Neu (C-erbB-2) Oncogene in Breast Cancer and its Possible Association with the Risk of Distant Metastases a Retrospective Study and Review of Literature

Ap, Makar; Ej, Desmedt; Cr, De Potter; Js, Vanderheyden; Ea, Schatteman

doi:10.3109/02841869009096392

Cited by 21 publications

(13 citation statements)

References 18 publications

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“…These results confirm those obtained from studies where an association between age of breast cancer patients and their tumour over expression of Her-2 was found [12][13][14][15]. Other studies, however, did not find any significant association between the former and the latter [16,17]. We also found that there is a significant association between the nature of the tumours' expression of ER and the age of the patients.…”

Section: Discussionsupporting

confidence: 82%

Pathobiological features of breast tumours in the State of Kuwait: a comprehensive analysis

Saleh¹,

Abdeen²

2008

European Journal of Cancer Supplements

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Section: Discussionsupporting

confidence: 82%

Pathobiological features of breast tumours in the State of Kuwait: a comprehensive analysis

Saleh¹,

Abdeen²

2008

European Journal of Cancer Supplements

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“…Over-expression of ErbB2, in particular, has been associated with a poor prognosis in breast carcinomas (Slamon et al, 1987) and is a possible indicator for the risk of distant metastases (Makar et al, 1990). Overexpression of the activated form of this receptor when driven by the MMTV promoter in mice leads to rapid induction of mammary gland tumors (Muller et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

The oncogene heregulin induces apoptosis in breast epithelial cells and tumors

1998

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The products of a growing number of genes have been shown to display seemingly contradictory functions; namely, the induction of tumorigenesis and the induction of apoptosis. Heregulin's involvement in oncogenesis occurs through its interactions with members of the EGF receptor tyrosine kinase family. Recently one isoform of heregulin, b2b, was isolated in an in vitro screen for dominant, apoptosis-inducing genes in kidney epithelial cells. Here we show that heregulin is also capable of mediating apoptosis in human and murine mammary tumor cell lines and murine tumors. Furthermore, through transfection of the human breast cancer cell line MCF-7 with the truncated transmembrane/cytoplasmic segment of the heregulin gene, we show that the intracellular region of the heregulin precursor is sucient for induction of apoptosis. Through the use of DNA fragmentation assays we also show that apoptosis occurs in cell lines established from heregulin-induced mammary gland tumors. TdT addition of digoxigenin labeled nucleotides to 3' OH ends of DNA breaks recapitulated these results in the actual tumors. Finally, over-expression of heregulin is shown to lead to the down-regulation of Bcl-2, an inhibitor of apoptosis. Conversely, the transfection of Bcl-2 into MCF-7 cells inhibits heregulin-mediated programmed cell death.

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“…It is a process that requires a tumor cell to leave its primary site, pass through the blood stream, then invade and break through basement membrane barriers at the secondary site. ERBB2 (HER2 and Neu), which is a member of the ERBB family of receptor tyrosine kinases, is amplified or overexpressed in ;25% of breast cancer patients, where it correlates with poor prognosis and high invasiveness (Slamon et al 1989;Makar et al 1990;Tiwari et al 1992). To date, there is very limited understanding of the roles of PTPs in the regulation of ERBB2 signaling.…”

mentioning

confidence: 99%

Identification of PTPN23 as a novel regulator of cell invasion in mammary epithelial cells from a loss-of-function screen of the ‘PTP-ome'

Lin¹,

Aranda²,

Muthuswamy³

et al. 2011

Genes Dev.

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We used an RNAi-mediated loss-of-function screen to study systematically the role of the protein tyrosine phosphatase (PTP) superfamily of enzymes in mammary epithelial cell motility in the absence or presence of the oncoprotein tyrosine kinase ERBB2. We report that although shRNAs directed against most of the PTP family were without effect, suppression of three PTPs-PRPN23, PTPRG, and PTPRR-enhanced cell motility. Furthermore, we found that suppression of PTPN23, but not PTPRG or PTPRR, induced cell invasion. Suppression of PTPN23 increased E-cadherin internalization, impaired early endosome trafficking of E-cadherin, induced the expression of mesenchymal proteins, and caused cell scattering. The activity of SRC and b-catenin was elevated when PTPN23 was suppressed. Moreover, we identified SRC, E-cadherin, and b-catenin as direct substrates of PTPN23. Inhibition of SRC with the small molecular inhibitor SU6656 blocked the effects of PTPN23 depletion. These findings suggest that loss of PTPN23 may increase the activity of SRC and the phosphorylation status of the E-cadherin/b-catenin signaling complex to promote tumor growth and invasive behavior in breast cancer. In addition, our studies highlight functional specificity among PTPs and reveal new roles for PTPs in mammary epithelial cell biology.

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Neu (C-erbB-2) Oncogene in Breast Cancer and its Possible Association with the Risk of Distant Metastases a Retrospective Study and Review of Literature

Cited by 21 publications

References 18 publications

Pathobiological features of breast tumours in the State of Kuwait: a comprehensive analysis

Pathobiological features of breast tumours in the State of Kuwait: a comprehensive analysis

The oncogene heregulin induces apoptosis in breast epithelial cells and tumors

Identification of PTPN23 as a novel regulator of cell invasion in mammary epithelial cells from a loss-of-function screen of the ‘PTP-ome'

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