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preclinical

A collection of 65 issues

GPR39 Protein Linked to Immunotherapy Resistance in Microsatellite-Stable CRC

Skip to content The CRC Digest ◇ RESEARCH GPR39 Protein Linked to Immunotherapy Resistance in Microsatellite-Stable CRC Research using GPR39 knockdown in human and mouse CRC cell lines found that GPR39, a protein overexpressed in colorectal cancer, suppresses ferroptosis (a form of cell death) and reduces the sensitivity of microsatellite-stable tumors

Review links colibactin-producing E. coli to early-onset colorectal cancer through distinct mutational signatures

Skip to content The CRC Digest ◇ RESEARCH Review links colibactin-producing E. coli to early-onset colorectal cancer through distinct mutational signatures Genomic profiling has identified mutational signatures SBS88 and ID18 in colorectal tumors exposed to colibactin from pks+ E. coli, with emerging data suggesting enrichment in early-onset CRC. (Infection, Genetics and

Preclinical study shows fruquintinib combined with TAS-102 has antitumor activity in colorectal and gastric cancer models

Skip to content The CRC Digest ▸ TREATMENT Preclinical study shows fruquintinib combined with TAS-102 has antitumor activity in colorectal and gastric cancer models Fruquintinib, an oral inhibitor of all three vascular endothelial growth factor receptors that has been approved for chemorefractory CRC, showed combined antitumor activity with TAS-102 in xenograft

KRAS mutations drive immune evasion through RNA modifications

Skip to content The CRC Digest ◇ RESEARCH KRAS mutations drive immune evasion through RNA modifications Preclinical research found that KRAS mutations remodel RNA m6A modifications to increase CD73 expression, promoting immune evasion in colorectal cancer. (Cancer Research) This content is informational only and does not constitute medical advice. Always consult

PLOD2 Protein Linked to Tumor Growth in Colorectal Cancer

Skip to content The CRC Digest ◇ RESEARCH PLOD2 Protein Linked to Tumor Growth in Colorectal Cancer Preclinical research using single-cell RNA sequencing found that PLOD2, often overexpressed in colorectal cancer, has been implicated in promoting tumor growth and epithelial-mesenchymal transition. Functional assays in CRC cell lines with PLOD2 knockdown showed

DHODH Identified as Metabolic Vulnerability in PIK3CA-Mutant Colorectal Cancer

Skip to content The CRC Digest DHODH Identified as Metabolic Vulnerability in PIK3CA-Mutant Colorectal Cancer Preclinical research identifies dihydroorotate dehydrogenase (DHODH) as a selective metabolic dependency in PIK3CA-mutant CRC; DHODH inhibition reduces cancer cell self-renewal and tumor initiation by disrupting PI3K-AKT signaling. (Cell Reports) This content is informational only and

KRAS G12D Inhibitor Reshapes Immune Landscape, Enhances NK Cell Therapy

Skip to content The CRC Digest ◇ RESEARCH KRAS G12D Inhibitor Reshapes Immune Landscape, Enhances NK Cell Therapy Preclinical research shows that KRAS G12D inhibition with MRTX1133 remodels the tumor immune environment by reducing immunosuppressive cells and facilitating infiltration of natural killer and CD8+ T cells, reversing systemic immunosuppression and restoring

Mitochondrial Metabolism Drives 5-FU Resistance in Colorectal Cancer

Skip to content The CRC Digest ◇ RESEARCH Mitochondrial Metabolism Drives 5-FU Resistance in Colorectal Cancer Preclinical research shows that 5-fluorouracil treatment promotes mitochondrial biogenesis and increased mitochondrial function in surviving colorectal cancer cells, and that targeting mitochondrial metabolism—particularly Complex I inhibition—can sensitize CRC cells to chemotherapy. (Nature Metabolism)

CRISPR Screens Reveal How MSI-H Tumors Depend on WRN Helicase

Skip to content The CRC Digest ◇ RESEARCH CRISPR Screens Reveal How MSI-H Tumors Depend on WRN Helicase Genome-wide CRISPR screens identified SMARCAL1 as a key modulator of WRN dependency in MSI-H colorectal cancer, with loss of SMARCAL1 rendering cells resistant to the WRN inhibitor HRO761. The findings shed light on

DR5/Ligase 3 feedback loop drives immunogenicity in dMMR/MSI CRC

Skip to content The CRC Digest DR5/Ligase 3 feedback loop drives immunogenicity in dMMR/MSI CRC Preclinical study investigated why dMMR/MSI colorectal cancers are intrinsically immunogenic and why some do not respond or develop resistance to immune checkpoint inhibitors. (Gastroenterology) This content is informational only and does not