Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest cancers. Significant
efforts have largely defined major genetic factors driving PDAC pathogenesis and …

One hundred years have passed since Warburg discovered alterations in cancer
metabolism, more than 70 years since Sidney Farber introduced anti-folates that …

Cancer-associated fibroblasts (CAFs) found in primary and metastatic tumours are highly
versatile, plastic and resilient cells that are actively involved in cancer progression through …

Cancer cells evade T cell-mediated killing through tumour–immune interactions whose
mechanisms are not well understood,. Dendritic cells (DCs), especially type-1 conventional …

Pancreatic ductal adenocarcinoma (PDAC) cells use glutamine (Gln) to support proliferation
and redox balance. Early attempts to inhibit Gln metabolism using glutaminase inhibitors …

Metabolic reprogramming enables cancer cell growth, proliferation, and survival. This
reprogramming is driven by the combined actions of oncogenic alterations in cancer cells …

Cancer cells continuously rewire their metabolism to fulfill their need for rapid growth and
survival while subject to changes in environmental cues. Thus, a vital component of a cancer …

Pancreatic ductal adenocarcinoma (PDAC) is a lethal cancer with a prominent extracellular
matrix (ECM) deposition and poor prognosis. High levels of ECM proteins derived from …

Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive disease with a 5-year
survival rate of< 10%. The tumour microenvironment (TME) of PDAC is characterized by …

A hallmark of pancreatic tumors is their highly desmoplastic stroma composed of fibroblasts,
immune cells, and a dense network of collagen fibers. Tumor-associated macrophages are …