ArticleOncology letters2014
Effect of tumor suppressor gene cyclin-dependent kinase inhibitor 2A wild-type and A148T mutant on the cell cycle of human ovarian cancer cells.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 10 citations in OpenAlex.
- Cuproptosis in inflammation and cancer: molecular mechanisms and therapeutic targets.Molecular cancer · 2026Review
- Role of cuproptosis in digestive system tumors (Review).International journal of molecular medicine · 2026Review
- Harnessing cuproptosis: a new avenue for targeted cancer therapies.Apoptosis : an international journal on programmed cell death · 2025Review
- Cuproptosis: a promising new target for breast cancer therapy.Cancer cell international · 2024Review
- A cuproptosis-related signature predicts prognosis and indicates cross-talk with immunocyte in ovarian cancer.Discover oncology · 2024Article
- Cuproptosis: mechanisms and links with cancers.Molecular cancer · 2023Review
- C-terminal binding protein-2 promotes cell proliferation and migration in breast cancer via suppression of p16INK4A.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Single-base substitution may affect the function of genes. This study identified a single-base substitution of G for A in codon 148 of cyclin-dependent kinase inhibitor 2A (CDKN2A/p16) by sequencing human ovarian cancer cell line UACC-1598. As a tumor suppressor gene, the expression of CDKN2A/p16 should be strictly controlled. In order to control CDKN2A/p16 gene expression, an inducible pTUNE vector system was selected. Using recombinant DNA technology, a CDKN2A/p16-A148T and CDKN2A/p16-wild-type gene expression system was successfully constructed to investigate whether this single-base substitution affects the function of CDKN2A/p16. For the wild-type and the mutant, expression of CDKN2A/p16-green fluorescent protein fusion protein increased markedly following isopropyl-β-D-thiogalactoside induction, and was accompanied by significant G1 arrest in the transfected human ovarian cancer SKOV3 cell line. The inducible vectors used in this study, CDKN2A/p16-wild-type and CDKN2A/p16-A148T open reading frame, may be useful for further investigation into whether this somatic mutation could alter the function of CDKN2A/p16 as a tumor suppressor gene. In summary, CDKN2A/p16-A148T was identified in ovarian cancer cells, and this single-base substitution did not affect the ability of CDKN2A/p16 to arrest the cell cycle.
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.