ArticleBritish journal of cancer2022
Topoisomerase I poison-triggered immune gene activation is markedly reduced in human small-cell lung cancers by impairment of the cGAS/STING pathway.
Article in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- BUB signaling in cancer and molecular insights into targeted therapies.Communications biology · 2026Review
- Exploring the immunological effects of antibody-drug conjugates.Nature reviews. Clinical oncology · 2026Review
- Review
- Advances in Cancer Immunotherapy for Solid Tumors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Understanding and Overcoming Antibody-Drug Conjugate Resistance: Biological Mechanisms and Emerging Analytical Frameworks in Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- cGAS-STING pathway regulated by spatiotemporal heterogeneity of tumor microenvironment and precision therapy strategies in lung cancer.Journal of experimental & clinical cancer research : CR · 2026Review
- cGAS-STING pathway in lung cancer and emerging therapeutic approaches.Drug discovery today · 2026Review
- Novel anti-HER2 nanobody-drug conjugates with enhanced penetration of solid tumor and BBB, reduced systemic exposure and superior antitumor efficacy.Acta pharmacologica Sinica · 2026Article
- The cGAS-STING pathway in tumor immunity: dual roles, regulatory mechanisms, and precision therapeutic strategies.Frontiers in pharmacology · 2026Review
- Lamin A/C loss promotes R-loop-mediated genomic instability and poor survival in small-cell lung cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- DNA remnants in red blood cells enable early detection of cancer.Cell research · 2025Article
- Nanocarrier-mediated modulation of cGAS-STING signaling pathway to disrupt tumor microenvironment.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Lamin A/C Deficiency Drives Genomic Instability and Poor Survival in Small-Cell Lung Cancer through Increased R-loop Accumulation.bioRxiv : the preprint server for biology · 2025Article
- Advances in radiotherapy enhancing the efficacy of immune checkpoint inhibitors in malignant.Frontiers in oncology · 2025Review
- Stimulation of cGAS-STING pathway as a challenge in the treatment of small cell lung cancer: a feasible strategy?British journal of cancer · 2024Review
- Immunomodulatory effects of trastuzumab deruxtecan through the cGAS-STING pathway in gastric cancer cells.Cell communication and signaling : CCS · 2024Article
- PLX038A, a long-acting SN-38, penetrates the blood-tumor-brain-barrier, accumulates and releases SN-38 in brain tumors to increase survival of tumor bearing mice.Scientific reports · 2024Article
- A platform technology for ultra-long acting intratumoral therapy.Scientific reports · 2024Article
- Human DNA topoisomerase I poisoning causes R loop-mediated genome instability attenuated by transcription factor IIS.Science advances · 2024Article
- Activation of STING by the novel liposomal TLC388 enhances the therapeutic response to anti-PD-1 antibodies in combination with radiotherapy.Cancer immunology, immunotherapy : CII · 2024Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundCurrent immunotherapy strategies have contrasting clinical results in human lung cancer patients as small-cell lung cancers (SCLC) often show features of immunological cold tumours. Topoisomerase 1 (TOP1) poisons are effective antitumor drugs with good efficacy against lung cancers.
methodsWe used molecular, genetic and bioinformatic approaches to determine the mechanism of micronuclei formation induced by two TOP1 poisons in different human cancer cells, including SCLC cell lines.
resultsTOP1 poisons stimulate similar levels of micronuclei in all tested cell lines but downstream effects can vary markedly. TOP1 poisons increase micronuclei levels with a mechanism involving R-loops as overexpression of RNaseH1 markedly reduces or abolishes both H2AX phosphorylation and micronuclei formation. TOP1 poison-induced micronuclei activate the cGAS/STING pathway leading to increased expression of immune genes in HeLa cells, but not in human SCLC cell lines, mainly due to lack of STING and/or cGAS expression. Moreover, the expression of STING and antigen-presenting machinery genes is generally downregulated in patient tumours of human lung cancer datasets.
conclusionsAltogether, our data reveal an immune signalling mechanism activated by TOP1 poisons, which is often impaired in human SCLC tumours.
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