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Issues

Cancer Research

Table of Contents


In the Spotlight

Review

Resource Report

The Lung Cancer Autochthonous Model Gene Expression Database (LCAMGDB) provides a comprehensive and accessible resource for the research community to investigate lung cancer biology in mouse models.

Cancer Biology

Palmitic acid accumulation activates the NF-κB pathway in colorectal cancer cells to promote cytokine secretion that facilitates the generation of matrix cancer-associated fibroblasts, driving extracellular matrix remodeling and development of obstructions.

CRISPR-knockout screen in 3D tumor spheroid revealed that SMARCA4, a SWI/SNF ATPase subunit, suppresses triple-negative breast cancer growth and metastasis by increasing ARHGAP29 transcription and inhibiting the RHOA signaling pathway.

Intratumoral F. nucleatum activates NF-κB signaling to facilitate gastric cancer immune evasion by promoting tumor-associated neutrophil recruitment that sensitizes tumors to immune checkpoint blockade therapy.

Cancer Immunology

Elevated itaconate production by macrophages induced by IFNγ is a critical negative feedback immunoregulatory metabolic response to anti-PD-1 immunotherapy that inhibits the cross-priming function of dendritic cells and confers immunotherapy resistance.

Cancer Metabolism and Molecular Mechanisms

Sunitinib treatment induces metabolic reprogramming to provide essential metabolite building blocks for tumor survival, resistance, and progression by upregulating serine biosynthesis, which represents a targetable dependency to enhance therapeutic efficacy.

Therapeutic Development and Chemical Biology

Sherpabodies represent a biological targeting technology that could help extend the success of CAR T-cell therapy from treating leukemias and lymphomas to the treatment of solid cancers.

Translational Cancer Biology

PARP inhibitor sensitivity is associated with cGAS–STING–IFN signaling, which can be harnessed by combining PARP inhibitors with STING agonists to overcome acquired resistance and requires NK cells to mediate antitumor immunity.

FADD promotes progression of tumors with chr11q13.3 amplification by binding to the DNA helicase complex, which can be targeted in combination with cyclin D1 as a viable therapeutic strategy for HNSCC patients.

Cancer Landscapes

Analysis of tumors from various populations can broadly characterize genomic landscapes and enhance precision medicine strategies.

Editor’s Note

Retractions

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