Poly(ADP-ribose) polymerase (PARP) inhibitors: Exploiting a synthetic lethal strategy in the clinic (Q37826009)

23 August 2017

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title

Poly(ADP-ribose) polymerase (PARP) inhibitors: Exploiting a synthetic lethal strategy in the clinic (English)

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23 August 2017

Timothy A Yap

1

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23 August 2017

Shahneen K Sandhu

series ordinal

2

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23 August 2017

Craig P Carden

series ordinal

3

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23 August 2017

Johann S de Bono

series ordinal

4

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23 August 2017

language of work or name

English

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publication date

4 January 2011

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23 August 2017

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23 August 2017

61

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23 August 2017

31-49

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23 August 2017

1

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Poly(ADP-ribose) polymerase null mouse cells synthesize ADP-ribose polymers

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DNA recombination: the replication connection.

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Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy

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PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination.

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Homologous recombination in cancer development, treatment and development of drug resistance.

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Poly(ADP-ribose) polymerase is hyperactivated in homologous recombination-defective cells

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53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks

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Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase

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Phase 0 clinical trial of the poly (ADP-ribose) polymerase inhibitor ABT-888 in patients with advanced malignancies

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Promoter hypermethylation and BRCA1 inactivation in sporadic breast and ovarian tumors

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EMSY links the BRCA2 pathway to sporadic breast and ovarian cancer

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Population BRCA1 and BRCA2 mutation frequencies and cancer penetrances: a kin-cohort study in Ontario, Canada

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Prevalence and penetrance of germline BRCA1 and BRCA2 mutations in a population series of 649 women with ovarian cancer

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BRCA1 and BRCA2 mutations account for a large proportion of ovarian carcinoma cases

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Somatic mutations in BRCA1 and BRCA2 could expand the number of patients that benefit from poly (ADP ribose) polymerase inhibitors in ovarian cancer

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ATM mutations that cause ataxia-telangiectasia are breast cancer susceptibility alleles

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ATM deficiency sensitizes mantle cell lymphoma cells to poly(ADP-ribose) polymerase-1 inhibitors

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Cell cycle checkpoint defects contribute to genomic instability in PTEN deficient cells independent of DNA DSB repair.

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Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors

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PTEN: a new guardian of the genome.

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PTEN loss compromises homologous recombination repair in astrocytes: implications for glioblastoma therapy with temozolomide or poly(ADP-ribose) polymerase inhibitors.

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Promising novel therapies for the treatment of endometrial cancer

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Frequent alteration of DNA damage signalling and repair pathways in human colorectal cancers with microsatellite instability.

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Repeated observation of breast tumor subtypes in independent gene expression data sets

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Gene-Expression Profiles in Hereditary Breast Cancer

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Gene expression profile of BRCAness that correlates with responsiveness to chemotherapy and with outcome in patients with epithelial ovarian cancer.

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Resistance to therapy caused by intragenic deletion in BRCA2

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Secondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated cancers

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Improved survival in women with BRCA-associated ovarian carcinoma

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gammaH2AX expression in tumors exposed to cisplatin and fractionated irradiation.

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DNA repair pathways in clinical practice: lessons from pediatric cancer susceptibility syndromes

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Development of a functional assay for homologous recombination status in primary cultures of epithelial ovarian tumor and correlation with sensitivity to poly(ADP-ribose) polymerase inhibitors.

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BRCA1 promoter methylation is associated with increased mortality among women with breast cancer

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Secondary BRCA1 mutations in BRCA1-mutated ovarian carcinomas with platinum resistance

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DNA repair pathways as targets for cancer therapy

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Poly(ADP-ribose) polymerase inhibitors in cancer treatment: a clinical perspective.

21 January 2018

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Proteasome function is required for DNA damage response and fanconi anemia pathway activation

21 January 2018

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Inhibitors of the proteasome suppress homologous DNA recombination in mammalian cells.

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Cyclin-dependent kinase 2 functions in normal DNA repair and is a therapeutic target in BRCA1-deficient cancers

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HDAC inhibitor PCI-24781 decreases RAD51 expression and inhibits homologous recombination

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Poly(ADP-ribose) polymerase-1 plays a role in suppressing mammary tumourigenesis in mice.

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Loss of poly(ADP-ribose) polymerase-2 leads to rapid development of spontaneous T-cell lymphomas in p53-deficient mice

21 January 2018

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PTEN mutations are common in sporadic microsatellite stable colorectal cancer

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Germ-Line Mutations in Mismatch Repair Genes Associated with Prostate Cancer

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“BRCAness” Syndrome in Ovarian Cancer: A Case-Control Study Describing the Clinical Features and Outcome of Patients With Epithelial Ovarian Cancer Associated WithBRCA1andBRCA2Mutations

21 January 2018

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21 January 2018

Identifiers

DOI

10.3322/CAAC.20095

1 reference

23 August 2017

1 reference