Characterization of chromosomal anomalies in human breast cancer

Dutrillaux, Bernard; Gerbault‐Seureau, Michèle; Zafrani, B

doi:10.1016/0165-4608(90)90143-x

Cited by 189 publications

(41 citation statements)

References 11 publications

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“…Indeed, abnormalities of this chromosome are also consistently observed in other cancers (Teyssier, 1989). Karyotyping of breast cancer cell lines has shown that the most frequent aberrations (Dutrillaux et al, 1990(Dutrillaux et al, , 1991. Loss of 16q was the sole abnormality detected by CGH in DCIS case 3325.…”

Section: Discussionmentioning

confidence: 84%

Comparative genomic hybridisation of ductal carcinoma in situ of the breast: identification of regions of DNA amplification and deletion in common with invasive breast carcinoma

et al. 1997

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Comparative genomic hybridisation has been used to map copy number changes in nine cases of ductal carcinoma in situ of the breast obtained from waxembedded archive material. A wide variety of abnormalities were detected including gain of regions of 1q, 17q, 19q, 20p and 20q and loss on 13q, 14q, 17p, 16q and 22q. Ampli®cation of areas on 10p, 8q and 20q were also observed. Chromosomal alterations were more frequent in higher grade DCIS and closely resemble those previously detected in invasive breast cancer using the same technique. These data provide strong molecular support for the view that DCIS is a precursor lesion of invasive breast carcinoma.

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Section: Discussionmentioning

confidence: 84%

Comparative genomic hybridisation of ductal carcinoma in situ of the breast: identification of regions of DNA amplification and deletion in common with invasive breast carcinoma

et al. 1997

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“…The human gene for S100A4 occurs in a cluster of S100 genes on chromosome 1 (Engelkamp et al, 1993), a region of the human genome which is often ampli®ed in breast cancer (Devilee et al, 1991;Dutrillaux et al, 1990;Gendler et al, 1990;Merlo et al, 1989;Micale et al, 1994;Pandis et al, 1992), and elevated levels of S100A4 mRNA have been associated with malignant, relative to benign, breast tumours (Lloyd et al, submitted). However, it is not yet known whether the human S100A4 gene has the same metastasis-inducing properties as its rodent counterparts , when it is overexpressed in non-metastatic epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

et al. 1998

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The rodent S100-related calcium-binding protein, S100A4 induces metastasis in non-metastatic rat and mouse benign mammary cells and co-operates with benign-tumour-inducing changes in two transgenic mouse models, to yield metastatic mammary tumours. Cotransfection of the human gene for S100A4 with pSV2neo into the benign rat mammary cell line, Rama 37, yielded cells which expressed a low level of the endogenous S100A4 mRNA, and either high or undetectable levels of human S100A4 mRNA. The cells which expressed a high level of human S100A4 mRNA induced metastasis in the benign rat mammary cell line Rama 37 in an in vivo assay, whereas the cells which expressed an undetectable level of human S100A4 did not induce any detectable metastases. The primary tumours arising from the S100A4-expressing cells contained high levels of immunocytochemically-detected S100A4 and this high level of S100A4 and the metastatic potential were maintained when cells from a metastasis were re-injected into syngeneic rats. The results show that the human S100A4 possesses metastasis-inducing capabilities.

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“…Generally one allele of the target gene is lost and the remaining allele contains a nonsense or missense mutation. The involvement of chromosome 6q in breast carcinomas has been noted in cytogenetic analysis of primary tumours (Dutrillaux et al, 1990;Lu et al, 1993;Thompson et al, 1993; Trent et al, 1985Trent et al, , 1993. Similarly, molecular analysis of primary breast tumour DNAs has shown that chromosome 6q is frequently affected by LOH (Devilee et al, 1991).…”

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confidence: 98%

“…Cytogenetic (Dutrillaux et al, 1990;Lu et al, 1993;Thompson et al, 1993;Trent et al, 1985Trent et al, , 1993 and molecular analyses (reviewed in Callahan et al, 1993) of primary human breast carcinomas have documented frequently occurring genetic alterations that take place during the evolution of tumour development. It is thought that these mutations either inactivate normal growth controls or give the tumour some selective advantage.…”

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Multiple regions of chromosome 6q affected by loss of heterozygosity in primary human breast carcinomas

Sheng

Marchetti²,

Buttitta³

et al. 1996

Br J Cancer

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Summary A total of 80 primary human breast carcinoma DNAs were analysed for loss of heterozygosity (LOH) on the long arm of chromosome 6, using microsatellite markers whose location has been defined physically and by linkage analysis. Loss of heterozygosity was observed in 38 of 80 (48%) tumours that were informative for at least one locus. The analysis revealed partial or interstitial deletions of chromosome 6q. Detailed mapping of chromosome 6q in these tumour DNAs identified two and perhaps three commonly deleted regions. One of these is located between markers D6S251 and D6S252 (6q14 -q16.2), another between D6S268 and D6S261 (6q 16.3 -q23) and a third between D6S287 and D6S270 (6q22.3 -q23. 1).Keywords: breast cancer; deletion; chromsome 6q; tumour-suppressor gene Cytogenetic (Dutrillaux et al., 1990;Lu et al., 1993;Thompson et al., 1993; Trent et al., 1985Trent et al., , 1993 and molecular analyses (reviewed in Callahan et al., 1993) of primary human breast carcinomas have documented frequently occurring genetic alterations that take place during the evolution of tumour development. It is thought that these mutations either inactivate normal growth controls or give the tumour some selective advantage. At the molecular level, loss of heterozygosity (LOH) is the most frequent type of genetic alteration in primary human breast tumours . LOH at specific chromosomal loci has been taken as evidence for the presence of putative tumour-suppressor genes within the affected regions (Knudson, 1989). In sporadic primary human breast carcinomas LOH has been detected on at least 12 different chromosome arms . However only in the case of chromosome l7pl3 has the target gene for LOH (TP53) been identified (Hollstein et al., 1991). Generally one allele of the target gene is lost and the remaining allele contains a nonsense or missense mutation. The involvement of chromosome 6q in breast carcinomas has been noted in cytogenetic analysis of primary tumours (Dutrillaux et al., 1990;Lu et al., 1993;Thompson et al., 1993; Trent et al., 1985Trent et al., , 1993. Similarly, molecular analysis of primary breast tumour DNAs has shown that chromosome 6q is frequently affected by LOH (Devilee et al., 1991). In this report, we describe studies aimed at defining the location of putative tumour-suppressor gene(s) on Table I. The PCR products were diluted with loading buffer (95% formamide, 20 mM EDTA, 0.05% bromophenol blue and 0.05% xylene cyanol), heat denatured and rapidly cooled. Samples were run in pairs (tumour and lymphocyte PCR product from the same patient) on a denaturing gel (7% acrylamide, 32% formamide, 6 M urea, 1 x TBE) at a constant 30-35 W. After electrophoresis the gel was transferred to 3MM Whatman paper and autoradiography performed with Kodak X-Omat AR film at -70'C. When the signal of an allele in tumour DNA was less than 50% of intensity observed in matching normal DNA from a heterozygous patient, LOH was considered to have occurred (Bieche et al., 1993). ResultsPreliminary results obtained at 6 loci (D6S254,...

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Characterization of chromosomal anomalies in human breast cancer

Cited by 189 publications

References 11 publications

Comparative genomic hybridisation of ductal carcinoma in situ of the breast: identification of regions of DNA amplification and deletion in common with invasive breast carcinoma

Comparative genomic hybridisation of ductal carcinoma in situ of the breast: identification of regions of DNA amplification and deletion in common with invasive breast carcinoma

Human S100A4 (p9Ka) induces the metastatic phenotype upon benign tumour cells

Multiple regions of chromosome 6q affected by loss of heterozygosity in primary human breast carcinomas

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