Expression of Bcl‐2 in human breast cancer: Correlation between hormone receptor status, p53 protein accumulation and DNA strand breaks associated with apoptosis

Hori, Masao; Nogami, Tatsuya; Itabashi, Michio; Yoshimi, Fuyo; Ono, Hisayuki; Koizumi, Sanae

doi:10.1111/j.1440-1827.1997.tb04453.x

Cited by 26 publications

(22 citation statements)

References 16 publications

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“…Apoptotic index and Ki67 also correlated positively with high pathological grade. Apoptotic index has been previously shown to be associated with p53 overexpression, but inversely with bcl-2 and ER (Lipponen et al, 1994;Hori et al, 1997;Rochaix et al, 1999). A high proliferation rate in breast tumours is associated with a poorer prognosis (Meyer and Lee, 1980;Silvestrini et al, 1985) as is p53 expression (Silvestrini et al, 1993), whereas ER overexpression is associated with a more favourable prognosis (EBCTCG, 1998b).…”

Section: Discussionmentioning

confidence: 99%

Early changes in apoptosis and proliferation following primary chemotherapy for breast cancer

et al. 2003

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Patients undergoing primary chemotherapy for invasive breast cancer consented to a core biopsy of the invasive breast primary preand 24 h postchemotherapy. The resulting tissue was analysed for apoptosis, Ki67, ER and HER-2 using immunohistochemical techniques. These data were then used to evaluate the relationship between these biological markers and response to chemotherapy and overall survival. Response rate to chemotherapy in this group was 86%, 16 patients (25%) achieved a clinical complete response and 41 (63%) a partial response. Prechemotherapy there was a significant correlation between Ki67 and apoptotic index (AI), r ¼ 0.6, (Po0.001). A significant rise in AI (Po0.001), and fall in Ki67 (P ¼ 0.002) was seen 24 h following chemotherapy. No relationship was seen between pretreatment AI and clinical response, but higher Ki67 and growth index (Ki67/AI ratio, GI) did correlate with clinical response (both r ¼ 0.31, Po0.025). No correlation was seen between the change in AI or Ki67 at 24 h and clinical response or survival. Significant changes in apoptosis and proliferation can be demonstrated 24 h following chemotherapy, but these changes do not relate to clinical response or outcome in this study. Pretreatment proliferation and GI are however predictive of response to chemotherapy in breast cancer.

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Section: Discussionmentioning

confidence: 99%

Early changes in apoptosis and proliferation following primary chemotherapy for breast cancer

et al. 2003

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“…Immunohistochemical studies on human cancer tissues had demonstrated a significant inverse relationship between Bcl-2 and p53 protein expression in non-small-cell lung cancers, 31,32 follicular lymphomas, 33 gastric carcinomas, 34 esophageal squamous cancers, 35 non-melanoma skin cancers, 36 and breast carcinomas. 37,38 In prostatic carcinomas 39 and colorectal adenomas and carcinomas, 40 the expressions of Bcl-2 and p53 proteins in the same tissue section were almost reciprocal. It appeared that alteration of both Bcl-2 and p53 proteins may be involved in a common genetic pathway that is shared by a number of different human cancers.…”

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confidence: 99%

Bcl-2 and p53 Protein Expression, Apoptosis, and p53 Mutation in Human Epithelial Ovarian Cancers

Chan

Cheung

Schorge

et al. 2000

The American Journal of Pathology

156

110

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Bcl-2 and p53 gene products have been both linked to cell death by apoptosis. In the present study, we examined the relationship of Bcl-2 and p53 protein expression, p53 mutation and apoptosis in normal human ovaries and different types of human ovarian epithelial tumors by immunohistochemical localization, in situ terminal transferase-mediated dUTP nick end labeling and polymerase chain reaction-single strand conformation polymorphism. It was found that Bcl-2 expressed strongly in the surface epithelium of normal ovaries and benign and borderline ovarian tumors but weakly in the malignant tumors. On the contrary, strong protein expression of p53 was found in 54% (25/46) of the malignant epithelial tumors examined but similar expression of p53 was not observed in borderline and benign tumors and normal ovarian surface epithelium. A significant inverse correlation between Bcl-2 and p53 expression was found in the malignant ovarian tumors examined. p53 gene mutation at exons 5-11 was however not a pre-requisite for p53 expression in both borderline and malignant tumors.

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“…6 The expression of this oncoprotein in breast cancers seems to be related to poor prognosis associated with a high histological grade, epidermal growth factor receptor (EGFR) positivity, and bcl-2 and oestrogen receptor (ER) negativity. [7][8][9][10][11][12][13][14][15][16] However, it should be noted that clinical pathological studies also report the coexpression of cytokeratin (CK) and vimentin in breast cancer as a more aggressive phenotype associated with poor prognosis. 17 18 This particular phenotype has been detected in a subset of normal breast epithelial cells that grows out of mammoplasty cultures, after most of the early passage cells have senesced.…”

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confidence: 99%

p53 mutation in breast cancer. Correlation with cell kinetics and cell of origin

Megha

Ferrari²,

Benvenuto³

et al. 2002

Journal of Clinical Pathology

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Aim: Several studies have investigated the expression of the cytokeratins (CKs), vimentin, the epithelial growth factor receptor (EGFR), the oestrogen receptor (ER), and the progesterone receptor (PgR), in breast cancer, but no study has directly compared p53 mutations with these phenotypic and differentiation markers in the same case. The present study was designed to provide some of this information. Methods: The expression of the p53 and bcl-2 proteins was evaluated by immunohistochemistry in relation to phenotypic characteristics and cellular kinetic parameters (mitotic index and apoptotic index) in 37 cases of ductal carcinoma in situ (DCIS) and 27 cases of infiltrating ductal carcinoma (IDC) of the breast. In addition, p53 gene mutation was examined by polymerase chain reaction single strand conformation polymorphism analysis (SSCP). Results: Thirteen cases (eight DCIS and five IDC) showed expression of CK8, CK14, CK18, vimentin, and EGFR, consistent with a stem cell phenotype, whereas 44 cases (27 DCIS and 17 IDC) showed expression of CK8 and CK1, weak or negative expression of CK18, but were negative for vimentin and EGFR, consistent with a luminal cell phenotype. DCIS and IDC cases with a stem cell phenotype were ER/PgR negative and intermediately or poorly differentiated. In contrast, the cases with luminal cell phenotype were ER/PgR positive and well or intermediately differentiated. In addition, intermediately or poorly differentiated cases with a stem cell phenotype showed higher proliferative activity (per cent of MIB-l positive cells) than did intermediately or well differentiated cases with a luminal cell phenotype. Both DCIS and IDC cases with a stem cell phenotype were p53 positive and bcl-2 negative by immunohistochemistry. In IDC, p53 expression was associated with a reduction of both mitotic index and apoptotic index compared with DCIS. Most of the tumours showing a more differentiated phenotype (luminal) were p53 negative and bcl-2 positive. In these cases, cell kinetic parameters increased from DCIS to IDC. These data suggest the existence of subsets of DCIS and IDC that, because of their phenotypic characteristics, could be derived from subpopulations of normal breast cells having different control mechanisms of cell proliferation and neoplastic progression. Conclusions: These results are compatible with the hypothesis that the phenotype of the cell of origin constrains both tumour phenotype and the choice of genetic events; however, the occurrence of p53 mutants by chance during neoplastic transformation cannot be excluded.

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Expression of Bcl‐2 in human breast cancer: Correlation between hormone receptor status, p53 protein accumulation and DNA strand breaks associated with apoptosis

Cited by 26 publications

References 16 publications

Early changes in apoptosis and proliferation following primary chemotherapy for breast cancer

Early changes in apoptosis and proliferation following primary chemotherapy for breast cancer

Bcl-2 and p53 Protein Expression, Apoptosis, and p53 Mutation in Human Epithelial Ovarian Cancers

p53 mutation in breast cancer. Correlation with cell kinetics and cell of origin

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