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Pancreatic cancer is a disease in which malignant cells originate in the pancreatic tissue. Cancer of the exocrine component of the pancreas (adenocarcinomas) represents the majority of pancreatic malignancies. Pancreatic cancer is generally characterized by a poor prognosis.
Effectively targeting deregulated KRAS signaling remains an unmet clinical need, as current approaches commonly lead to the development of chemoresistance in clinical settings. ADAM9-mediated lysosomal KRAS degradation is now shown to counteract PDAC chemoresistance independently of mutational status.
The tumour microenvironment produces nutrients that propel cancer development. New work finds that pancreatic ductal adenocarcinoma cells use one such nutrient, acetate, to alter protein acetylation, rerouting polyamine metabolism and promoting cell growth under acidosis—a finding with potential implications for treating this cancer.
The MAPK pathway is an important therapeutic target in pancreatic ductal adenocarcinoma (PDAC), but success is limited by pathway reactivation, which drives resistance. Here, the authors investigate the mechanism underlying HER2-reactivation post KRAS-MAPK inhibition, identifying combination of MAPK and HER2 inhibition as a therapeutic strategy.
Therapeutic options for pancreatic ductal adenocarcinoma (PDAC) are limited. Here the authors report the characterization of a CEACAM6-targeting antibody drug conjugate loaded with a BET protein degrader, showing antitumour activity in PDAC preclinical models.
Effectively targeting deregulated KRAS signaling remains an unmet clinical need, as current approaches commonly lead to the development of chemoresistance in clinical settings. ADAM9-mediated lysosomal KRAS degradation is now shown to counteract PDAC chemoresistance independently of mutational status.
The tumour microenvironment produces nutrients that propel cancer development. New work finds that pancreatic ductal adenocarcinoma cells use one such nutrient, acetate, to alter protein acetylation, rerouting polyamine metabolism and promoting cell growth under acidosis—a finding with potential implications for treating this cancer.
We applied an artificial intelligence (AI) approach to a dataset of clinical and advanced multi-omic molecular features from patients with pancreatic adenocarcinoma to predict survival. The results reveal a tumor-type-agnostic platform that can identify parsimonious and robust clinical prediction biomarkers, catalyzing the vision to democratize precision oncology worldwide.
In a recent Developmental Cell paper, Falvo et al. establish a role for epigenetic memory of inflammatory injury in promoting pancreatic tumorigenesis.