ArticleScience advances2022
Therapeutic inhibition of the SRC-kinase HCK facilitates T cell tumor infiltration and improves response to immunotherapy.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Integrated network pharmacology and serum metabolomics to reveal the protective mechanism of methanolic extract of BaiYangJie on cisplatin-induced acute kidney injury in mice.Experimental and therapeutic medicine · 2026Article
- Review
- Hematopoietic cell kinase regulates microglial/macrophage activation to drive neuroinflammation after traumatic brain injury.Cell communication and signaling : CCS · 2026Article
- A trispecific antibody engaging T cells with tumour and myeloid cells augments antitumour immunity.Nature biomedical engineering · 2026Article
- Microenvironmental regulation of solid tumour resistance to CAR T cell therapy.Nature reviews. Immunology · 2026Review
- The myeloid SRC family kinase HCK regulates breast cancer growth by activating tumor-associated macrophage-led invasion and inhibiting cytotoxic T cell activity.Frontiers in immunology · 2026Article
- CAR T Cell Therapy in Lung Cancer: Overcoming Tumor Microenvironment-Mediated Barriers.International journal of biological sciences · 2026Review
- Hck promotes IL-1β-induced extracellular matrix degradation, inflammation, and apoptosis in osteoarthritis via activation of the JAK-STAT3 signaling pathway.Advances in rheumatology (London, England) · 2024Article
- Generation of novel lipid metabolism-based signatures to predict prognosis and immunotherapy response for colorectal adenocarcinoma.Scientific reports · 2024Article
- Mechanisms of cellular crosstalk in the gastric tumor microenvironment are mediated by YAP1 and STAT3.Life science alliance · 2024Article
- A tuft cell - ILC2 signaling circuit provides therapeutic targets to inhibit gastric metaplasia and tumor development.Nature communications · 2023Article
- HCK induces macrophage activation to promote renal inflammation and fibrosis via suppression of autophagy.Nature communications · 2023Article
- The proto-oncogene SRC phosphorylates cGAS to inhibit an antitumor immune response.JCI insight · 2023Article
- Small-molecule toosendanin reverses macrophage-mediated immunosuppression to overcome glioblastoma resistance to immunotherapy.Science translational medicine · 2023Article
- Tumor Growth Remains Refractory toCells · 2022Article
- Enhancing therapeutic anti-cancer responses by combining immune checkpoint and tyrosine kinase inhibition.Molecular cancer · 2022Review
- The role of lipid metabolism in tumor immune microenvironment and potential therapeutic strategies.Frontiers in oncology · 2022Review
- Comprehensive analysis of the HCK gene in myeloid neoplasms: Insights into biological functions, prognosis, and response to antineoplastic agents.Hematology, transfusion and cell therapyArticle
Corrections and comments
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Authors and funding
23 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although immunotherapy has revolutionized cancer treatment, many immunogenic tumors remain refractory to treatment. This can be largely attributed to an immunologically "cold" tumor microenvironment characterized by an accumulation of immunosuppressive myeloid cells and exclusion of activated T cells. Here, we demonstrate that genetic ablation or therapeutic inhibition of the myeloid-specific hematopoietic cell kinase (HCK) enables activity of antagonistic anti-programmed cell death protein 1 (anti-PD1), anti-CTLA4, or agonistic anti-CD40 immunotherapies in otherwise refractory tumors and augments response in treatment-susceptible tumors. Mechanistically, HCK ablation reprograms tumor-associated macrophages and dendritic cells toward an inflammatory endotype and enhances CD8
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.