At least four different chromosomal regions are involved in loss of heterozygosity in human breast carcinoma

Devilee, Peter; Broek, Martijn van den; Kuipers-Dukshoorn, Nel; Kolluri, Rukmini; Khan, P. Meera; Pearson, P. L.; Cornelisse, Cees J.

doi:10.1016/0888-7543(89)90023-2

Cited by 173 publications

(83 citation statements)

References 20 publications

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“…Up to two-thirds of tumours may show allelic imbalance at the YNZ22 locus at 17pl3.3 (Mackay et al, 1988;Devilee et al, 1989;Thompson et al, 1990;Chen et al, 1991;Singh et al, 1993;Thorlacius et al, 1993;Cornelis et al, 1994;Harada et al, 1994;Stack et al, 1995) and this finding has been associated with markers of tumour aggression Chen et al, 1991;Merlo et al, 1992;Harada et al, 1994;Ito et al, 1995).…”

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confidence: 99%

Allelic imbalance at chromosome 17p13.3 (YNZ22) in breast cancer is independent of p53 mutation or p53 overexpression and is associated with poor prognosis at medium-term follow-up

Thompson

Crichton²,

Elton³

et al. 1998

Br J Cancer

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Summary Molecular and immunohistochemical studies of genetic events on chromosome 17p were prospectively compared with conventional clinical and pathological parameters and disease behaviour at a minimum of 72 months follow-up. In a series of 91 patients with primary operable breast cancer, 37 out of 91 (41 %) patients had disease relapse and 23 out of 91 (25%) had died during the follow-up period. Allelic imbalance at the YNZ22 locus (1 7p1 3.3), demonstrated in 33 out of 63 (52%) informative patients, was significantly associated with disease recurrence (P < 0.01, 2 d.f. Cox analysis) and showed a trend towards impaired survival (P = 0.08, 2 d.f. Cox analysis) after a mean follow-up of 84 months for survivors. By contrast, p53 mutation (in 10 out of 60, 17% of cancers), p53 allelic imbalance (in 23 out of 56, 41% informative patients), p53 mRNA expression (in 47 out of 87, 54% patients), p53 mRNA overexpression (in 24 out of 87, 28%) or p53 protein expression (detected in 25/76, 32%) were not associated with disease behaviour. There was no significant association between allelic imbalance at YNZ22 and any abnormality of p53 DNA, RNA or protein. Allelic imbalance at 17p13.3 (YNZ22) serves as a marker of poor prognosis in breast cancer. As yet unidentified genes on 17p13.3, distinct from and telomeric to p53, are therefore likely to be of clinical importance in breast cancer.

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confidence: 99%

Allelic imbalance at chromosome 17p13.3 (YNZ22) in breast cancer is independent of p53 mutation or p53 overexpression and is associated with poor prognosis at medium-term follow-up

Thompson

Crichton²,

Elton³

et al. 1998

Br J Cancer

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“…Techniques using restriction fragment length polymorphisms (RFLP) and radiolabelled probes mapping to known regions of the human genome (Hayes, 1989) (Eccles, 1990;Russell, 1990), breast (MacKay, 1988;Devilee, 1989), and colon (Vogelstein, 1989).…”

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confidence: 99%

Overexpression of the p53 protein and allele loss at 17p13 in ovarian carcinoma

Eccles

Brett²,

Lessells³

et al. 1992

Br J Cancer

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Mouse monoclonal antibodies PAb 240 and PAb 1801 which specifically immunoprecipitate p53 protein, were used to examine 27 fresh ovarian tumours (16 serous adenocarcinomas, six endometrioid carcinomas, one mucinous adenocarcinoma, one mucinous borderline tumour and three benign adenomas). Eleven out of 16 (69%) serous adenocarcinomas and one endometrioid tumour showed positive staining with one or both antibodies and none of the mucinous or benign tumours stained with either antibody. DNA from tumour and peripheral blood leukocytes was used to identify allelic deletions on chromosome 17p in tumours. 11/12 positively staining tumours showed less of heterozygosity (LOH) on 17p at the nearest informative locus to the p53 gene. In this series of ovarian tumours, LOH on 17p correlates closely with the aberrant expression of the p53 protein in a high proportion of advanced stage serous adenocarcinomas. This observation suggests that the p53 tumour suppressor gene is involved in the evolution of epithelial ovarian cancer (EOC) and may have prognostic significance. Images Figure 2 Figure 3

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“…Deletions of 3p have been demonstrated in breast cancer by cytogenetic and LOH studies, indicating several regions (3p24-26, 3p21.3, and 3p13-14.3) involved in breast cancer (Chen et al, 1994;Devilee et al, 1989;Pandis et al, 1995;Pandis et al, 1993;Sato et al, 1991). LOH at 3p21.3 was initially shown in seven of the 17 informative cases of 28 primary tumors with the D3F15S2 (previously called DNF15S2) probe (Devilee et al, 1989).…”

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confidence: 99%

Cloning of a breast cancer homozygous deletion junction narrows the region of search for a 3p21.3 tumor suppressor gene

et al. 1998

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Chromosome 3p abnormalities and allele loss are frequent in lung and breast cancers, and several lung cancer cell lines exhibit homozygous deletions of 3p indicating potential sites of tumor suppressor genes at regions 3p21.3, 3p14.2 and 3p12. We have identi®ed and characterized a new 3p21.3 homozygous deletion in a breast cancer cell line and the primary tumor that overlaps those previously described in small cell lung cancer (SCLC). This homozygous deletion is approximately 220 kb in length and represents a somatically acquired change in the primary breast cancer. Cloning and sequencing of the breakpoint demonstrated that this resulted from an interstitial deletion and precisely pinpoints this deletion within the three SCLC homozygous deletions previously reported. This deletion signi®cantly narrows the minimum common deleted region to 120 kb and is distinct from the previously reported region that suppresses tumor formation of the murine A9 ®brosarcoma cells. These ®ndings suggest that a common homozygous deletion region on 3p21.3 is important in both lung and breast cancers. It is likely that this very well characterized region either contains one tumor suppressor gene common to both tumor types or two closely linked tumor suppressor genes speci®c for each tumor.

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At least four different chromosomal regions are involved in loss of heterozygosity in human breast carcinoma

Cited by 173 publications

References 20 publications

Allelic imbalance at chromosome 17p13.3 (YNZ22) in breast cancer is independent of p53 mutation or p53 overexpression and is associated with poor prognosis at medium-term follow-up

Allelic imbalance at chromosome 17p13.3 (YNZ22) in breast cancer is independent of p53 mutation or p53 overexpression and is associated with poor prognosis at medium-term follow-up

Overexpression of the p53 protein and allele loss at 17p13 in ovarian carcinoma

Cloning of a breast cancer homozygous deletion junction narrows the region of search for a 3p21.3 tumor suppressor gene

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