Literature DB >> 22968923

Higher cytoplasmic and nuclear poly(ADP-ribose) polymerase expression in familial than in sporadic breast cancer.

Marie-Luise Klauke1, Nicoline Hoogerbrugge, Jan Budczies, Peter Bult, Judith Prinzler, Cornelia Radke, J Han J M van Krieken, Manfred Dietel, Carsten Denkert, Berit Maria Müller.   

Abstract

Poly(ADP-ribose) polymerase 1 (PARP) is a key element of the single-base excision pathway for repair of DNA single-strand breaks. To compare the cytoplasmic and nuclear poly(ADP-ribose) expression between familial (BRCA1, BRCA2, or non BRCA1/2) and sporadic breast cancer, we investigated 39 sporadic and 39 familial breast cancer cases. The two groups were matched for hormone receptor status and human epidermal growth factor receptor 2 status. Additionally, they were matched by grading with a maximum difference of ±1 degree (e.g., G2 instead of G3). Cytoplasmic PARP (cPARP) expression was significantly higher in familial compared to sporadic breast cancer (P = 0.008, chi-squared test for trends) and a high nuclear PARP expression (nPARP) was significantly more frequently observed in familial breast cancer (64 %) compared with sporadic breast cancer (36 %) (P = 0.005, chi-squared test). The overall PARP expression was significantly higher in familial breast cancer (P = 0.042, chi-squared test). In familial breast cancer, a combination of high cPARP and high nPARP expression is the most common (33 %), whereas in sporadic breast cancer, a combination of low cPARP and intermediate nPARP expression is the most common (39 %). Our results show that the overall PARP expression in familial breast cancer is higher than in sporadic breast cancer which might suggest they might respond better to treatment with PARP inhibitors.

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Year:  2012        PMID: 22968923     DOI: 10.1007/s00428-012-1311-2

Source DB:  PubMed          Journal:  Virchows Arch        ISSN: 0945-6317            Impact factor:   4.064


  28 in total

1.  Cytoplasmic poly(adenosine diphosphate-ribose) polymerase expression is predictive and prognostic in patients with breast cancer treated with neoadjuvant chemotherapy.

Authors:  Gunter von Minckwitz; Berit Maria Müller; Sibylle Loibl; Jan Budczies; Claus Hanusch; Silvia Darb-Esfahani; Jörn Hilfrich; Erich Weiss; Jens Huober; Jens Uwe Blohmer; Andreas du Bois; Dirk-Michael Zahm; Fariba Khandan; Gerald Hoffmann; Bernd Gerber; Holger Eidtmann; Falko Fend; Manfred Dietel; Keyur Mehta; Carsten Denkert
Journal:  J Clin Oncol       Date:  2011-04-25       Impact factor: 44.544

2.  High nuclear poly(adenosine diphosphate-ribose) polymerase expression is predictive for BRCA1- and BRCA2-deficient breast cancer.

Authors:  Luka Ozretić; Kerstin Rhiem; Sebastian Huss; Barbara Wappenschmidt; Birgid Markiefka; Peter Sinn; Rita K Schmutzler; Reinhard Buettner
Journal:  J Clin Oncol       Date:  2011-10-24       Impact factor: 44.544

3.  Failure of iniparib to inhibit poly(ADP-Ribose) polymerase in vitro.

Authors:  Anand G Patel; Silvana B De Lorenzo; Karen S Flatten; Guy G Poirier; Scott H Kaufmann
Journal:  Clin Cancer Res       Date:  2012-01-30       Impact factor: 12.531

Review 4.  The clinical development of inhibitors of poly(ADP-ribose) polymerase.

Authors:  H Calvert; A Azzariti
Journal:  Ann Oncol       Date:  2011-01       Impact factor: 32.976

5.  Poly(ADP-ribose) polymerase-2 (PARP-2) is required for efficient base excision DNA repair in association with PARP-1 and XRCC1.

Authors:  Valérie Schreiber; Jean-Christophe Amé; Pascal Dollé; Inès Schultz; Bruno Rinaldi; Valérie Fraulob; Josiane Ménissier-de Murcia; Gilbert de Murcia
Journal:  J Biol Chem       Date:  2002-04-10       Impact factor: 5.157

6.  Inhibition of poly(ADP-ribose) polymerase down-regulates BRCA1 and RAD51 in a pathway mediated by E2F4 and p130.

Authors:  Denise Campisi Hegan; Yuhong Lu; Gregory C Stachelek; Meredith E Crosby; Ranjit S Bindra; Peter M Glazer
Journal:  Proc Natl Acad Sci U S A       Date:  2010-01-19       Impact factor: 11.205

7.  Pathologic complete response rates in young women with BRCA1-positive breast cancers after neoadjuvant chemotherapy.

Authors:  Tomasz Byrski; Jacek Gronwald; Tomasz Huzarski; Ewa Grzybowska; Magdalena Budryk; Malgorzata Stawicka; Tomasz Mierzwa; Marek Szwiec; Rafal Wisniowski; Monika Siolek; Rebecca Dent; Jan Lubinski; Steven Narod
Journal:  J Clin Oncol       Date:  2009-12-14       Impact factor: 44.544

Review 8.  Understanding and treating triple-negative breast cancer.

Authors:  Carey Anders; Lisa A Carey
Journal:  Oncology (Williston Park)       Date:  2008-10       Impact factor: 2.990

Review 9.  Hallmarks of 'BRCAness' in sporadic cancers.

Authors:  Nicholas Turner; Andrew Tutt; Alan Ashworth
Journal:  Nat Rev Cancer       Date:  2004-10       Impact factor: 60.716

Review 10.  The pathology of familial breast cancer: Immunohistochemistry and molecular analysis.

Authors:  P P Osin; S R Lakhani
Journal:  Breast Cancer Res       Date:  1999-10-27       Impact factor: 6.466

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  3 in total

Review 1.  Mechanisms of resistance to therapies targeting BRCA-mutant cancers.

Authors:  Christopher J Lord; Alan Ashworth
Journal:  Nat Med       Date:  2013-10-07       Impact factor: 53.440

Review 2.  Targeting DNA damage response in cancer therapy.

Authors:  Noriko Hosoya; Kiyoshi Miyagawa
Journal:  Cancer Sci       Date:  2014-03-21       Impact factor: 6.716

3.  Resistance to PARP-Inhibitors in Cancer Therapy.

Authors:  Alicia Montoni; Mihaela Robu; Emilie Pouliot; Girish M Shah
Journal:  Front Pharmacol       Date:  2013-02-27       Impact factor: 5.810

  3 in total

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