作者: Milind Javle , Talia Golan , Anirban Maitra
DOI: 10.1016/J.CTRV.2016.01.004
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摘要: In the past decade, insightful preclinical research has led to important breakthroughs in our understanding of pancreatic cancer. Even though vast majority cancers are KRAS mutated, not all cancer tumors "KRAS equal"; there seems be varying dependencies on pathway. While KRAS-targeting therapies have been disappointing clinic, 'synthetic lethal' approaches hold promise this setting. The stromal microenvironment appears contradictory roles. is evidence suggest that barrier prevents drug delivery, other circumstances, stroma can play a protective role and its disruption enhances tumor dissemination. Clinical trials aimed at manipulating various components progress. BRCA mutation-related illustrate unique subtype with enhanced susceptibility DNA damaging agents PARP-inhibition. repair defects extend beyond germ line mutation may indications for repair-targeting agents. Immune strategies an area active investigation Although initial single-agent checkpoint inhibitors negative, combinational using immune-modifying vaccines appear promising goal identify 'immune-therapy responsive' profile