ArticleBritish journal of cancer2012
The cyclin-dependent kinase inhibitor p57(Kip2) is epigenetically regulated in carboplatin resistance and results in collateral sensitivity to the CDK inhibitor seliciclib in ovarian cancer.
Article in British journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 25 citations in OpenAlex.
- Multifaceted Integrated Analysis of CDK1 and TOP2A Signaling Pathways for Multi-Target Therapeutic Intervention in Epithelial Ovarian Cancer.International journal of molecular sciences · 2026Article
- Development and validation of a computational tool to predict treatment outcomes in cells from high-grade serous ovarian cancer patients.Bioengineering & translational medicine · 2025Article
- Integrated Analysis, Machine Learning, Molecular Docking and Dynamics of CDK1 Inhibitors in Epithelial Ovarian Cancer: A Multifaceted Approach Towards Targeted Therapy.International journal of molecular sciences · 2025Article
- DNA Methylation Biomarkers for Prediction of Response to Platinum-Based Chemotherapy: Where Do We Stand?Cancers · 2022Review
- Article
- Resistance to cis- and carboplatin initiated by epigenetic changes in ovarian cancer patients.Cancer drug resistance (Alhambra, Calif.) · 2019Review
- Epigenetic silencing of downstream genes mediated by tandem orientation in lung cancer.Scientific reports · 2017Article
- Tumor suppressor genes and their underlying interactions in paclitaxel resistance in cancer therapy.Cancer cell international · 2016Review
- Broad targeting of resistance to apoptosis in cancer.Seminars in cancer biology · 2015Review
- Relevance of immunohistochemical expression of p57kip2 in epithelial ovarian carcinoma- A systematic literature review.Journal of ovarian research · 2012Article
- Polo Like Kinase 2 Tumour Suppressor and cancer biomarker: new perspectives on drug sensitivity/resistance in ovarian cancer.Oncotarget · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCarboplatin remains a first-line agent in the management of epithelial ovarian cancer (EOC). Unfortunately, platinum-resistant disease ultimately occurs in most patients. Using a novel EOC cell line with acquired resistance to carboplatin: PEO1CarbR, genome-wide micro-array profiling identified the cyclin-dependent kinase inhibitor p57(Kip2) as specifically downregulated in carboplatin resistance. Presently, we describe confirmation of these preliminary data with a variety of approaches.
methodsCytotoxicity testing (MTT) and cell cycle blockade assessed drug responsiveness. Methylation specific PCR and pyrosequencing identified sites of promoter methylation in p57(Kip2). siRNA to p57(Kip2) was used to look at the changes in apoptosis of carboplatin treated EOC cells. EOC tissues (20 cases) were assessed for mRNA levels of p57(Kip2).
resultsCarboplatin resistance was reversed using 5-aza-cytidine in vitro. Promoter methylation sites and preferential sensitivity to seliciclib were seen in PEO1CarbR cells. Silencing p57(Kip)2 decreased the apoptotic response to the effects of platinum but produced sensitisation to seliciclib. EOC biopsies indicated an association of high levels of p57(Kip2)mRNA with complete responses to chemotherapy and improved outcome.
conclusionWe conclude that p57(Kip2) is a candidate biomarker of platinum sensitivity/resistance in EOC and such cases may show preferential response to the cyclin-dependent kinase inhibitor seliciclib.
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.