Loss of heterozygosity at D3S2 locus of short arm of chromosome 3 in chronic myelogenous leukemia

Tanaka, Kimio; Mansoor, Ahmed; Shigeta, Chiharu; Nobuo,; Oguma,; Kamada, Nanao

doi:10.1016/0165-4608(92)90368-i

Cited by 8 publications

(3 citation statements)

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“…LOH at chromosomes 8q22 and 11q23 have frequently been seen in acute myeloid leukaemia (AML) (Pabst et al, 1996). Though deletion of the short arm of chromosome 3 is rare in leukaemia, region 3p14-p21 is prone to gene rearrangements (Smith et al, 1993;Tanaka et al, 1992). Recently, the FHIT gene has been cloned and characterized.…”

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“…In malignancies a loss of heterozygosity (LOH) of genomic sequences which accompanies the inactivation of tumour suppressor genes have been noted, and this is thought to be involved in a multistep accumulation of gene alterations crucial to leukaemogenesis (Rabbitts, 1994;Cline, 1994;Yokota & Sugimura, 1993). Loss of the short arm of chromosome 3 has been noted in many solid and haematological malignancies, most notably small cell lung carcinoma (SCLC) (Naylor et al, 1987;Brauch et al, 1990), non-small-cell lung carcinoma Miura et al, 1990), renal cell carcinoma Kovacs et al, 1988;Kovacs & Kung, 1991), breast carcinoma (Ali et al, 1989;Devilee et al, 1989), cervical carcinoma (Yokota et al, 1989) and chronic myeloid leukaemia (Tanaka et al, 1992). The putative tumour suppressor genes are thought to be most probably located in the 3p11-p21 region , the 3p21-p25 region and the 3p25 region (Seizinger et al, 1988).…”

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Aberrant FHIT transcripts in acute myeloid leukaemia

et al. 1997

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Summary.Recently the FHIT gene (fragile histidine triad gene) has been identified at chromosome 3p14.2 and a high frequency of abnormalities in this gene has been demonstrated in various cancers. To determine the role of the FHIT gene in leukaemia, bone marrow or peripheral blood from 62 acute myeloid leukaemia patients and five haemopoietic cell lines (HL60, U937, Raji, KG-1, K562) were analysed by reverse transcription of the FHIT mRNA followed by PCR amplification and sequencing of the products. To detect the deletion of the FHIT gene, 17 cases were evaluated using microsatellite polymorphism analysis. In this study, 17/62 (27%) AML patients expressed aberrant transcripts which lack two or more exons of the FHIT gene, and all the cell lines exhibited the aberrant FHIT transcripts. No cases exhibited a loss of the FHIT alleles. Our data indicated that the FHIT gene may play a role in myeloid carcinogenesis and may be indicated in the late progression of the disease.

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Aberrant FHIT transcripts in acute myeloid leukaemia

et al. 1997

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“…Tumor promoters are not themselves carcinogenic, but may promote tumors in systems already exposed to carcinogens. 13–15 Homologous mitotic recombination, the exchange of genetic material between homologous chromosomes, is an essential mechanism for faithful DNA replication in vertebrate cells and is an important repair pathway of DNA double-strand breaks. This recombinational repair, however, may result in the loss of the functional allele ( s+ ) in a heterozygous cell of a defective tumor suppressor gene ( s+ / s ).…”

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Mitotic recombination: a genotoxic effect of the antidepressant citalopram in Aspergillus nidulans

Franco

Castro-Prado

Rosada

et al. 2010

Exp Biol Med (Maywood)

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This report evaluates the potential of the antidepressant drug citalopram to induce homozygotization of genes previously present in a heterozygous condition, by homologous recombination. In order to address this question, a heterozygous diploid strain of the filamentous fungus Aspergillus nidulans and the homozygotization assay were utilized. Non-cytotoxic concentrations of citalopram (50, 75 and 100 μmol/L) showed a strong recombinogenic effect in A. nidulans, inducing homozygosis of the diploid strain's nutritional markers. The genetic markers exhibited homozygotization index (HI) rates higher than 2.0 and significantly different from HI control ones. Since citalopram has been previously characterized as a DNA synthesis inhibitor, the recombinogenic potential of this antidepressant in A. nidulans may be associated with the recombinational repair of citalopram-induced DNA strand breaks.

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