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

Translocations involving chromosome 11, band q23, are frequent recurring abnormalities in human acute lymphoblastic and acute myeloid leukemia. We used 19 biotin-labeled probes derived from genes and anonymous cosmids for hybridization to metaphase chromosomes from leukemia cells that contained four translocations involving band 11q23: t(4;11)(q21;q23), t(6;11)(q27;q23), t(9;11)(p22;q23), and t(11;19)(q23;p13). The location of the cosmid probes relative to the breakpoint in 11q23 was the same in all translocations. Of the cosmid clones containing known genes, CD3D was proximal and PBGD, THY1, SRPR, and ETS1 were distal to the breakpoint on 11q23. Hybridization of genomic DNA from a yeast clone containing yeast artificial chromosomes (YACs), that carry 320 kilobases (kb) of human DNA including CD3D and CD3G genes, showed that the YACs were split in all four translocations. These results indicate that the breakpoint at 11q23 in each of these translocations occurs within the 320 kb encompassed by these YACs; whether the breakpoint within the YACs is precisely the same in the different translocations is presently unknown.
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PMID:Mapping chromosome band 11q23 in human acute leukemia with biotinylated probes: identification of 11q23 translocation breakpoints with a yeast artificial chromosome. 225 Dec 77

An interferon-inducible cytokine, IP-10, containing homology to a family of proteins having chemotactic (platelet factor 4, beta-thromboglobulin) and mitogenic (connective tissue-activating peptide III) activities has been mapped to chromosome 4 at band q21, a locus associated with an acute monocytic/B-lymphocyte lineage leukemia that exhibits the nonrandom translocation t(4;11)(q21;q23). In situ hybridization of t(4;11)(q21;q23)-carrying leukemic cells revealed that the IP-10 gene is proximal to the breakpoint of this translocation. No DNA rearrangement was evident when the IP-10 gene was hybridized to genomic DNA isolated from two patients' leukemic cells that contain t(4;11)(q21;q23). However, restriction fragment length polymorphism in the 5' region of the IP-10 gene was detected. The ETS1 protooncogene is located at 11q23 and is known to translocate to chromosome 4 in t(4;11) (q21;q23) and into the interferon gene cluster in (9;11) (p22;q23). Both translocations are associated with acute monocytic leukemia. These results suggest a model in which juxtaposition of genetic loci regulated by antiproliferative signals, such as interferon, next to an oncogene, like ETS1, could effectively short circuit homeostatic control circuits and contribute to the neoplastic state.
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PMID:Interferon-inducible gene maps to a chromosomal band associated with a (4;11) translocation in acute leukemia cells. 243 86

We studied chromosomes of BM cells from four neurofibromatosis (NF) patients with leukemia. One patient had a normal diploid karyotype in the chronic phase of juvenile chronic myelogenous leukemia (JCML). When the the leukemia evolved into the accelerated phase, she had cells with 46,XX,-7,+der(7)t(3;7)(q21;p22); the abnormalities resulted in a partial 7p deletion. In another patient with JCML, BM cells in the accelerated phase had 45,XY,-7. The abnormal cells with monosomy 7 disappeared from the BM after chemotherapy but reappeared later in the course. Another patient developed refractory anemia with excess of blasts in transformation (RAEB-T) and had cells with 46,XX,-6,+r(6)(p23?q21?); the abnormalities resulted in partial 6p and 6q deletions. The other patient with ANLL had cells with 45,XX,-7. Our findings and review of data on nine other patients suggest that BM cells of NF patients with JCML in chronic phase have no microscopically detectable chromosome changes and that cells with chromosomal deletion emerge when JCML evolve into the accelerated or blast phase. Thus, deletion of the whole or part of certain chromosomes, such as chromosomes 6, 7, etc., may be an important step towards the evolution of JCML cells or the development of de novo acute leukemias in NF patients.
Leukemia 1989 Jan
PMID:Chromosome pattern in juvenile chronic myelogenous leukemia, myelodysplastic syndrome, and acute leukemia associated with neurofibromatosis. 249 96

A human leukemia cell line, PER-255, was established from the bone marrow of a 5-year-old boy with features typical of lymphomatous T-acute lymphoblastic leukemia (T-ALL). The leukemic origin of cell line PER-255 is indicated by its cytochemical and immunologic similarity to the patient's fresh leukemic cells, which correspond to immature cortical thymocytes. Southern blot analysis showed that the IgJH genes were in germline configuration, whereas both alleles of the T-cell receptor-beta (TCR-beta) gene were rearranged in PER-255 cells, with identical rearrangements present in the patient's leukemic cells. Cytogenetic analysis of the cell line revealed a single abnormal clone with the karyotype 46,XY,t(7;10)(q32-34;q24),t(9;12) (p22;p12-13). Reciprocal translocations involving chromosome bands 7q32-36, containing the gene for the TCR-beta chain, have been reported for a number of tumors of T-cell origin. Translocations involving the 7q32-36 region appear to be nonrandomly associated with childhood T-ALL, whereas abnormalities of 9p and 12p have been reported to be nonrandomly involved in ALL but not specifically associated with the T-cell phenotype.
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PMID:Establishment and characterization of a childhood T-cell acute lymphoblastic leukemia cell line, PER-255, with chromosome abnormalities involving 7q32-34 in association with T-cell receptor-beta gene rearrangement. 254 23

A case of congenital monocytic leukemia that underwent a lineage switch to acute lymphocytic leukemia (ALL) is described. The original leukemia had typical monocytic features, as evidenced by morphology (FAB M5), cytochemistry (nonspecific esterase) and immunophenotype (My4 positive). Cytogenetic study showed a pseudodiploid clone t(9;11)(p22;q21) that could be interpreted as a variant of the t(9;11)(p22;q23) reported in patients with the M5 type of leukemia. After successful remission induction with single-agent chemotherapy (VM-26) and subsequent sustained remission for 12 months with alternating VM-26 and VP-16-213, lineage switch to ALL (FAB L1) occurred. The presence of both lymphoid and myeloid markers on leukemic cells at lineage switch suggested the biphenotypic character of the patient's ALL. Our observation indicates that a lineage switch can occur from monocytic leukemia to ALL, although most of the cases previously reported have been in the reverse direction. This case emphasizes again the need to carry out careful and comprehensive marker studies to gain insight into the possible prognostic significance and the application of appropriate therapy.
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PMID:A lineage switch in acute monocytic leukemia. A case report. 275 Oct 72

Sera from 11 Japanese patients with hairy cell leukemia and 4B122, an anti-hairy cell serum produced by the authors, were surveyed by Western blot analyses for cross-reacting antibodies to human T cell leukemia virus (HTLV)-I and -II virions released, respectively, from Lma-66 and Mo-T cell lines. Sera from the majority of the patients showed positive reactions with p15, p19, and/or p24 of HTLV-I and with p21 and/or p22 or HTLV-II. 4B122 was weakly cross-reactive with HTLV-II but not with HTLV-I. These results militate against the involvement of HTLV-I or -II but may implicate a role by a cross-reacting, previously unrecognized retrovirus in the pathogenesis of hairy cell leukemia in Japanese patients.
Leukemia 1987 Apr
PMID:Cross-reacting antibodies to human T cell leukemia virus-I and -II in Japanese patients with hairy cell leukemia. 282 19

Cytogenetic analysis of the leukemic cells from a 1-day-old baby with an acute myelomonocytic leukemia revealed them to contain a chromosome change of t(11;19)(q23;p13). Molecular studies using a 980 bp HindIII/HpaI digested v-ets probe showed no DNA rearrangements, deletions, or amplification in the leukemic cells, including the JH immunoglobulin and T-cell receptor (alpha or beta) genes. The findings indicate that the leukemic cells with t(11;19)(q23;p13) appear not to contain a transposition or rearrangement of the protooncogene Hu-ets-1 located at 11q23, as previously described in leukemic cells with t(4;11)(q21;q23) and t(9;11)(p22;q23). The leukemic cases with t(11;19)(q23;p13) studied by us showed a phenotype compatible with their myelomonocytic nature, although it is possible that other cases may have a lymphoid phenotype.
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PMID:Hu-ets-1 gene in congenital leukemia with t(11;19)(q23;p13). 283 11

The t(9;11)(p22;q23) is a recurring abnormality in acute nonlymphocytic leukemia. The analysis of complex 9;11 translocations will aid in the identification of the conserved chromosomal junction or the critical genetic alteration created by the rearrangement; however, variant translocations involving chromosomes #9 and #11 have not been reported. We have identified such variants in two patients who had acute myelomonocytic leukemia and acute monocytic leukemia, characterized by a t(9;11;18)(p22;q23;q12) and a t(9;11;13)(p22;q23;q34), respectively. The conserved junction resulting from these rearrangements is created by the translocation of chromosomal material from 9p to 11q.
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PMID:Variant translocations (9;11): identification of the critical genetic rearrangement. 342 44

A 69-year-old male patient with refractory anemia with excess blasts (RAEB) was found to have a consistent chromosomal abnormality, t(6;9)(p22.3;q34), in the bone marrow and unstimulated peripheral blood cells. Twenty patients with t(6;9) and leukemia have been reported; some of them had a myelodysplastic syndrome (MDS) before developing overt ANLL. Our patient was still in the MDS stage when the t(6;9) was found. This result suggests that t(6;9) represents one of the pathways from MDS to leukemia in patients with ANLL.
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PMID:Translocation t(6;9)(p22.3;q34) in myelodysplastic syndrome--refractory anemia with excess blasts. 366 44

A fragile site on the long arm of chromosome #16 (q22) was detected in a 24-year-old man with pancytopenia. During the course of the disease he developed an inverted duplication of region q11-12 of chromosome #1 and a translocation between chromosomes #9 and #13: t(9;13)(p22;q32). These abnormalities, as well as an additional iso-like marker chromosome that consisted of one normal 9p and the abnormal 9p arm, were detected in Epstein-Barr nuclear antigen-positive B-cell cultures. Two years later, evolution of the abnormal clone with loss of chromosome #7 and, subsequently, chromosome #22 occurred in connection with development of acute myeloid leukemia. Although the heritable fragile site on chromosome #16 was present in all cell populations investigated, it was not involved in the evolution of the abnormal karyotype. This fragile chromosome #16 also was found in 4 of 11 family members in whom chromosome analysis was performed, thus suggesting this aberration was inherited in a dominant autosomal pattern. The incidence of the heritable fragile site in normal and leukemic cells of the patient, as well as stimulated blood cultures of his relatives, are reported. In addition, the possible relationship between this constitutional chromosome breakage syndrome and the occurrence of leukemia is analyzed.
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PMID:Noninvolvement of chromosome 16 in karyotype evolution of acute myeloid leukemia in a patient with a heritable fragile site on 16q22. 385 7


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