Newsletters

US FDA Grants Full Approval to Pfizer’s BRAFTOVI Combination Regimen in First-Line Metastatic Colorectal Cancer

[Pfizer Inc. ] Pfizer Inc., announced that the US FDA has granted full approval to BRAFTOVI® in combination with cetuximab and fluorouracil-based chemotherapy for the treatment of adult patients with metastatic colorectal cancer with a BRAF V600E mutation based on results from the global Phase III BREAKWATER trial.

Five Global Teams Awarded $125 Million to Take on the Toughest Challenges at the Frontiers of Cancer Science

[Cancer Grand Challenges (Business Wire)] Cancer Grand Challenges, a global initiative co-founded by the National Cancer Institute in the US and Cancer Research UK, announced a major $125m commitment to propel cancer research into uncharted territory.

Villification of the Intestinal Epithelium Is Driven by Foxl1 through Activation of PDGFRα and BMPs

[Nature Communications] Investigators set out to determine the molecular targets and pathways controlled by Foxl1 during intestinal villification

Systematic Analysis of Functional Genetic and Epigenetic Variants in Colorectal Cancer

[Science Advances] Scientists adapted and applied two high-throughput techniques, SNP-STARR-seq and Methyl-STARR-seq, to systematically evaluate the influence of 30,790 noncoding SNPs and more than 134,000 CpG sites on enhancer activity in primary and metastatic CRC cells.

PKM2 Lactylation Promotes Colorectal Cancer Vasculogenic Mimicry and Bevacizumab Resistance by Facilitating FOSL1 Super-Enhancer Formation

[Cancer Research] Researchers revealed lactylation as a metabolic switch linking cancer glycolytic reprogramming to transcriptional rewiring and proposes targeting PKM2 lactylation to enhance the anti-tumor activity of bevacizumab in colorectal cancer.

P53 and Fatty Acids Collaborate to Trigger Ferroptosis via the FBXO2-FABP5 Axis in Colorectal Cancer

[Redox Biology] The authors revealed that p53 induces ferroptosis in the presence of abundant polyunsaturated fatty acids (PUFAs). They uncovered that the availability of PUFAs is crucial for p53 to exert a pro-ferroptotic function in colorectal cancer.

Glucose Metabolism Sustains Aberrant STAT3 Signaling in Colorectal Cancer through Glycosylated Local Signaling Factor

[Science Signaling] Investigators demonstrated that glucose sustained STAT3 activation independently of cytokine availability. Their findings showed how glucose metabolism supports sustained STAT3 activation in colorectal cancer.

Claudin18.2 Promote Gastric Cancer Proliferation by Activating MCM2/5

[Scientific Reports] Researchers found that knockdown of claudin18.2 (CLDN18.2) inhibited tumor growth in vivo and in vitro. Additionally, CLDN18.2 knockdown down-regulated minichromosome maintenance (MCM) proteins and decreased phosphorylation of ERK, CDK, and MCM2 in gastric cancer cells.

The TAAR1 Antagonist EPPTB Ameliorates Colitis via Serotonin Inhibition

[Biochemistry and Biophysics Reports] Scientists evaluated the effects of the TAAR1 antagonist EPPTB in a DSS-induced colitis model, focusing on inflammation, barrier function, and serotonin signaling, to explore its therapeutic potential.

Reshaping the Colorectal Cancer Immune Microenvironment: Insights from Single-Cell and Spatial Omics

[Cancer Cell International] Investigators synthesize single-cell RNA sequencing and spatial transcriptomic studies of colorectal cancer to characterize cellular heterogeneity and to delineate spatial niche organization and functional crosstalk within the tumor microenvironment.

Lipid Metabolism Drives Dietary Effects on T Cell Ferroptosis and Immunity

[Nature] Ferroptosis resistance of human T cells correlated with plasma lipid profiles across multiple healthy cohorts, exhibiting negative associations with polyunsaturated and monounsaturated fatty acids ratios in major lipid classes.

Immune Mechanisms of Viral, Autoimmune, and Immune Checkpoint Inhibitor-Associated Myocarditis

[Immunological Reviews] The authors integrate human studies with mechanistic models to map convergent pathways that connect pattern-recognition signaling, antigen presentation, and T- and B cell responses with monocyte and macrophage networks that drive injury, fibrosis, and electrical instability.
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