ArticleGenes & development2004
Hypoxia and defective apoptosis drive genomic instability and tumorigenesis.
Article in Genes & development, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
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Who cites it
131 citing papers in PubMed.
- Response prediction of neoadjuvant chemoradiation therapy in locally advanced rectal cancer using CT-based fractal dimension analysis.European radiology · 2022Trial
- Hypoxia-inducible factors: Regulatory functions and status as a therapeutic target in gastric cancer (Review).Oncology letters · 2026Review
- Magnetic resonance imaging signal variation for the effective quantitative evaluation of treatment response to neoadjuvant immunotherapy of osteosarcoma: a comparative study with Response Evaluation Criteria in Solid Tumors version 1.1.Quantitative imaging in medicine and surgery · 2026Article
- MRI-derived radiomics for risk stratification of tumor deposits in rectal cancer: a dual-center study.Insights into imaging · 2026Article
- Generative adversarial networks: multiparametric, multiregion super-resolution MRI in predicting lymph node metastasis in rectal cancer.Insights into imaging · 2026Article
- Research progress in multimodal radiomics of rectal cancer tumors and peritumoral regions in MRI.Abdominal radiology (New York) · 2025Review
- Habitat-based transformer model in pretreatmentBMC cancer · 2025Article
- Tumor microenvironment and immunotherapy: from bench to bedside.Medical oncology (Northwood, London, England) · 2025Review
- Integrating radiomics features and CT semantic characteristics for predicting visceral pleural invasion in clinical stage Ia peripheral lung adenocarcinoma.Discover oncology · 2025Article
- Texture analysis of CT colonography to develop a novel imaging biomarker for the management of colorectal cancer.Annals of gastroenterological surgery · 2025Article
- Hypoxia and activation of hypoxia inducible factor alpha as influencers of inflammatory helper T cells in autoimmune disease - a link between cancer and autoimmunity.Frontiers in immunology · 2025Review
- Autophagy and cancer therapy.Cancer letters · 2024Review
- Nomogram of magnetic resonance imaging (MRI) histogram analysis to predict telomerase reverse transcriptase promoter mutation status in glioblastoma.Quantitative imaging in medicine and surgery · 2024Article
- Perinatal arterial ischemic stroke: how informative is the placenta?Virchows Archiv : an international journal of pathology · 2024Article
- Nanoparticles in tumor microenvironment remodeling and cancer immunotherapy.Journal of hematology & oncology · 2024Review
- T2WI-based MRI radiomics for the prediction of preoperative extranodal extension and prognosis in resectable rectal cancer.Insights into imaging · 2024Article
- Tumor Heterogeneity of Breast Cancer Assessed with Computed Tomography Texture Analysis: Association with Disease-Free Survival and Clinicopathological Prognostic Factor.Diagnostics (Basel, Switzerland) · 2023Article
- MRI-based multiregional radiomics for preoperative prediction of tumor deposit and prognosis in resectable rectal cancer: a bicenter study.European radiology · 2023Article
- Radiomics from Mesorectal Blood Vessels and Lymph Nodes: A Novel Prognostic Predictor for Rectal Cancer with Neoadjuvant Therapy.Diagnostics (Basel, Switzerland) · 2023Article
- A Comprehensive Pan-Cancer Analysis of the Regulation and Prognostic Effect of Coat Complex Subunit Zeta 1.Genes · 2023Article
71 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors.
Funding
Abstract
Genomic instability is a hallmark of cancer development and progression, and characterizing the stresses that create and the mechanisms by which cells respond to genomic perturbations is essential. Here we demonstrate that antiapoptotic BCL-2 family proteins promoted tumor formation of transformed baby mouse kidney (BMK) epithelial cells by antagonizing BAX- and BAK-dependent apoptosis. Cell death in vivo correlated with hypoxia and induction of PUMA (p53 up-regulated modulator of apoptosis). Strikingly, carcinomas formed by transformed BMK cells in which apoptosis was blocked by aberrant BCL-2 family protein function displayed prevalent, highly polyploid, tumor giant cells. Examination of the transformed BMK cells in vivo revealed aberrant metaphases and ploidy changes in tumors as early as 9 d after implantation, which progressed in magnitude during the tumorigenic process. An in vitro ischemia system mimicked the tumor microenvironment, and gain of BCL-2 or loss of BAX and BAK was sufficient to confer resistance to apoptosis and to allow for accumulation of polyploid cells in vitro. These data suggest that in vivo, even in cells in which p53 function is compromised, apoptosis is an essential response to hypoxia and ischemia in the tumor microenvironment and that abrogation of this response allows the survival of cells with abnormal genomes and promotes tumorigenesis.
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