemia cell lines, MOLM-13 and MOLM-14, established from the peripheral blood of a patient at relapse of acute monocytic leukemia, FAB M5a, which had evolved from myelodysplastic syndrome (MDS). Both cell lines express monocyte-specific esterase (MSE) and MLL-AF9 fusion mRNA. Gene fusion is associated with a minute chromosomal insertion, ins(11;9)(q23;p22p23). MOLM-13 and MOLM-14 are the first cell lines with, and represent the third reported case of, MLL gene rearrangement arising via chromosomal insertion. Both cell lines carry trisomy 8 which was also present during the MDS phase, as well as the most frequent trisomies associated with t(9;11), ie, +6, +13, +19 variously present in different subclones. Despite having these features in common, differences in antigen expression were noted between the two cell lines: that of MOLM-13 being CD34+, CD13-, CD14-, CD15+, CD33+; whereas MOLM-14 was CD4+, CD13+, CD14+, CD15+, CD33+. Differentiation to macrophage-like morphology could be induced in both cell lines after stimulation with INF-gamma alone, or in combination with TNF-alpha, which treatment also induced or upregulated, expression of certain myelomonocyte-associated antigens, including CD13, CD14, CD15, CD64, CD65 and CD87. Together, these data confirm that both cell lines are likely to be novel in vitro models for studying monocytic differentiation and leukemogenesis.
Leukemia 1997 Sep
PMID:Two acute monocytic leukemia (AML-M5a) cell lines (MOLM-13 and MOLM-14) with interclonal phenotypic heterogeneity showing MLL-AF9 fusion resulting from an occult chromosome insertion, ins(11;9)(q23;p22p23). 930

Thirty patients representing 5.5% of those collected by the 11q23 workshop had a t(6;11)(q27;q23). They included 27cases of acute myeloid leukemia (AML) (M1, three cases; M2, two cases; M4, nine cases; M4/M5, one case; M5, 12 cases) of age range 3-72 years and three cases of acute lymphoblastic leukemia (ALL) (B-lineage ALL, two cases; T-ALL, one case) of age range 0.5-13 years. In 20 cases the t(6;11) was the sole abnormality. In 10 cases the recurrent additional abnormalities were extra copies of chromosomes 8, 19, 21, or the der(6). Translocation t(6;11) was identified by cytogenetics alone in 13 cases. In three cases it was confirmed by fluorescence in situ hybridization (FISH) using whole chromosome paints (wcps) 6 and 11. In a further 14 cases involvement of MLL was demonstrated by FISH, by reverse transcriptase polymerase chain reaction (RT-PCR), by Southern blotting (SB) or by a combination of these methods. One case had a direct insertion of 11 into 6-dir ins(6;11)(q27;q13q23). Molecular investigations showed that one case had a 3' deletion of MLL. The median overall survival for the patients was 12 months, indicating a poor prognosis for patients with a t(6;11) translocation.
Leukemia 1998 May
PMID:The t(6;11)(q27;q23) translocation in acute leukemia: a laboratory and clinical study of 30 cases. EU Concerted Action 11q23 Workshop participants. 959 82

Analyzable G-banded metaphases were normal in bone marrow from a 26-year-old male having 80% blasts. Fluorescence in situ hybridization (FISH) using the centromeric probe, D7Z1, revealed 85% of interphase cells with one signal for chromosome 7. Chromosome painting revealed a chromosome 7 rearrangement in a few metaphases that were otherwise unanalyzable. A repeat bone marrow confirmed 3 of 20 metaphases, by G-banding, to have multiple rearrangements and aneuploidy, including a large derivative chromosome involving a complex rearrangement of chromosomes 5, 7, and 9; that is, der(5)t(5;9)(q31;q13)ins(5;7)(p15;q?31q?34), with loss of most of chromosome 7 (7 pter-->7q?31); one normal 7 was present. Immunophenotyping characterized the patient's condition as an early T-cell acute lymphocytic leukemia (ALL), with a population of cells suggesting biphenotypic leukemia. He attained a complete clinical remission with chemotherapy. Six months after the initial presentation he received an allogeneic bone marrow transplant. Three months later a CNS relapse was followed by a bone marrow relapse. At this time, eight months after transplant, repeat study of his bone marrow revealed the majority of metaphases had structural and numerical chromosome abnormalities similar to the small clone in the earlier study, including der(5)t(5;9)ins(5;7), but with two normal 7s. FISH showed two 7-centromere signals in interphase. The patient expired one month later.
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PMID:Discrepant cytogenetic and fluorescence in situ hybridization results in a 26-year-old male with early T-cell acute lymphocytic leukemia. 979 75

We report a case of acute myelocytic leukemia (AML) showing a chromosomal abnormality, ins(21;8), with AML1/MTG8 chimeric mRNA. The patient, a 73-year-old woman, was admitted to our hospital because of AML relapse. Bone marrow aspiration showed 44% blasts and ins(21;8)(q12;q13q22) by cytogenetic study. Moreover, the size of chimeric AML1/MTG8 mRNA detected by RT-PCR in this case was shorter than that of previously reported. The patient was diagnosed as having relapse of AML (M2), but achieved complete remission with DCP therapy. Four months later, extramedullary relapse occurred, and this was followed five months later by bone marrow relapse. However, the patient again achieved complete remission. Most cases of AML1/MTG8 fusion gene are caused by t(8;21), and only very rarely by ins(21;8). In this case, the AML1/MTG8 fusion gene is thought to have been involved in the onset of leukemia.
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PMID:[Acute myelocytic leukemia with ins(21;8)(q22;q13q22) presenting with AML1/MTG8 chimeric mRNA]. 1107 Sep 37


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