ArticlePathology2013
Prohibitin expression is associated with high grade breast cancer but is not a driver of amplification at 17q21.33.
Article in Pathology, 2013. 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
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Structural basis for prohibitin-mediated regulation of mitochondrial m-AAA protease.Nature communications · 2026Article
- Pan-cancer Analysis Combined with Experiments Deciphers PHB Regulation for Breast Cancer Cell Survival and Predicts Biomarker Function.Combinatorial chemistry & high throughput screening · 2024Article
- Targeting Prohibitins to Inhibit Melanoma Growth and Overcome Resistance to Targeted Therapies.Cells · 2023Article
- Prohibitin participates in the HIRA complex to promote cell metastasis in breast cancer cell lines.FEBS open bio · 2020Article
- Prohibitin is a prognostic marker and therapeutic target to block chemotherapy resistance in Wilms' tumor.JCI insight · 2019Article
- Review
- Estrogen Enhances Endometrial Cancer Cells Proliferation by Upregulation of Prohibitin.Journal of Cancer · 2019Article
- Genetic determinants of sporadic breast cancer in Sri Lankan women.BMC cancer · 2018Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 2 countries.
Funding
Abstract
aimsIn a study of ductal carcinoma in situ of the breast, we identified five genes at chromosome 17q21.33 that were over-expressed in high grade cases, and showed a correlation between expression and gene copy number. The aim of this study was to investigate potential drivers of genomic amplification at 17q21.33.
methodsAnalysis of high resolution comparative genomic hybridisation and published data specified a minimum region of amplification at 17q21.33. Prohibitin (PHB) expression was examined by immunohistochemistry in 285 invasive breast cancers. Gene copy number was examined by fluorescence in situ hybridisation.
resultsThe minimum region of amplification at 17q21.33 included ten genes with PHB selected as a candidate driver. Increased PHB expression was associated with higher grade breast cancer and poorer survival. Amplification of PHB was detected in 13 of 235 cases (5.5%) but was not associated with PHB expression. PHB amplification was most common in the ERBB2+ breast cancer subtype, although high expression was most prevalent in basal-like and luminal B cancers.
conclusionsAmplification at 17q21.33 is a recurrent feature of breast cancer that forms part of a 'firestorm' pattern of genomic aberration. PHB is not a driver of amplification, however PHB may contribute to high grade breast cancer.
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