ArticleMethods in molecular biology (Clifton, N.J.)2017
Senescence-Like Phenotypes in Human Nevi.
Article in Methods in molecular biology (Clifton, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- The Molecular and Cellular Strategies of Glioblastoma and Non-Small-Cell Lung Cancer Cells Conferring Radioresistance.International journal of molecular sciences · 2022Review
- Targeting tumor cell senescence and polyploidy as potential therapeutic strategies.Seminars in cancer biology · 2022Review
- Breast Cancer and p16: Role in Proliferation, Malignant Transformation and Progression.Healthcare (Basel, Switzerland) · 2021Article
- Simple Detection Methods for Senescent Cells: Opportunities and Challenges.Frontiers in aging · 2021Review
- A new model to investigate UVB-induced cellular senescence and pigmentation in melanocytes.Mechanisms of ageing and development · 2020Article
- Detection of Gene Mutations in Liquid Biopsy of Melanoma Patients: Overview and Future Perspectives.Current treatment options in oncology · 2020Review
- Aberrant expression of p16Cancer reports and reviews · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cellular senescence is an irreversible arrest of cell proliferation at the G1 stage of the cell cycle in which cells become refractory to growth stimuli. Senescence is a critical and potent defense mechanism that mammalian cells use to suppress tumors. While there are many ways to induce a senescence response, oncogene-induced senescence (OIS) remains the key to inhibiting progression of cells that have acquired oncogenic mutations. In primary cells in culture, OIS induces a set of measurable phenotypic and behavioral changes, in addition to cell cycle exit. Senescence-associated β-Galactosidase (SA-β-Gal) activity is a main hallmark of senescent cells, along with morphological changes that may depend on the oncogene that is activated, or on the primary cell type. Characteristic cellular changes of senescence include increased size, flattening, multinucleation, and extensive vacuolation. At the molecular level, tumor suppressor genes such as p53 and p16
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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.