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

The United Kingdom Cancer Cytogenetics Group (UKCCG) collected retrospective data on 73 cases of acquired, single autosomal trisomies associated with haematological disorders, excluding trisomy 8 cases in myeloid conditions and trisomy 12 in lymphoid conditions. The bone marrow and/or blood smear morphology was reviewed in 49 cases. Trisomies for chromosomes 21, 11, 9 and 13 respectively were represented most frequently. Trisomy was not reported for chromosomes 1, 2, 5, 7, 16 or 17 and there was only one case of trisomy 8 in a non-myeloid condition and one case of trisomy 18. Of the 73 patients, 60 had myeloid disorders, 12 had lymphoid disorders and there was one case of acute undifferentiated leukaemia. There was no evidence of predisposing factors involved in the etiology of trisomy associated with haematological disorders.
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PMID:Primary, single, autosomal trisomies associated with haematological disorders. United Kingdom Cancer Cytogenetics Group (UKCCG). 140 15

Analysis of the chromosomal changes in various neoplasia is being increasingly carried out not only to evaluate its relationship with the prognosis and biological behaviour of the tumour but also for diagnostic purposes in some cases. Leukaemias are one such group of haematological malignancies which have been most extensively studied in this regard. Karyotypic analysis with Giemsa banding technique was carried out in 35 consecutive cases of Acute Lymphoblastic Leukaemia. Eighteen cases were in children (less than 15 years age) and 17 cases were in adults. M.F. ratio was 1.8:1 FAB classification of these cases showed 31 cases of L1 type and 4 cases of L2 type including one case of T-ALL. Fifteen cases (43%) had no karyotypic abnormality, 6 cases (17%) showed pseudodiploidy, one case each having (-20 + 21), t (9:22), (+ 2-6), (-6 + 8), while two cases had 6 q-.13 cases (37%) showed hyperdiploidy with 6 cases showing trisomy 8 alone, one case (+ 8 + 21), one case trisomy 18, one case + 15(r), one case trisomy 21 plus t (9:22) and one case with trisomy 21 only. Two cases showed more complex abnormalities i.e. + 2 + 8, t (13:22) and -11 + MR + Min + Min. There was one (3%) case of hypodiploidy showing monosomy 6. The above findings are in agreement with studies carried out in other countries except t (13:22) which is rather a scarcely reported abnormality.
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PMID:Chromosomal pattern in acute lymphoblastic leukaemia. 210 33

In the western part of the Netherlands during 1973-80 leukaemia was diagnosed in 293 patients aged under 15 years. An overall incidence rate of 2.91 per 100000 person years was calculated. No seasonal influence on months of birth or months of diagnosis of these patients could be traced by the method of Edwards. Time space clustering was looked for by both methods of Mantel and Knox. No significant time space clustering of date and place of diagnosis of childhood leukaemia was found in all types of leukaemia, acute lymphocytic leukaemia (ALL), ALL in boys and girls, ALL in children under 6 years at diagnosis, and in acute non-lymphocytic leukaemia.
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PMID:Time space distribution of childhood leukaemia in the Netherlands. 657 27

Chromosomes of 30 patients with adult T-cell leukemia were analyzed. Chromosome abnormalities were found in all the patients examined. The modal chromosome number of abnormal cells was hypodiploid in 2 patients, diploid in 14, and hyperdiploid in 9. The remaining 5 patients had bimodal chromosome numbers (diploid and hyperdiploid modes). Although all the patients showed various numerical or structural chromosome abnormalities, they also had common chromosome abnormalities. Aberrations of chromosome 1 were noted in 20 of the 30 patients, aberrations of chromosome 3 were seen in 20, trisomy 6 or 6q- was found in 17, aberrations of chromosome 10 were noted in 16, aberrations of the long arm of chromosome 14 were seen in 9, and trisomy 18 was seen in 7. There was no particular relationship between the difference in clinical symptoms and disparity in chromosome abnormalities.
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PMID:Chromosome abnormalities of leukemia cells in adult patients with T-cell leukemia. 661 41

Acute nonlymphocytic leukemia developed in a 57-year-old woman following adjuvant therapy with melphalan for ovarian carcinoma. Maturation of differentiating marrow myeloid and erythroid precursors was megaloblastic. The serum vitamin B12 level was low, and Schilling test revealed vitamin B12 malabsorption correctable with intrinsic factor. Megaloblastic maturation of the marrow cells was converted to normoblastic following treatment with vitamin B12 and folic acid. However, blast cells persisted in the marrow, and cytogenetic analysis revealed aneuploidy and trisomy 18. In contrast to the marrow blast cells, there was a decline in circulating blast cells following vitamin replacement, suggesting that these cells were capable of maturation but required vitamin B12 for this purpose.
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PMID:Unusual case of acute leukemia. Coexisting acute leukemia and pernicious anemia. 673 67

Female first cousins, aged 21 and 2 1/2 years, with many of the characteristic features of trisomy 18, were found to have identical unbalanced translocations, 46,XX,--13, + der(13)t(13;18) (p13;q12)mat. Clinical features of another cousin, two uncles, and an aunt suggested that they, too, had a partial trisomy 18 phenotype. The long survival and normal menstrual and secondary sexual development in one case are remarkable. A heritable balanced translocation, 46,XX or XY, t(13;18) (p13;q12), was detected in the mothers of the cases, a sib, an aunt, and two uncles. Translocation carriers had abnormalities in gonadal structure or function, with aspermia in males and polycystic ovaries with infertility in several females, suggesting that some gene controlling reproductive development occurs on the long arm of chromosome 18, with normal function interrupted at the breakpoint. Balanced translocation carriers may also be at greater risk for both benign and malignant neoplasms, which included acute leukaemia in an uncle and adenocarcinoma of the stomach at an early age in the grandmother. Although aetiological laboratory studies identified no premalignant state, the clinical findings suggest a defect that may predispose to cytogenetic abnormalities and malignancy.
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PMID:Clinical manifestations of familial 13;18 translocation. 721 77

The putative tumor suppressor gene deleted in colorectal carcinoma (DCC), located on human chromosome band 18q21, is deleted or inactivated in many solid tumors. Its role in the pathogenesis of non-Hodgkin's lymphoma (NHL) has not been studied. Recently, inactivation of this gene was reported in cases of leukemia with monosomy 18. As monosomy 18 is frequently observed in low-grade NHL, we investigated the incidence of altered DCC gene expression in patients with NHL, and correlated it with the number of copies of chromosome 18. Fifteen unselected cases of NHL were studied for evidence of DCC gene expression by reverse transcriptase-polymerase chain reaction. The results were correlated with Southern blot analysis of the DCC gene and with the number of copies of chromosome 18 determined by fluorescent in situ hybridization (FISH). The controls were tissues from normal colon mucosa and normal tonsils. Eight of 15 (53%) NHL cases lacked DCC mRNA, and one expressed substantially less than normal. Southern blot analysis showed normal configuration of the DCC gene in all samples. Two copies of chromosome 18 were found in 9 of 11 samples studied by FISH: one case had a subpopulation of cells with monosomy 18 and one had trisomy 18. All controls expressed DCC. We conclude that DCC gene expression is frequently absent or decreased in NHL and may be involved in the pathogenesis of NHL. Monosomy 18 was not required for DCC inactivation.
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PMID:Decreased expression of the deleted in colorectal carcinoma gene in non-Hodgkin's lymphoma. 774 42

In malignant non-Hodgkin lymphomas (NHL), cytogenetic analysis may provide prognostic information including prediction of histologic evolution and responsiveness to therapy. In this study, we correlate clinical data and chromosomal aberrations in 70 adult patients with newly diagnosed NHL followed for a median of 20 months. Clonal aberrations were detected in 68/70 patients (97%). Besides t(2;5)(p23;q35), observed exclusively in three patients with anaplastic large cell lymphoma, Ki-1 positive, none of the characteristic aberrations observed was specific for a given histological subtype. Aberrations of chromosome 7 (n = 21) occurred in all histological subtypes together with aberrations of chromosome 3 and of the short arm of chromosome 17. They were clinically associated with a high serum lactate dehydrogenase level (LDH) and a trend to short survival. Anomalies of the long arm of chromosome 13 (n = 10) were found in patients with high grade B-cell lymphomas and bulky disease. In t(14;18)(q32;q21) bearing lymphomas (n = 27), distinct patterns of additional aberrations were observed in low grade and high grade lymphomas: trisomy 3 and trisomy 18 occurred concomitantly in high grade lymphomas (n = 6, p < 0.001) as well as aberrations of 1q, 5q, 6q and +der (18)(q21). In conclusion, cytogenetic analysis provides information about the complexity of genetic changes in NHL. These changes act not only as indicators of disease activity, but influence clinical outcome as demonstrated by their stringent correlation to the International Index and might reveal more general rules of tumor growth and spreading.
Leukemia 1994 Nov
PMID:Karyotype and prognosis in non-Hodgkin lymphoma. 796 39

One can roughly divide disease cluster tests into area-based (using regional data) and point-based (using exact locations). We have compared the power of two area-based methods (Moran's I and I* (pop), a new method) to that of two point-based methods (the Cuzick-Edwards test and Grimson's test), using three realistic simulations of disease (fox rabies in England, childhood leukaemia in North Humberside, England, and Lyme disease in Georgia). The naive belief that point-based methods should be better is not supported: for the complex data simulated here, I* (pop) and the Cuzick-Edwards test had higher power than Grimson's method or Moran's I. I* (pop) capitalizes on high inter-region variability, while Moran's I cannot.
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PMID:Realistic power simulations compare point- and area-based disease cluster tests. 913 5

Marginal zone B cell lymphoma (MZBCL) represents a distinct subtype of B cell non-Hodgkin's lymphoma, which has been recently recognized and defined as a disease entity. We investigated 25 cases (18 at primary diagnosis and seven during the course of disease) of MZBCL by comparative genomic hybridization (CGH) and compared these results with cytogenetic, fluorescence in situ hybridization (FISH), and Southern blot data. Twenty of the 25 cases (80%) showed gains (total 49) or losses (total 15) of genetic material. In extranodal, nodal, and splenic MZBCL, material of chromosomes 3 (52% of cases), 18 (32%), X (24%), and 1q (16%) was most frequently gained, whereas losses predominantly involved chromosomes 17 (16%) and 9 (12%). High-level amplifications involving the regions 18q21-23 and 18q21-22, respectively, were detected in two cases. Gains of chromosomes 1q and 8q and losses of chromosome 17 or 17p occurred more frequently in relapsed or progressive lymphomas. For all of the frequently affected chromosomes, CGH allowed narrowing of the relevant subregions including 3q21-23, 3q25-29 and 18q21-23. By Southern blot analysis, the BCL2, BCL6, and CMYC proto-oncogenes were found to be a part of the over-represented regions in two cases, one case, and two cases, respectively, with gains involving 18q, 3q or 8q. In 13 cases, CGH revealed chromosomal imbalances which were not detected by cytogenetic analysis but could be confirmed by FISH or Southern blot analysis in all cases investigated. On the other hand, CGH failed to detect trisomy 3, trisomy 18, and deletion 7q in three cases with a low proportion of tumor cells bearing these abnormalities, as shown by interphase FISH. The characteristic pattern of chromosomal gains and losses detected in this study confirms the distinct nature of MZBCL and may point to chromosomal regions involved in the pathogenesis of these neoplasms.
Leukemia 1997 May
PMID:Characteristic pattern of chromosomal gains and losses in marginal zone B cell lymphoma detected by comparative genomic hybridization. 918 Mar 2


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