ArticleNeoplasia (New York, N.Y.)2025
Kv11.1-dependent senescence activates a lethal immune response via tumor necrosis factor alpha.
Article in Neoplasia (New York, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
5 citing papers in PubMed.
- Potassium channels in cancer: from hallmarks to therapeutic targeting.Journal of physiology and biochemistry · 2026Review
- Immune surveillance and immune evasion of senescent cells.Nature reviews. Immunology · 2026Review
- The double-edged sword of SASP in breast cancer: from tumor suppression to progression and therapy resistance.Frontiers in oncology · 2026Review
- Article
- Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.Molecular cancer · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding the complex relationship between cancer and immune surveillance is essential for leveraging the immune system to control tumor growth. In our study, we discovered that activating the Kv11.1 potassium channel in ER+ breast cancer cells induces a senescent phenotype, which in turn triggers a potent immune response against these senescent cells. Specifically, we found that the senescence-associated secretory phenotype (SASP) plays a crucial role in activating CD4+ T-helper 1 (Th1) cells and memory T cell phenotypes. This activation led to the release of tumor necrosis factor-alpha (TNFα), which induced the death of senescent breast cancer cells, independent of their resistance to endocrine therapy. Our findings suggest that Kv11.1 channel-induced cellular senescence in ER+ breast cancer cells is a key mechanism in immune surveillance, driving a lethal immune response through TNFα. These results highlight the potential immunomodulatory role of Kv11.1 activation in ER-positive breast cancer and provide a foundation for future therapeutic investigations.
Indexed as
Identifiers
What OpenQuestion holds
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.