O. J. Sansom

This study identifies an oncofetal cell state that contributes to resistance in colorectal cancer and shows that targeting both this state and LGR5+ CSCs is needed for effective treatment.

This study shows eIF4A1 is critical for supporting translational demands in Wnt-driven colorectal cancers, while eIF4A2 loss accelerates tumourigenesis, and eFT226 inhibits eIF4A1 function in these models.

This study shows ALDH1A3 and ACSS2 coordinate acetaldehyde-acetyl-CoA metabolism with histone acetylation in melanoma, contributing to transcriptional heterogeneity and drug resistance.

This study shows that wild-type KRAS suppresses tumour growth and metastasis in KRAS mutant colorectal cancer while enhancing resistance to MEK inhibition.

This study shows that loss of wild-type Kras enhances oncogenic Kras signaling and promotes pancreatic ductal adenocarcinoma, while also increasing sensitivity to MEK1/2 inhibitors.

The paper shows that eIF4A2, a negative regulator of mRNA translation, promotes ECM deposition to accelerate HCC initiation by influencing integrin-mediated signaling and senescence exit.

This study uses metabolomics to stratify colorectal cancer tissues and identifies adenosylhomocysteinase as a potential therapeutic target.

This study identifies mutation-induced phenotypic plasticity as a driver of a pro-metastatic tumour-intrinsic niche in BRAF-mutant colorectal cancer.

This study identifies SHANK3 as a RAS interactor that limits oncogenic KRAS signaling, and shows that disrupting its interaction with KRAS induces cell death in KRAS-mutant cancers.

This study uses spatial transcriptomics to identify prognostic immune and stromal subgroups in colorectal cancer liver metastases, revealing distinct transcriptomic programs associated with survival outcomes.

This study shows aspirin reprograms colorectal cancer cell metabolism and increases sensitivity to glutaminase inhibition, suggesting potential for improved metabolic therapies in CRC.

The paper develops three methods to classify mouse colorectal cancer models into human CMS subtypes, finding that pathway-level classifiers outperform gene-level ones for accurate subtype identification.

This study shows that β-catenin signaling in colon cancer cells reduces BTNL expression, impairing γδ T cell immunosurveillance and promoting tumor progression.

This study shows that mTORC1 is essential for CLL progression in mice, with rapamycin effectively targeting eEF2 to inhibit proliferation and MCL1 expression.

The paper shows that transcriptional signatures in tumour samples can be misinterpreted due to stromal influences, affecting alignment with preclinical data.

This study shows that loss of BCL-3 increases DNA damage and reduces homologous recombination in colorectal cancer cells, suggesting BCL-3 as a potential target to enhance DNA damage therapy response.

This study identifies Ly6G expression levels as a marker for neutrophil maturation stages and shows spleen-derived neutrophils mature faster with distinct transcriptional profiles.

The paper shows that Rpl24Bst mutation suppresses colorectal cancer by enhancing eEF2 phosphorylation through eEF2K, reducing protein synthesis and tumorigenesis.

This study shows that extracellular matrix components, specifically laminin, control stem cell specification and crypt morphology in the gut, with laminin promoting adult stem cell features and crypt-like structures.

This study identifies cyclocreatine as a dual-action inhibitor of prostate cancer by blocking the phosphagen system and increasing S-adenosyl methionine levels.

This study re-evaluates lineage tracing in Axin2CreERT2 mice and reports absence of pericentral hepatocyte expansion and altered Wnt pathway physiology.

The paper shows cancer cells in organoids eliminate wild-type cells through apoptosis and JNK signaling, promoting their own growth by forcing cell death and fate change in competing cells.

This study shows that LRG1 promotes tumor vascular dysfunction and suppresses immunotherapy effectiveness, with its inhibition enhancing therapeutic outcomes in mouse cancer models.

This study shows RAL GTPases activate EGFR/MAPK signaling in intestinal stem cells, promoting proliferation and tumorigenesis, but are independent of oncogenic RAS.

This study shows that KRASG12D mutant cells are outcompeted by wild-type cells in the adult pancreas, dependent on EphA2 signaling, leading to tissue clearance and reduced premalignant lesions.

This study identifies EpCAMlo colon cancer cells with phenotypic plasticity, linking Wnt/β-catenin signaling and EMT activation to metastasis and poor prognosis.

The paper shows aspirin reduces Wnt-driven stem-like traits in intestinal organoids by increasing DKK-1, suggesting a mechanism for its anti-cancer effects.

This study shows that non-canonical HIF-1 stabilization is crucial for intestinal tumorigenesis, independent of hypoxia, by affecting both epithelial and microenvironmental oncogenic processes.