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Despite of severe clinical and scientific efforts, treatment of pancreatic ductal adenocarcinoma (PDAC) remains a major challenge. Significant improvement of PDAC prognosis is hampered by restricted therapy response of PDAC patients which is—on the molecular level—primarily caused by an extreme intertumoral heterogeneity.1 Besides the core genetic alterations (oncogenic mutation of KRAS, inactivation of the core tumour suppressors TP53, CDKN2A and DPC4) PDAC is characterised by a plethora of additional molecular events that, although occurring less frequently, are of prognostic and predictive significance.2 3 For instance, approximately one-third of PDAC tumours carry mutations in genes coding for chromatin regulatory proteins.2 Epigenetic alterations installed by changes of the chromatin landscape critically impact on tissue homeoestasis and can foster malignant transformation and tumour progression.1 This is particularly true for the SWI/SNF (SWItch/sucrose non-fermentable) complex of chromatin remodelling proteins, which physiologically disrupts the tight contact between DNA and histones and mobilises nucleosomes to reveal previously …
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