pancreatic-cancer

A newly characterized cell death pathway may bypass treatment resistance in the hardest cancers.

Alkaliptosis is a pH-dependent cell death mechanism driven by JTC801 that disrupts intracellular pH homeostasis. Because it is mechanistically distinct from apoptosis, cells resistant to standard treatments remain susceptible. Particularly effective against pancreatic ductal adenocarcinoma. This…

A newly characterized cell death pathway may bypass treatment resistance in the hardest cancers.

Key Findings

Alkaliptosis is pH-dependent, distinct from apoptosis/necroptosis/ferroptosis
Driven by JTC801 via disruption of pH-regulatory proteins
Effective against apoptosis-resistant cancers including PDAC
Detection methods include dynamic pH measurement and protein expression analysis

Implications

Alkaliptosis-targeting therapies could benefit patients with pancreatic and other apoptosis-resistant cancers.

Caveats

Methods/protocol paper; abstract-only. JTC801 is a research tool compound; significant translational gap.

Source: Methods in cell biology — 2026-01-01

Landmark DCIS trial, CRC microbiome & AML combos

Two themes cut across this week’s 236 posts. The first is de-escalation: researchers are building rigorous evidence that patients can safely do less — skip lymph node surgery, forgo radiotherapy, watch pre-invasive lesions instead of cutting them out. The landmark result here is a randomized trial confirming that active surveillance

Colorectal Cancer Microbiome Discovery Platform

Analysis of 9,000+ patients revealed that only colorectal cancer — not other cancer types — consistently harbors distinct microbial communities, suggesting the gut microbiome has a unique relationship with colorectal carcinogenesis that could be exploited for diagnostics and treatment.

GBM Tumor Microenvironment Drug Target Atlas

Non-cancerous brain support cells were found to promote glioblastoma growth through paracrine signaling, and blocking this communication dramatically slowed tumor growth — revealing that GBM's microenvironment contains targetable vulnerabilities that are being systematically overlooked by drug…

BET Inhibitor Target Selectivity Database

BRD2 and BRD4 have fundamentally distinct functions — BRD2 prepares genes for activation while BRD4 triggers transcription — meaning that pan-BET inhibitors have been disrupting gene regulation in counterproductive ways, and the field now needs selective BRD4 inhibitors.

A newly characterized cell death pathway may bypass treatment resistance in the hardest cancers.

Key Findings

Implications

Caveats

Read more

Landmark DCIS trial, CRC microbiome & AML combos

Colorectal Cancer Microbiome Discovery Platform

GBM Tumor Microenvironment Drug Target Atlas

BET Inhibitor Target Selectivity Database