Mark Pinese

TL;DR: In this paper, the authors performed whole-genome sequencing of 102 primary pancreatic neuroendocrine tumours and defined the genomic events that characterize their pathogenesis, including a deficiency in G:C,>T:A base excision repair due to inactivation of MUTYH, which encodes a DNA glycosylase.

TL;DR: The second version of PINA enhances its utility for studies ofprotein interactions at a network level, by including multiple collections of interaction modules identified by different clustering approaches from the whole network of protein interactions (‘interactome’) for six model organisms.

TL;DR: A graded response to priming is demonstrated in stratified patient-derived tumors, indicating that fine-tuned tissue manipulation before chemotherapy may offer opportunities in both primary and metastatic targeting of pancreatic cancer.

TL;DR: It is found that LOX expression is upregulated in metastatic tumors from Pdx1‐Cre KrasG12D/+ Trp53R172H/+ (KPC) mice and that inhibition of LOX in these mice suppressed metastasis, and LOX inhibition is able to reverse many of the features that make PDAC inherently refractory to conventional therapies.

TL;DR: The methylation profiles of 167 untreated resected PDACs and a panel of 29 adjacent nontransformed pancreata using high‐density arrays suggest that aberrant methylation plays an important role in pancreatic carcinogenesis affecting core signaling pathways with potential implications for the disease pathophysiology and therapy.