De novo amplification within a "silent" human cholinesterase gene in a family subjected to prolonged exposure to organophosphorous insecticides.

Prody, Catherine A.; Dreyfus, Patrick A.; Zamir, R.; Zakut, Haim; Soreq, Hermona

doi:10.1073/pnas.86.2.690

Cited by 69 publications

(30 citation statements)

References 25 publications

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“…cently cloned human ACHEcDNA (1) and CHEcDNA (2), we found that the CHE gene is capable of being heritably amplified in humans (8). Further analysis revealed the occurrence of coamplified ACHEDNA and CHEDNA sequences in genomic DNA from peripheral blood cells of leukemic patients (9).…”

Section: Introductionmentioning

confidence: 90%

“…32P and 35S-labeled cDNA and plasmid probes were labeled by the multi-prime labeling method (Boehringer Mannheim Biochemicals, Indianapolis, IN) to specific activities of 1-5 X 10 9 dpm/gg DNA using enzymatically restricted and gel electroeluted DNA fragments (2,8). DNA (9) and RNA (2) blot hybridizations were performed as previously described, and washes were at 65°C at low ionic strength (0.…”

Section: Methodsmentioning

confidence: 99%

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Acetylcholinesterase and butyrylcholinesterase genes coamplify in primary ovarian carcinomas.

Zakut

Ehrlich²,

Ayalon³

et al. 1990

J. Clin. Invest.

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The genes for acetylcholinesterase (ACHE) and butyrylcholinesterase (CHE) are expressed in multiple tumor tissues, including ovarian carcinomas. Both CHE and ACHE genes coamplify in leukemias. To examine the relationship of gene amplification to the expression of these genes in tumors, ACHE and CHE genes and their expression were studied in primary ovarian carcinomas. DNA blot hybridization demonstrated a significant amplification and mutagenesis of both genes in 6 of 11 malignant tumors studied. This was greater or of the same order of magnitude as the amplification of the oncogenes c-rafi, v-sis, and c-fes in these tumors. No amplification was found in normal ovarian tissues or benign ovarian cysts. Xenopus oocyte microinjections, blot and in situ hybridizations, and immuno-and cytochemical staining revealed translatable CHEmRNA and its active protein product in discrete tumor foci. The frequent coamplification in ovarian carcinomas of ACHE and CHE genes implicates cholinesterases in neoplastic growth and/or proliferation. (J. Clin. Invest. 1990. 86:900-908.)

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Section: Introductionmentioning

confidence: 90%

Section: Methodsmentioning

confidence: 99%

Acetylcholinesterase and butyrylcholinesterase genes coamplify in primary ovarian carcinomas.

Zakut

Ehrlich²,

Ayalon³

et al. 1990

J. Clin. Invest.

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“…Yet another possibility is that of the insertion of a retroviral sequence, followed by the extension of its amplification into the chromosomal region of the ChoEase genes. The amplification of the CHE gene on chromosome 3 that we recently found in a family exposed to chronic doses of parathion, a potent ChoEase inhibitor (19), could be an example for the first option. It should be noted, however, that in that particular family the CHE gene was the only one to be amplified (H.S., C.A.P., and H.Z., unpublished observation).…”

Section: Methodsmentioning

confidence: 99%

Coamplification of human acetylcholinesterase and butyrylcholinesterase genes in blood cells: correlation with various leukemias and abnormal megakaryocytopoiesis.

Lapidot-Lifson

Prody

Ginzberg

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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To study the yet unknown role of the ubiquitous family of cholinesterases (ChoEases) in developing blood cells, the recently isolated cDNAs encoding human acetyicholinesterase (AcChoEase; acetylcholine acetyihydrolase, EC 3.1.1.7) and butyrylcholinesterase (BtChoEase; cholinesterase; acylcholine acylhydrolase, EC 3.1.1.8) were used in blot hybridization with peripheral blood DNA from various leukemic patients. Hybridization signals (10-to 200-fold intensifled) and modified restriction patterns were observed with both cDNA probes in 4 of the 16 leukemia DNA preparations examined. These reflected the amplification of the corresponding AcChoEase and BtChoEase genes (ACHE and CHE) and alteration in their structure. Parallel analysis of 30 control samples revealed nonpolymorphic, much weaker hybridization signals for each of the probes. In view of previous reports on the effect of acetylcholine analogs and ChoEase inhibitors in the induction of megakaryocytopoiesis and production of platelets in the mouse, we further searched for such phenomena in nonleukemic patients with platelet production disorders. Amplifications of both ACHE and CHE genes were found in 2 of the 4 patients so far examined. Pronounced coamplification of these two related but distinct genes in correlation with pathological production of blood cells suggests a functional role for members of the ChoEase family in megakaryocytopoiesis and raises the question whether the coamplification of these genes could be causally involved in the etiology of hemocytopoietic disorders.

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“…In addition, the amplification of oncogenes occurs at a very high frequency in human malignancies and is usually correlated with the more progressive stages of the particular disease {Bishop 1987; Hamlin et al 1991). With very rare exceptions (see Prody et al 1989), DNA sequence amplification has not been observed in normal, non-neoplastic cells (Sager et al 1985;Otto et al 1989;Tlsty 1990;Wright et al 1990). …”

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Sister chromatid fusion initiates amplification of the dihydrofolate reductase gene in Chinese hamster cells.

Ma¹,

Martin²,

Trask³

et al. 1993

Genes Dev.

185

103

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We have utilized a dihydrofolate reductase (DHFR) probe in combination with selected probes from other positions along the 2q chromosome arm in a two-color fluorescence in situ hybridization analysis of early DHFR gene amplification events in CHO cells. These studies show clearly that the most frequent initiating event is the formation of a giant inverted duplication, resulting either from chromosome breakage and terminal fusion or a reverse unequal sister chromatid exchange. The dicentric chromosomes thus formed initiate bridge/breakage/fusion cycles that appear to mediate subsequent amplification steps to higher copy number.

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De novo amplification within a "silent" human cholinesterase gene in a family subjected to prolonged exposure to organophosphorous insecticides.

Abstract: A 100-fold DNA amplification in the CHE gene, coding for serum butyryicholinesterase (BtChoEase), was found in a farmer expressing the "silent" CHE phenotype.

Cited by 69 publications

References 25 publications

Acetylcholinesterase and butyrylcholinesterase genes coamplify in primary ovarian carcinomas.

Acetylcholinesterase and butyrylcholinesterase genes coamplify in primary ovarian carcinomas.

Coamplification of human acetylcholinesterase and butyrylcholinesterase genes in blood cells: correlation with various leukemias and abnormal megakaryocytopoiesis.

Sister chromatid fusion initiates amplification of the dihydrofolate reductase gene in Chinese hamster cells.

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