The extracellular matrix (ECM) is a complex assembly of proteins surrounding cells. It is a critical component of the tumor microenvironment that plays an active role in tumor progression and modulati...

A recent study published in Cancer Research by scientists at The University of Texas MD Anderson Cancer Center (USA) and collaborators aimed to identify and characterize a target that elicits an antic...

Abstract. Purpose: Treatment of pancreatic ductal adenocarcinoma (PDAC) has been advanced by the development of KRAS inhibitors. Despite this progress, PDACs invariably develop resistance to these age...

Despite constitutive Ras/Raf/MAPK pathway activation in most pancreatic ductal adenocarcinomas (PDACs), treatment approaches targeting this pathway ha…

KRAS mutations are ubiquitous in pancreatic adenocarcinomas (PDACs) and are associated with poor outcomes. We leveraged a cohort of 2,336 PDAC tumors to characterize genomic subtypes and their prognos...

KRAS mutations are ubiquitous in pancreatic adenocarcinomas (PDACs) and are associated with poor outcomes. We leveraged a cohort of 2,336 PDAC tumors to characterize genomic subtypes and their prognos...

Tumors driven by cancer-driving KRAS mutations are often susceptible to ferroptosis, a type of cell death that can be harnessed for cancer therapy. Given that more than 95% of pancreatic ductal adenocarcinomas (PDACs) harbor such mutations, one might expect these tumors to be similarly vulnerable. Yet, in keeping with PDAC's notorious intractability, its tumors show no such vulnerability. Why this is so has been something of a mystery.

Clinically available KRAS inhibitors mainly target G12C, which is rare in PDAC and often acquires resistance. Oncogenic KRAS inactivates RB1 via CDK4/6, while RB1 mutation is rare. Thus, CDK4/6 inhibition offers an indirect strategy to counter KRAS-driven malignancy without direct KRAS targeting. Virtually all pancreatic ductal adenocarcinomas (PDACs) are initiated by activating mutations in the oncogene KRAS, which occur in multiple distinct allelic forms. Although considerable efforts have led to the development of inhibitors targeting specific mutant KRAS proteins, the only agents currently approved for clinical use selectively target the KRASG12C variant. However, KRASG12C mutations are exceedingly rare in pancreatic cancer. Furthermore, in patients with KRASG12C-mutant pancreatic cancer, treatment with KRASG12C inhibitors has shown only modest clinical benefit, comparable to that of conventional chemotherapeutic regimens, and even in cases with an initial objective response, acquired resistance almost invariably emerges within a limited time frame. More broadly, direct pharmacological inhibition of driver oncogenes frequently precipitates the rapid development of durable therapeutic resistance. These observations underscore a critical unmet need for therapeutic strategies that circumvent direct targeting of driver mutant proteins while achieving antitumor efficacy comparable to that of their direct inhibition. Zhang et al. addressed how to cure PDAC patients with...

The South Korean BDACS CRYPTO Cortodian PDACS launched XRP institutional reservation support after the February Partnership Agreement with Ripple. This step provides organized access to one of the most trading digital assets in the world. Subtraction, Declare Through the X -BDACS account on Tuesday, the institutions enable the storage and management of XRP (XRP) safely using Ripple Custody, Reble's Pressing Ragen. "We are happy to provide nursery support to XRP, one of the most popular digital assets in Korea, for our institutional customers," BDACS wrote. "This launch enhances our long -term partnership with Ripple and emphasizes our commitment to the Korean market."

Nature Medicine - KRAS mutations are ubiquitous in pancreatic adenocarcinomas (PDACs) and are associated with poor outcomes. We leveraged a cohort of 2,336 PDAC tumors to characterize genomic...

Nature Medicine - KRAS mutations are ubiquitous in pancreatic adenocarcinomas (PDACs) and are associated with poor outcomes. We leveraged a cohort of 2,336 PDAC tumors to characterize genomic...

Pancreatic ductal adenocarcinomas (PDACs) are lethal cancers resistant to immunotherapies. In this issue of Cancer Cell, Kureshi et al. show that combining checkpoint blockade with STING-mediated innate immune stimulation unlocks cDC2-driven CD4+ T cell immunity in mice, promoting PDAC immune control. This cellular axis may be exploited for PDAC therapy.

Pancreatic ductal adenocarcinomas (PDACs) are lethal cancers resistant to immunotherapies. In this issue of Cancer Cell, Kureshi et al. show that combining checkpoint blockade with STING-mediated innate immune stimulation unlocks cDC2-driven CD4+ T cell immunity in mice, promoting PDAC immune control. This cellular axis may be exploited for PDAC therapy.

Wang et al. analyze IPMNs, normal samples, pancreatic cyst fluids, and PDACs using proteomics and glycoproteomics, identify high-grade-IPMN-associated proteins in both tissues and cyst fluids, and link ECM protein alterations to disease progression. These findings offer insights into neoplastic progression in the pancreas and highlight potential biomarkers for early detection and therapy.

Wang et al. analyze IPMNs, normal samples, pancreatic cyst fluids, and PDACs using proteomics and glycoproteomics, identify high-grade-IPMN-associated proteins in both tissues and cyst fluids, and link ECM protein alterations to disease progression. These findings offer insights into neoplastic progression in the pancreas and highlight potential biomarkers for early detection and therapy.

Wang et al. analyze IPMNs, normal samples, pancreatic cyst fluids, and PDACs using proteomics and glycoproteomics, identify high-grade-IPMN-associated proteins in both tissues and cyst fluids, and lin...

Pancreatic ductal adenocarcinomas (PDACs) are lethal cancers resistant to immunotherapies. In this issue of Cancer Cell, Kureshi et al. show that combining checkpoint blockade with STING-mediated innate immune stimulation unlocks cDC2-driven CD4+ T cell immunity in mice, promoting PDAC immune control. This cellular axis may be exploited for PDAC therapy.

Pancreatic ductal adenocarcinomas (PDACs) are lethal cancers resistant to immunotherapies. In this issue of Cancer Cell, Kureshi et al. show that comb…

Pancreatic ductal adenocarcinomas (PDACs) with wild-type KRAS constitute a small fraction of PDACs, and these tumors were recently shown to harbor frequent actionable oncogenic mutations and fusions....