Toronto, Ontario--(Newsfile Corp. - November 3, 2026) - The Prospectors & Developers Association of Canada (PDAC) is pleased to announce the six recipients of the 2027 PDAC Awards, recognizing outstanding accomplishments in mineral exploration and development in Canada and around the world."The 2027 recipients reflect the exceptional talent, leadership and innovation found across our industry," said Karen Rees, PDAC President. "We're especially proud to introduce the Emerging Leaders Award this...

AbstractBackground:. Pancreatic ductal adenocarcinoma (PDAC) is projected to become the second leading cause of cancer-related death in the US, yet current treatments remain largely ineffective. The i...

Read the full paper: Quantitative ECM Profiling Reveals a Recapitulation Gap in a Subcutaneous KPC-Derived Syngeneic PDAC Model

Abstract. KRAS inhibitors (KRASi) are reshaping the treatment of aggressive tumors such as pancreatic ductal adenocarcinoma (PDAC), but it is appreciated that patients will eventually acquire resistan...

The European Investment Bank (EIB) and the Government of Canada have taken an important step toward strengthening cooperation on critical raw materials. At the PDAC 2026 conference in Toronto, the two...

Abstract. Pancreatic Ductal Adenocarcinoma (PDAC) remains one of the deadliest solid malignancies, with only 13% of patients surviving beyond five years. This dismal prognosis is largely attributed to...

Abstract. Chemotherapy remains the mainstay for treatment in patients with advanced pancreatic ductal adenocarcinoma (PDAC), but acquired therapeutic resistance remains a major challenge to sustaining...

AbstractBackground:. Pancreatic ductal adenocarcinoma (PDAC) is frequently driven by oncogenic KRASG12D/+ and exacerbated by obesity-induced metabolic inflammation, driving immune suppression and meta...

Il carcinoma duttale pancreatico (PDAC) rimane tra le neoplasie solide con la prognosi più sfavorevole. Nonostante decenni di ricerca, la sopravvivenza a cinque anni si attesta ancora intorno al 12%, un dato che non accenna a migliorare in modo sostanziale. Il principale responsabile di questa stagnazione prognostica è, da sempre, lo stesso: la diagnosi tardiva. Nella quasi totalità dei casi, quando il paziente sviluppa i primi sintomi significativi — dolore epigastrico irradiato al dorso, ittero, calo ponderale — la malattia è già localmente avanzata o metastatica, e le opzioni terapeutiche si riducono drammaticamente.

AbstractBackground:. Pancreatic ductal adenocarcinoma (PDAC) patients with concurrent type 2 diabetes mellitus (T2DM) exhibit significantly worse treatment responses and shorter survival rates. Howeve...

To define how PDAC cells take up exogenous lipids in vivo, we followed the transit of blood-borne low-density lipoprotein (LDL) particles into cancer cells within the tumor mass (Fig. 1 and Extended Data Fig. 1). Using cytokeratin as a PDAC lineage biomarker in cryosections of autochthonous KPC tumors6 (Pdx1-Cre;KrasLSL-G12D;Trp53f/f), we traced intravenously injected LDL particles labeled with BODIPY-cholesterol; these 25-nm particles concentrate in endosomes11 large enough to resolve by optical microscopy. At 15 min, the lipid signal localized to blood vessels and intercellular spaces (Extended Data Fig. 1a) and serum BODIPY-cholesterol peaked at 15 min and declined by 90 min as tissues took up LDL (Extended Data Fig. 1b). Between 90 min and 20 h, the signal migrated progressively into cytokeratin-positive carcinoma cells (Extended Data Fig. 1c,d). Because blood BODIPY-cholesterol was already low at these later times (Extended Data Fig. 1b), delayed uptake by PDAC cells relative to fibroblasts was unlikely to reflect slower LDL uptake kinetics despite upregulation of LDL receptors in PDAC12 and intratumoral redistribution from CAFs to cancer cells was a more plausible explanation. We next implanted syngeneic IRFP720-labeled murine KPCN349 PDAC cells into the pancreas of fibroblast reporter Col1a1-CreERT;Ai9 mice and induced CAF tdTomato expression with...

To define how PDAC cells take up exogenous lipids in vivo, we followed the transit of blood-borne low-density lipoprotein (LDL) particles into cancer cells within the tumor mass (Fig. 1 and Extended Data Fig. 1). Using cytokeratin as a PDAC lineage biomarker in cryosections of autochthonous KPC tumors6 (Pdx1-Cre;KrasLSL-G12D;Trp53f/f), we traced intravenously injected LDL particles labeled with BODIPY-cholesterol; these 25-nm particles concentrate in endosomes11 large enough to resolve by optical microscopy. At 15 min, the lipid signal localized to blood vessels and intercellular spaces (Extended Data Fig. 1a) and serum BODIPY-cholesterol peaked at 15 min and declined by 90 min as tissues took up LDL (Extended Data Fig. 1b). Between 90 min and 20 h, the signal migrated progressively into cytokeratin-positive carcinoma cells (Extended Data Fig. 1c,d). Because blood BODIPY-cholesterol was already low at these later times (Extended Data Fig. 1b), delayed uptake by PDAC cells relative to fibroblasts was unlikely to reflect slower LDL uptake kinetics despite upregulation of LDL receptors in PDAC12 and intratumoral redistribution from CAFs to cancer cells was a more plausible explanation. We next implanted syngeneic IRFP720-labeled murine KPCN349 PDAC cells into the pancreas of fibroblast reporter Col1a1-CreERT;Ai9 mice and induced CAF tdTomato expression with...

We previously showed that eEF1AK55me2 promotes global protein synthesis and proposed a model in which KRAS-driven lung adenocarcinoma (LUAD) and pancreatic ductal adenocarcinoma (PDAC) tumours become dependent on the METTL13–eEF1AK55me2 axis to meet their heightened translation demands13. In support of this model, METTL13 ablation inhibits tumorigenesis and extends median survival by 40–50% in KRASG12D-driven LUAD and PDAC mouse models13 (Extended Data Fig. 2a,b). Consistent with these experimental findings, METTL13 is commonly amplified or gained in patients with LUAD and PDAC (Extended Data Fig. 2c,d), and its mRNA is overexpressed across multiple cancer types, correlating with poor patient prognosis13,17,18,19,20,21. For example, METTL13 mRNA is increased in tumour tissue compared with normal lung tissue in 90% of patients with LUAD (Extended Data Fig. 2c). METTL13 protein and eEF1AK55me2 are increased in tumours compared with normal tissue, with higher levels correlating with an approximately twofold reduction in median patient survival (Extended Data Fig. 2e,f). These data are consistent with the METTL13–eEF1AK55me2 axis being a potential contributor to malignant disease in humans. Conversely, despite its role in tumorigenesis, tissue-specific METTL13 deletion produces no discernible phenotypes in normal pancreas or lung13. Moreover, METTL13 ablation at the germinal stage had no apparent effect on mouse development...

We previously showed that eEF1AK55me2 promotes global protein synthesis and proposed a model in which KRAS-driven lung adenocarcinoma (LUAD) and pancreatic ductal adenocarcinoma (PDAC) tumours become dependent on the METTL13–eEF1AK55me2 axis to meet their heightened translation demands13. In support of this model, METTL13 ablation inhibits tumorigenesis and extends median survival by 40–50% in KRASG12D-driven LUAD and PDAC mouse models13 (Extended Data Fig. 2a,b). Consistent with these experimental findings, METTL13 is commonly amplified or gained in patients with LUAD and PDAC (Extended Data Fig. 2c,d), and its mRNA is overexpressed across multiple cancer types, correlating with poor patient prognosis13,17,18,19,20,21. For example, METTL13 mRNA is increased in tumour tissue compared with normal lung tissue in 90% of patients with LUAD (Extended Data Fig. 2c). METTL13 protein and eEF1AK55me2 are increased in tumours compared with normal tissue, with higher levels correlating with an approximately twofold reduction in median patient survival (Extended Data Fig. 2e,f). These data are consistent with the METTL13–eEF1AK55me2 axis being a potential contributor to malignant disease in humans. Conversely, despite its role in tumorigenesis, tissue-specific METTL13 deletion produces no discernible phenotypes in normal pancreas or lung13. Moreover, METTL13 ablation at the germinal stage had no apparent effect on mouse development...