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

A translocation t(1;7)(p11;p11), previously reported in patients with myelodysplasia or leukemia has been found in seven new cases. The present report briefly reviews the cytogenetic and clinical features of 22 patients with this translocation. The majority of these patients had a history of occupational or therapeutic exposure to toxic substances or radiation. Trisomy 8 or 21 were the most common additional abnormalities, especially in leukemic patients. The t(1;7) should be added to the group of specific cytogenetic abnormalities observed frequently in secondary myelodysplasia and leukemia.
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PMID:Translocation 1;7 in hematologic disorders: a brief review of 22 cases. 405 82

Rickard's strain of feline leukemia virus (FeLV) contains two large glycoproteins and five smaller polypeptides of molecular weights 100,000 (gp >/= 100), 70,000 (gp70), 30,000 (p30), 21,000 (p21), 15,000 (p15), 11,200 (p11), and 10,000 (p10) when chromatographed on 6% agarose in the presence of 6 M guanidine hydrochloride (GuHCl). P21 is a minor component which was not previously described for mammalian leukemia-sarcoma viruses and may be analogous to the seventh protein found in avian viruses. Analysis on 4% agarose and by sodium dodecyl sulfate polyacrylamide gel electrophoresis revealed that gp >/= 100 is actually >/= 200,000 daltons and dissociates to polypeptides of approximately 100,000 to 115,000 daltons, whereas gp70 can be resolved into six stained bands ranging from 40,000 to 80,000 daltons despite being rechromatographed as a single symmetrical peak on 6% agarose. Rechromatography on 8% agarose was found to be more effective than on 6% agarose or sodium dodecyl sulfate polyacrylamide gel electrophoresis for obtaining the five small polypeptides, especially p11 and p10, in a highly purified form suitable for further analysis and for obtaining more precise estimates of their molecular weights, especially when done by co-chromatography with iodinated standard proteins markers. Rechromatographed p30, p21, p15, p11, and p10 had molecular weights of 27,000, 18,000, 15,000, 12,000, and 12,000 respectively, by co-electrophoresis with the marker proteins on sodium dodecyl sulfate polyacrylamide gel electrophoresis, clearly establishing that the latter two FeLV polypeptides comigrate to form one less band when compared to elution from agarose. The isoelectric points of p30 and p15 were 5.5 and 8.9, respectively, after renaturation from GuHCl and 5.6 and 8.7, respectively, when isolated from Tween-ether treated virus. Rechromatographed p30, p15, and p11, renatured by removing GuHCl with dialysis, reacted only with their homologous antisera in immunodiffusion analysis, indicating that they are immunologically unrelated. Also the interspecies gs-3 determinant associated with p30 could be regained by removal of GuHCl.
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PMID:Properties of feline leukemia virus. I. Chromatographic separation and analysis of the polypeptides. 413 30

We describe chromosome abnormalities in 6 patients with hairy cell leukaemia (HCL) variant, a rare B-cell disorder with clinical and laboratory features intermediate between HCL and B-prolymphocytic leukaemia (B-PLL). All but one had marked splenomegaly and a raised white blood cell count (median 40 x 10(9)/l) with over 80% nucleolated hairy cells. These cells had a B-cell immunophenotype distinct from that of typical HCL. All patients but one are alive with stable disease with a median follow-up of 60 months. Numerical chromosome changes included loss of chromosomes 2, 3, 4, 6, 10, 19, 21, and X. three cases had translocations involving the immunoglobulin gene regions: t(14;17)(q32;q11), t(14;22)(q32;q11), and t(2;8)(p11.12;q24). Immunocytochemistry demonstrated the presence of the MYC protein in cells from the case with t(2;8) but not in two others. Other structural abnormalities included t(3;10)(q27;q22) and t(3;12)(q27;q13) in the same patient, der(17)t(7;10;17)(p11;q27;q22), t(1;3)(q25;p21), t(8;21)(p12;q11), t(17;21)(p11;p11), del(6)(q15), del(7)(q34), and del(14)(q24).
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PMID:Chromosome abnormalities in hairy cell leukaemia variant. 752 43

There are five reported cases of an atypical myeloproliferative disorder in which the leukemia cells have a consistent t(8;13)(p11;q12) translocation. We analyzed the breakpoint in metaphases from two of these patients by fluorescence in situ hybridization using a series of yeast artificial chromosomes (YACs) derived from the 13q12 region. We found that a YAC containing the FLT1 and FLT3 oncogenes was localized distal to the 13q12 breakpoint and was not rearranged. YAC66, a YAC that lies immediately adjacent to the chromosome 13 centromere, was localized proximal to the 13q12 breakpoint and was not rearranged. A third YAC, which is located between FLT1 and YAC66, was unrearranged in normal metaphase chromosomes, but showed hybridization signals on both derivative chromosomes in both cases. Thus, the breakpoints in these two cases are localized to the same 1.5 Mbp region of 13q12. This may be the site of an unidentified gene involved in the pathogenesis of some types of leukemia.
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PMID:Localization of the 8;13 translocation breakpoint associated with myeloproliferative disease to a 1.5 Mbp region of chromosome 13. 753 83

Loss of chromosome 20 and rearrangement of the short arm of chromosome 9 were identified by banding analysis of three adult patients with acute lymphoblastic leukemia (ALL). The G-banding pattern suggested an identical deletion of 9p, but, also, an unbalanced translocation with chromosome 20 was taken into consideration. Dual-color chromosome painting with probes for chromosomes 9 and 20 revealed the presence of material from chromosome 20 at the short arm of the abnormal chromosome 9 in all three cases. Centromeric alpha-satellite DNA of both chromosome 9 and chromosome 20 was demonstrated by fluorescence in situ hybridization and indicated the presence of a dicentric chromosome. The hybridization of a YAC clone of the short arm of chromosome 20 proved that the dicentric chromosome contained the short arm of chromosome 20, which had been suspected from the G-banding pattern. Thus, the rearrangement was interpreted as dic(9;20)(p11;q11.?1). Because this was the sole chromosome abnormality in two patients, dic(9;20) may be a primary chromosome aberration in ALL. In one case, a 9q+ chromosome derived from a Philadelphia (Ph) translocation was involved in the formation of the dicentric chromosome. Immunophenotyping revealed CD10+ B-cell precursor ALL in all three cases. Whereas the two patients in whom dic(9;20) was the sole cytogenetically detectable change are in continuous complete remission for 10 and 45 months, respectively, the Ph+ patient relapsed with leukemia and died 8 months after diagnosis.
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PMID:dic(9;20): a new recurrent chromosome abnormality in adult acute lymphoblastic leukemia. 754 44

Chromosomal breakpoints associated with malignancy are known to cluster at particular regions of the karyotype. Based on a review of the literature we have identified a novel leukaemia syndrome associated with translocations involving 8p11. This syndrome is distinct from the previously described translocation t(8;16)(p11;p13) associated with acute monoblastic leukaemia. We have summarized the clinical and cytogenetic features of 13 case reports which describe a myeloproliferative syndrome with eosinophilia, lymphadenopathy and a high incidence of T cell non-Hodgkin's lymphoma with progression to acute myeloid leukaemia. The translocations involving 8p11 were: either t(8;13)(p11-12;q11-12), t(8;9) (p11;q32-34) or t(6;8)(q27;p12). In two cases of t(8;13) molecular studies have mapped the chromosome 13 breakpoint to a 1.5 Mbp region, but a full molecular characterization of these translocations is required. In view of the striking clinicopathological and karyotypic similarities between these cases we propose that they be considered a single nosological entity and termed '8p11 myeloproliferative syndrome'.
Leukemia 1995 Oct
PMID:A new myeloproliferative disorder associated with chromosomal translocations involving 8p11: a review. 868 12

Acute myeloblastic leukemia (AML) with t(8:16) or its variant t(8:V) has been rarely reported. A high proportion of patients are infants and children, often with a bleeding tendency and disseminated intravascular coagulopathy (DIC). Only one-third of the de novo patients remain in the first complete remission following multiagent chemotherapy and bone marrow transplantation (BMT). Morphocytochemically, the disorder is classified as an M5, M4, or M4/M5 variant. In the presented case, with the variant t(8:19)(p11:q13), comprehensive light and electron microscopic blast cell characterization showed monocytic and granulocytic features compatible with the M4 subtype (on the monocytic predominance range of the French-American-British classification scale). Although hemophagocytosis, one of the hallmarks of the disease, was rare in our patient, numerous autophagic vacuoles were present. Immuno- and genotyping showed a myelomonocytic phenotype with no evidence of early progenitor antigen expression or mixed leukemia. These results and those of previous reports support the high specificity of t(8:16) or its variants to the unique M4/M5 type leukemia and the role of a gene on 8p11 in this specific transformation.
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PMID:A distinct subtype of M4/M5 acute myeloblastic leukemia (AML) associated with t(8:16)(p11:p13), in a patient with the variant t(8:19)(p11:q13)--case report and review of the literature. 759 49

In Drosophila the Notch gene controls differentiation to various cell fates in many tissues. Three mammalian Notch homologs have recently been identified: Notch 1, 2, and 3. All three homologs are very highly conserved relative to the Drosophila Notch gene, which suggests that they are important for cell differentiation in mammals. This notion is supported by the previous finding of a truncated, translocated form of the human NOTCH1 gene (formerly TAN1) in three cases of leukemia. Given this genetic link between NOTCH1 and tumor formation, it is of interest to establish the chromosomal positions of the other two homologs. We report the identification of cosmid clones for the human NOTCH1, 2, and 3 genes. These clones were used as probes in fluorescence in situ hybridization to human metaphase chromosomes, and the results, combined with data from somatic cell hybrid panels, show that the NOTCH2 and 3 genes are located at positions 1p13-p11 and 19p13.2-p13.1, respectively, which are regions of neoplasia-associated translocation.
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PMID:The human NOTCH1, 2, and 3 genes are located at chromosome positions 9q34, 1p13-p11, and 19p13.2-p13.1 in regions of neoplasia-associated translocation. 769 46

Karyotype analysis of a case of acute megakaryoblastic leukaemia revealed an X;6 translocation as the sole abnormality. Using fluorescence in situ hybridisation on leukaemic metaphases we demonstrated that the breakpoint on the X-chromosome occurred at p11.21, within a region spanned by a YAC probe which has also been found to be disrupted in synovial sarcomas and some papillary renal cell carcinomas.
Leukemia 1995 Apr
PMID:A case of acute megakaryoblastic leukaemia with t(X;6)(p11.21;q23) having an X chromosome breakpoint within a 450-Kb region which is also disrupted in two classes of solid tumours. 772 9

The t(16;21)(p11;q22) translocation is an infrequent chromosomal abnormality, but seems specific to acute non-lymphocytic leukaemia (ANLL). We established two cell lines with t(16;21)(p11;q22) from the bone marrow of a patient with ANL in relapse. Their morphological, karyotypic, immunohistochemical and genetic features are examined. Although both cell lines show monocytoid features morphologically, they express only CD13 (My7) and CD34, and neither expressed monocytoid or lymphoid markers. Reverse transcription-polymerase chain reaction showed that both cell lines expressed a similar TLS-ERG chimaeric mRNA as a result of the t(16;21)(p11;q22) translocation. As far as we know, there is no report of a leukaemia cell line with t(16;21). These cell lines represent a useful tool for leukaemia research.
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PMID:Establishment and characterization of IRTA17 and IRTA21, two novel acute non-lymphocytic leukaemia cell lines with t(16;21) translocation. 779 65


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