ArticleAmerican journal of cancer research2011
Targeting Rb inactivation in cancers by synthetic lethality.
Article in American journal of cancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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
13 citing papers in PubMed, 19 citations in OpenAlex.
- Cross-species identification of PIP5K1-, splicing- and ubiquitin-related pathways as potential targets for RB1-deficient cells.PLoS genetics · 2021Article
- NatB regulates Rb mutant cell death and tumor growth by modulating EGFR/MAPK signaling through the N-end rule pathways.PLoS genetics · 2020Article
- Synthetic lethal therapies for cancer: what's next after PARP inhibitors?Nature reviews. Clinical oncology · 2018Review
- ESCRT-0 complex modulates Rbf-mutant cell survival by regulating Rhomboid endosomal trafficking and EGFR signaling.Journal of cell science · 2016Article
- Regulation of cell polarity determinants by the Retinoblastoma tumor suppressor protein.Scientific reports · 2016Article
- Collateral Lethality: A new therapeutic strategy in oncology.Trends in cancer · 2015Article
- Down-regulation of SOSTDC1 promotes thyroid cancer cell proliferation via regulating cyclin A2 and cyclin E2.Oncotarget · 2015Article
- Hyperactivated Wnt signaling induces synthetic lethal interaction with Rb inactivation by elevating TORC1 activities.PLoS genetics · 2014Article
- Mutation of the retinoblastoma tumor suppressor gene sensitizes cancers to mitotic inhibitor induced cell death.American journal of cancer research · 2014Article
- Systems genetics in "-omics" era: current and future development.Theory in biosciences = Theorie in den Biowissenschaften · 2013Review
- Functional inactivation of Rb sensitizes cancer cells to TSC2 inactivation induced cell death.Cancer letters · 2013Article
- Conserved RB functions in development and tumor suppression.Protein & cell · 2011Review
- Osteosarcoma: prognosis plateau warrants retinoblastoma pathway targeted therapy.Signal transduction and targeted therapyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The retinoblastoma protein, pRb, is a key regulator of cell proliferation, differentiation, apoptosis, as well as checkpoint and stress responses. The function of Rb is often inactivated in many types of cancers, a feature that can potentially be used to target this specific subset of cancers. However little is known about how the loss of Rb function can be exploited in cancer therapies. In this review, we overview the functions of Rb, and discuss a genetic screen that led to the finding that inactivation of TSC2 and Rb induces synergistic cell death in both Drosophila developing tissues and human cancer cells. The mechanisms for synergistic cell death involve the accumulation of cellular stress, suggesting that inactivation of TSC2 and chemotherapeutic agents that result in induction of cellular stress can potentially be combined to treat cancers harboring inactivated Rb.
Indexed as
Identifiers
21814623PMC3147291W194799890What 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.