Association of genetic alterations on chromosome 17 and loss of hormone receptors in breast cancer

Ito, Isao; Yoshimoto, Masataka; Iwase, Takuji; Watanabe, Satoshi; Katagiri, Toyomasa; Harada, Yousuke; Kasumi, Fujio; Yasuda, Shigeru; Mitomi, T; Emi, Mitsuru

doi:10.1038/bjc.1995.89

Cited by 44 publications

(36 citation statements)

References 16 publications

(6 reference statements)

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“…British Journal of Cancer (1998) 77(5) YNZ22 allelic imbalance reported in this study (52%) lies within the range (37-65%) previously published by other groups (Chen et al, 1991;Singh et al, 1993;Thorlacius et al, 1993;Comelis et al, 1994;Harada et al, 1994;Ito et al, 1995;Stack et al, 1995). The proportion of cancers with p53 mutation (20%), p53 allele loss (41%), p53 mRNA expression (54%) and overexpression (28%) or p53 protein expression (32%) are similar to the reported series (Cattoretti et al, 1988;Davidoff, 1991;Iwaya, 1991;Kovach et al, 1991;Osborne et al, 1991;Runnebaum et al, 1991;Varley et al, 1991;Vojtesek et al, 1992;Andersen et al, 1993;Barnes, 1993;Friedrichs, 1993;Martinazzi, 1993;Thorlacius et al, 1993;Tsuda et al, 1993;Marks et al, 1994;Bergh et al, 1995;Borressen et al, 1995;Stenmark-Askmalm et al, 1995).…”

Section: Discussionsupporting

confidence: 86%

“…Thus, the associations between YNZ22 allelic imbalance and a high proliferation index (Chen et al, 1991;Merlo et al, 1992), DNA aneuploidy (Chen et al, 1991), with absence of progesterone receptor expression (Ito et al, 1995), low oestrogen receptor expression and the presence of axillary lymph node metastasis at the time of diagnosis (Takhita et al, 1992;Harada et al, 1994) have now been supported in this study by prospective patient follow-up beyond 6 years. In addition to the evidence presented here of a gene or genes from 17pl3.3 associated with disease recurrence and poor prognosis in breast cancer, this gene(s) is also implicated in neoplastic proliferation even at the early stages of breast carcinogenesis, including atypical ductal hyperplasia (Lakhani et al, 1995) and ductal carcinoma in situ (Radford et al, 1993;Harada et al, 1994;Munn et al, 1996).…”

Section: Discussionsupporting

confidence: 63%

“…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).…”

mentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 86%

Section: Discussionsupporting

confidence: 63%

mentioning

confidence: 99%

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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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“…Expression of ER is often linked to progression of breast cancers from a hormone-dependent, nonmetastatic, antiestrogen-sensitive phenotype to a hormone-independent, antiestrogen-and chemotherapy-resistant phenotype with invasive and metastatic properties (Ito et al, 1995). One of the characteristics of the ER negative invasive breast cancer cells is constitutive high levels of NFkB activity.…”

Section: Expression Of Estrogen Receptor (Er) or Progesterone Receptomentioning

confidence: 99%

Overexpression of the Tpl-2/Cot oncogene in human breast cancer

1999

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“…[1][2][3] Many tumor suppressor genes are inactivated by intragenic mutations in one allele accompanied by the loss of a chromosomal region containing the other allele, termed loss of heterozygosity (LOH). In primary breast cancers frequent LOH in many chromosome arms, including 1p, 3p, 6q, 13q, 16q, 17, 18q, and 22q, [4][5][6][7][8][9][10][11][12][13][14][15][16][17] suggests that many putative tumor suppressor genes may influence the development and/or progression of breast cancer.…”

mentioning

confidence: 99%

Frequent Allelic Loss at 7p14‐15 Associated with Aggressive Histologic Types of Breast Cancer

Kurose

Iida

Araki

et al. 1998

Japanese Journal of Cancer Research

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We examined 142 primary human breast cancers to determine their patterns of loss of heterozygosity (LOH) at 19 microsatellite markers over the entire length of chromosome 7. Allelic loss at one or more loci on the short arm of chromosome 7 was observed in 37 of the tumors (26%). We found a new target region of allelic loss on 7p between D7S1802 and D7S817 at 7p14-15. LOH on 7p was found more frequently in tumors of the invasive solid tubular and scirrhous type (31 of 87; 36%) than in other less aggressive types (2 of 27; 7%) (P= = = =0.0047). The results suggest that inactivation of putative tumor suppressor gene(s) located at 7p14-15 may play a role in the development and/or progression of primary breast cancers, particularly those of the invasive solid tubular and scirrhous type. Allelic loss was also found in 56 of 142 tumors on the long arm, and a commonly deleted region was defined between D7S522 and D7S1801 at 7q31. Key words: Breast cancer -Loss of heterozygosity -Tumor suppressor gene -Chromosome 7Breast cancer is the most common malignancy in women. One in nine Caucasian women and one in 40-50 Japanese women will develop breast cancer in their lifetimes, and the incidence has been increasing worldwide. Human solid tumors are now believed to develop through a multistep process involving activation of oncogenes and inactivation of tumor suppressor genes.

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Association of genetic alterations on chromosome 17 and loss of hormone receptors in breast cancer

Cited by 44 publications

References 16 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 Tpl-2/Cot oncogene in human breast cancer

Frequent Allelic Loss at 7p14‐15 Associated with Aggressive Histologic Types of Breast Cancer

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