Targeting BRCA1-BER deficient breast cancer by ATM or DNA-PKcs blockade either alone or in combination with cisplatin for personalized therapy.
Nada Albarakati,Tarek M. A. Abdel-Fatah,Rachel Doherty,Roslin Russell,Devika Agarwal,Paul M. Moseley,Christina Perry,Arvind Arora,Nouf Alsubhi,Claire Seedhouse,Emad A. Rakha,Andrew R. Green,Graham Ball,Stephen Chan,Carlos Caldas,Ian O. Ellis,Srinivasan Madhusudan +16 more
TLDR
XRCC1 and pol β expression status in BRCA1 negative tumours may have prognostic significance and be targeted by ATM or DNA‐PKcs inhibitors for personalized therapy.About:
This article is published in Molecular Oncology.The article was published on 2015-01-01 and is currently open access. It has received 65 citations till now. The article focuses on the topics: Base excision repair & Low protein.read more
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Mechanisms of Multidrug Resistance in Cancer Chemotherapy.
TL;DR: The aim of this review is to demonstrate the latest data on the mechanisms of cellular resistance to anticancer agents currently used in clinical treatment but also to present the mechanism of action of novel potential antitumor drugs which have been designed to overcome these resistance mechanisms.
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ATM and ATR as therapeutic targets in cancer.
Anika M. Weber,Anderson J. Ryan +1 more
TL;DR: Preclinical data have provided a strong rationale for clinical testing of these compounds both in combination with radio- or chemotherapy, and in synthetic lethal approaches to treat tumours with deficiencies in certain DDR components, suggesting that a synthetic lethal approach with ATM or ATR inhibitors could have widespread utility, providing that appropriate biomarkers are developed.
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DNA repair pathways and cisplatin resistance: an intimate relationship
Clarissa Ribeiro Reily Rocha,Matheus Molina Silva,Annabel Quinet,Januário B. Cabral-Neto,Carlos Frederico Martins Menck +4 more
TL;DR: This review describes how cisplatin-induced DNA lesions are repaired or tolerated by cells and focuses on the pivotal role of DNA repair and tolerance mechanisms in tumor resistance to cisPlatin.
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Not breathing is not an option: How to deal with oxidative DNA damage.
TL;DR: The differential origins of 8-oxo-G in DNA and its consequences for genetic stability will be covered, followed by a thorough discussion of the different mechanisms in place to cope with 7,8-dihydro-8xo-deoxyGuanine.
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Advances in synthetic lethality for cancer therapy: cellular mechanism and clinical translation
Win Topatana,Win Topatana,Sarun Juengpanich,Sarun Juengpanich,Shijie Li,Jiasheng Cao,Jiahao Hu,Jiyoung Lee,Kenneth Suliyanto,Diana Ma,Bin Zhang,Mingyu Chen,Mingyu Chen,Xiu-Jun Cai,Xiu-Jun Cai +14 more
TL;DR: The characterization of potential synthetic lethal interactions and novel technologies to develop a more effective targeted drug for cancer patients will be explored and the clinical development and drug resistance mechanisms of synthetic lethality in cancer therapy will be discussed.
References
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Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments
TL;DR: The hierarchical model of Lonnstedt and Speed (2002) is developed into a practical approach for general microarray experiments with arbitrary numbers of treatments and RNA samples and the moderated t-statistic is shown to follow a t-distribution with augmented degrees of freedom.
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The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups
Christina Curtis,Christina Curtis,Sohrab P. Shah,Suet-Feung Chin,Gulisa Turashvili,Oscar M. Rueda,Mark J Dunning,Doug Speed,Doug Speed,Andy G. Lynch,Shamith A. Samarajiwa,Yinyin Yuan,Stefan Gräf,Gavin Ha,Gholamreza Haffari,Ali Bashashati,Roslin Russell,Steven McKinney,Anita Langerød,Andrew R. Green,Elena Provenzano,Gordon C. Wishart,Sarah E Pinder,Peter H. Watson,Peter H. Watson,Florian Markowetz,Leigh C. Murphy,Ian O. Ellis,Arnie Purushotham,Arnie Purushotham,Anne Lise Børresen-Dale,Anne Lise Børresen-Dale,James D. Brenton,Simon Tavaré,Carlos Caldas,Samuel Aparicio +35 more
TL;DR: The results provide a novel molecular stratification of the breast cancer population, derived from the impact of somatic CNAs on the transcriptome, and identify novel subgroups with distinct clinical outcomes, which reproduced in the validation cohort.
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Cytoscape 2.8
TL;DR: Version 2.8 introduces two powerful new features—Custom Node Graphics and Attribute Equations—which can be used jointly to greatly enhance Cytoscape's data integration and visualization capabilities.
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Diagnosis of multiple cancer types by shrunken centroids of gene expression
TL;DR: The method of “nearest shrunken centroids” identifies subsets of genes that best characterize each class, which was highly efficient in finding genes for classifying small round blue cell tumors and leukemias.
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Hallmarks of 'BRCAness' in sporadic cancers
TL;DR: There are properties that define 'BRCAness' — that is, traits that some sporadic cancers share with those occurring in either BRCA1- or BRCa2-mutation carriers, which might have important implications for the clinical management of these cancers.