ArticleThe Journal of investigative dermatology2017
Oncogene-Expressing Senescent Melanocytes Up-Regulate MHC Class II, a Candidate Melanoma Suppressor Function.
Article in The Journal of investigative dermatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 47 citations in OpenAlex.
- Immune surveillance and immune evasion of senescent cells.Nature reviews. Immunology · 2026Review
- The aryl hydrocarbon receptor (AHR) drives human leukocyte antigen (HLA)-II expression in human melanoma.Journal of experimental & clinical cancer research : CR · 2026Article
- Biological mechanism and immune response of MHC-II expression in tumor cells.Cancer biology & medicine · 2025Review
- The states of senescent cells.Biochemical Society transactions · 2025Review
- Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.Molecular cancer · 2025Review
- Sendotypes predict worsening renal function in chronic kidney disease patients.Clinical and translational medicine · 2025Article
- The Regulation of Cellular Senescence in Cancer.Biomolecules · 2025Review
- Article
- Inhibitory immune checkpoints suppress the surveillance of senescent cells promoting their accumulation with aging and in age-related diseases.Biogerontology · 2024Review
- Review
- Article
- T-cell immunity against senescence: potential role and perspectives.Frontiers in immunology · 2024Review
- Exploring the Complex and Multifaceted Interplay between Melanoma Cells and the Tumor Microenvironment.International journal of molecular sciences · 2023Review
- Cellular senescence and the host immune system in aging and age-related disorders.Biomedical journal · 2023Review
- Cellular Senescence Is Immunogenic and Promotes Antitumor Immunity.Cancer discovery · 2023Article
- The aging kidney is characterized by tubuloinflammaging, a phenotype associated with MHC-II gene expression.Frontiers in immunology · 2023Article
- Senescence and the tumor-immune landscape: Implications for cancer immunotherapy.Seminars in cancer biology · 2022Review
- Comprehensive assessment of cellular senescence in the tumor microenvironment.Briefings in bioinformatics · 2022Article
- Novel cellular senescence-related risk model identified as the prognostic biomarkers for lung squamous cell carcinoma.Frontiers in oncology · 2022Article
- Cellular senescence in cancer: from mechanisms to detection.Molecular oncology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
On acquisition of an oncogenic mutation, primary human and mouse cells can enter oncogene-induced senescence (OIS). OIS is characterized by a stable proliferation arrest and secretion of proinflammatory cytokines and chemokines, the senescence-associated secretory phenotype. Proliferation arrest and the senescence-associated secretory phenotype collaborate to enact tumor suppression, the former by blocking cell proliferation and the latter by recruiting immune cells to clear damaged cells. However, the interactions of OIS cells with the immune system are still poorly defined. Here, we show that engagement of OIS in primary human melanocytes, specifically by melanoma driver mutations NRASQ61K and BRAFV600E, causes expression of the major histocompatibility class II antigen presentation apparatus, via secreted IL-1ß signaling and expression of CIITA, a master regulator of major histocompatibility class II gene transcription. In vitro, OIS melanocytes activate T-cell proliferation. In vivo, nonproliferating oncogene-expressing melanocytes localize to skin-draining lymph nodes, where they induce T-cell proliferation and an antigen presentation gene expression signature. In patients, expression of major histocompatibility class II in melanoma is linked to favorable disease outcome. We propose that OIS in melanocytes is accompanied by an antigen presentation phenotype, likely to promote tumor suppression via activation of the adaptive immune system.
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.