ArticleCancer cell2011
Mad2 is a critical mediator of the chromosome instability observed upon Rb and p53 pathway inhibition.
Article in Cancer cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
117 citing papers in PubMed, 1 synthesis or guideline pooled it, 180 citations in OpenAlex.
- Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.Nucleic acids research · 2016Pooled it
- Dual Inhibition of TRIP13 and Aurora A Induces Mitotic DNA Damage and Concurrent Pyroptotic-Apoptotic Cell Death in Rb-Deficient Cancer Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Identification of targetable vulnerabilities of PLK1-overexpressing cancers by synthetic dosage lethality.Cell genomics · 2025Article
- MAD2L1 supports MYC-driven liver carcinogenesis in mice and predicts poor prognosis in human hepatocarcinoma.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- TSG101 depletion dysregulates mitochondria and PML NBs, triggering MAD2-overexpressing interphase cell death (MOID) through AIFM1-PML-DAXX pathway.Cell death & disease · 2024Article
- Targeting chromosomal instability in patients with cancer.Nature reviews. Clinical oncology · 2024Review
- Mechanical stress during confined migration causes aberrant mitoses and c-MYC amplification.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Genomic and transcriptomic profiling of combined small-cell lung cancer through microdissection: unveiling the transformational pathway of mixed subtype.Journal of translational medicine · 2024Article
- RB loss sensitizes cells to replication-associated DNA damage after PARP inhibition by trapping.Life science alliance · 2023Article
- Biallelic MAD2L1BP (p31comet) mutation is associated with mosaic aneuploidy and juvenile granulosa cell tumors.JCI insight · 2023Article
- Targeting TRIP13 for overcoming anticancer drug resistance (Review).Oncology reports · 2023Article
- Pathogenesis of cancers derived from thyroid follicular cells.Nature reviews. Cancer · 2023Review
- HPV16 E6 induces chromosomal instability due to polar chromosomes caused by E6AP-dependent degradation of the mitotic kinesin CENP-E.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Combined TRIP13 and Aurora Kinase Inhibition Induces Apoptosis in Human Papillomavirus-Driven Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Chromosomal instability as a source of genomic plasticity.Current opinion in genetics & development · 2022Review
- BUB3, beyond the Simple Role of Partner.Pharmaceutics · 2022Review
- Kinetochore-associated protein 1 promotes the invasion and tumorigenicity of cervical cancer cells via matrix metalloproteinase-2 and matrix metalloproteinase-9.Bioengineered · 2022Article
- SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7.Cell death & disease · 2022Article
- Hepatocellular Carcinoma: Current Therapeutic Algorithm for Localized and Advanced Disease.Journal of oncology · 2022Review
- Phosphorylation of MAD2 at Ser195 Promotes Spindle Checkpoint Defects and Sensitizes Cancer Cells to Radiotherapy in ATM Deficient Cells.Frontiers in cell and developmental biology · 2022Article
57 more citing papers are in PubMed but not listed here.
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5 authors at 1 institution in 1 country.
Funding
Abstract
Multiple mechanisms have been proposed to explain how Rb and p53 tumor suppressor loss lead to chromosome instability (CIN). It was recently shown that Rb pathway inhibition causes overexpression of the mitotic checkpoint gene Mad2, but whether Mad2 overexpression is required to generate CIN in this context is unknown. Here, we show that CIN in cultured cells lacking Rb family proteins requires Mad2 upregulation and that this upregulation is also necessary for CIN and tumor progression in vivo. Mad2 is also repressed by p53 and its upregulation is required for CIN in a p53 mutant tumor model. These results demonstrate that Mad2 overexpression is a critical mediator of the CIN observed upon inactivation of two major tumor suppressor pathways.
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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.