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EGFR

Combined Inhibition of SHP2 and CXCR1/2 Promotes Anti-Tumor T Cell Response in NSCLC

[Cancer Discovery] The authors found that SHP2 inhibitor treatment depleted alveolar and M2-like macrophages, induced tumor-intrinsic CCL5/CXCL10 secretion and promoted B and T lymphocyte infiltration in Kras- and Egfr-mutant non-small cell lung cancer.

Coregulation of Pathways in Lung Cancer Patients with EGFR Mutation: Therapeutic Opportunities

[British Journal of Cancer] Scientists highlight regulatory mechanisms and signaling pathways that cause therapy-induced resistance to epidermal growth factor receptor tyrosine kinase inhibitors.

Integrative Oncogene-Dependency Mapping Identifies RIT1 Vulnerabilities and Synergies in Lung Cancer

[Nature Communications] Scientists investigated the oncogene-specific dependencies conferred by the lung cancer oncogene, RIT1. Genome-wide CRISPR screening in KRAS, EGFR, and RIT1-mutant isogenic lung cancer cells identifies shared and unique vulnerabilities of each oncogene..

STAT3 Mediated Upregulation of C-MET Signaling Acts as a Compensatory Survival Mechanism upon EGFR Family Inhibition in Chemoresistant Breast Cancer Cells

[Cancer Letters] Investigators reported that the upregulated C-MET signaling acted as a compensatory mechanism that sustained the proliferation of chemoresistant cells in which EGFR family signaling was attenuated.

Targeting Gi/O Protein-Coupled Receptor Signaling Blocks HER2-Induced Breast Cancer Development and Enhances HER2-Targeted Therapy

[JCI Insight] In mammary epithelial cells of transgenic mouse models, and breast cancer cell lines, HER2 hyperactivation altered GPCR expression, particularly, Gi/o-GPCRs.

CRYβB2 Enhances Tumorigenesis through Upregulation of Nucleolin in Triple Negative Breast Cancer

[Oncogene] Researchers reported that the expression of CRYβB2 in breast cancer cells increased stemness, growth, and metastasis. Transcriptomics data revealed that CRYβB2 upregulated genes that were functionally associated with unfolded protein response, oxidative phosphorylation, and DNA repair, while down-regulating genes related to apoptosis.

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