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Network rewiring,adaptive resistance and combating strategies in breast cancer

Cancer Drug Resistance 2019年第4期2卷 1106-1126页

作者： Constance Gaya Cremers Lan k.Nguyen Department of Biochemistry and Molecular Biology School of Biomedical SciencesMonash UniversityClaytonVictoria 3800Australia Biomedicine Discovery Institute Monash UniversityClaytonVictoria 3800Australia

Resistance to targeted anti-cancer drugs is a complex phenomenon and a major challenge in cancer *** is becoming increasingly evident that a form of acquired drug resistance known as“adaptive resistance”is a common cause of treatment failure and patient relapse in many *** classical resistance mechanisms that are acquired via genomic alterations,adaptive resistance is instead driven by non-genomic changes involving rapid and dynamic rewiring of signalling and/or transcriptional networks following therapy,enabled by complex pathway crosstalk and feedback *** network rewiring allows tumour cells to adapt to the drug treatment,circumvent the initial drug challenge and continue to survive in the presence of the *** its great clinical importance,adaptive resistance remains largely under-studied and poorly *** review is focused on recent findings which provide new insights into the mechanisms underlying adaptive resistance in breast cancer,highlighting how breast tumour cells rewire intracellular signalling pathways to overcome the stress of initial targeted *** particular,we investigate adaptive resistance to targeted inhibition of two major oncogenic signalling axes frequently dysregulated in breast cancer,the pi3k-AkT-mTOR and RAS-MAPk signalling pathways;and discuss potential combination treatment strategies that overcome such *** addition,we highlight application of quantitative and computational modelling as a novel integrative and powerful approach to gain network-level understanding of network rewiring,and rationally identify and prioritise effective drug combinations.

关键词： Network rewiring adaptive resistance pi3k signalling MAPk signalling breast cancer mathematical modelling systems analysis

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前列腺癌印记基因表达的特殊变化一前列腺癌发展和表观遗传调控的预示

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Asian Journal of Andrology 2012年第3期14卷 436-450,I0007页

作者： Teodora Ribarska klaus-Marius Bastian Annemarie koch Wolfgang A Schulz Department of Urology Heinrich Heine University 40225 Duesseldorf Germany 1

Epigenetic dysregulation comprising DNA hypermethylation and hypomethylation, enhancer of zeste homologue 2 （EZH2） overexpression and altered patterns of histone modifications is associated with the progression of prostate cancer. DNA methylation, EZH2 and histone modifications also ensure the parental-specific monoallelic expression of at least 62 imprinted genes. Although it is therefore tempting to speculate that epigenetic dysregulation may extend to imprinted genes, expression changes in cancerous prostates are only well documented for insulin-like growth factor 2 （IGF2）. A literature and database survey on imprinted genes in prostate cancer suggests that the expression of most imprinted genes remains unchanged despite global disturbances in epigenetic mechanisms. Instead, selective genetic and epigenetic changes appear to lead to the inactivation of a sub-network of imprinted genes, which might function in the prostate to limit cell growth induced via the pi3k/Akt pathway, modulate androgen responses and regulate differentiation. Whereas dysregulation of IGF2 may constitute an early change in prostate carcinogenesis, inactivation of this imprinted gene network is rather associated with cancer progression.

关键词： androgen signalling imprinted genes loss of imprinting pi3k signalling prostate cancer

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