ArticleJournal of clinical pathology2005
Increased E2F-1 expression via tumour cell proliferation and decreased apoptosis are correlated with adverse prognosis in patients with squamous cell carcinoma of the oesophagus.
Article in Journal of clinical pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- CD70 drives cSCC growth by linking DNA damage response, inflammation, and tumor-stromal signaling.Cell death & disease · 2026Article
- CD70 drives cSCC growth by linking DNA damage response, inflammation, and tumor-stromal signaling.Research square · 2025Article
- Expression of PIM-1 in salivary gland adenoid cystic carcinoma: Association with tumor progression and patients' prognosis.Oncology letters · 2018Article
- Analysis of salivary microRNA expression profiles and identification of novel biomarkers in esophageal cancer.Oncology letters · 2017Article
- Identification of Predictive DNA Methylation Biomarkers for Chemotherapy Response in Colorectal Cancer.Frontiers in pharmacology · 2017Article
- ZNF282 (Zinc finger protein 282), a novel E2F1 co-activator, promotes esophageal squamous cell carcinoma.Oncotarget · 2014Article
- Transcription addiction: can we garner the Yin and Yang functions of E2F1 for cancer therapy?Cell death & disease · 2014Review
- Role of E2F-1 and its involving pathway in esophageal squamous cell carcinoma.Thoracic cancer · 2014Article
- E2F transcription factors and digestive system malignancies: how much do we know?World journal of gastroenterology · 2013Review
- Clinical significance of E2F1 protein expression in non-small cell lung cancer.Experimental hematology & oncology · 2012Article
- E2F-1 is overexpressed and pro-apoptotic in human hepatocellular carcinoma.Virchows Archiv : an international journal of pathology · 2012Article
- Glycogen synthase kinase 3 beta: can it be a target for oral cancer.Molecular cancer · 2010Review
- Modulation of the E2F1-driven cancer cell fate by the DNA damage response machinery and potential novel E2F1 targets in osteosarcomas.The American journal of pathology · 2009Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe retinoblastoma (Rb) pathway, which governs cell cycle progression, is frequently genetically altered in cancer, causing deregulated expression of the E2F-1 transcription factor, which promotes DNA synthesis and cell cycle progression. Recent studies show that E2F-1 also participates in apoptosis induction in a p53 dependent or independent manner. Despite its crucial role and paradoxical effects on cell turnover, the function of E2F-1 in human cancer is unclear.
aimsTo evaluate E2F-1 expression using immunohistochemistry in 43 surgically resected oesophageal squamous cell carcinoma (OSCC) specimens.
methodsThis study analysed the association of E2F-1 with tumour cell proliferation and apoptosis and the upstream regulators modulating these processes, and its impact on patient outcome. Tumour cell proliferation and apoptosis were assessed as percentage of MIB-1 positive or apoptotic cells (MIB-1 labelling index (MI) and apoptotic index (AI)), respectively.
resultsEntire specimens showed abnormal expression of one or more upstream regulators of pRb/E2F-1. Although E2F-1 positivity was not associated with the expression of upstream regulators, it showed a linear and positive correlation with MI but not AI. Patients with high MI, low AI, or high E2F-1 positivity had significantly shorter recurrence free survival. By multivariate analysis, high MI and low AI were independently associated with recurrence free survival, but E2F-1 was not.
conclusionsIncreased cell proliferation and decreased apoptosis are associated with adverse prognosis in patients with OSCC. Although E2F-1 remains a controversial prognostic factor, its expression was closely associated with tumour cell proliferation and might influence clinical outcome, mainly via cell cycle progression.
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