ArticleCancers2013
Synthetic genetic targeting of genome instability in cancer.
Article in Cancers, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
20 citing papers in PubMed.
- Article
- PROTACs: Current and Future Potential as a Precision Medicine Strategy to Combat Cancer.Molecular cancer therapeutics · 2024Review
- Unveiling the vulnerabilities of synthetic lethality in triple-negative breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
- Development of Metabolic Synthetic Lethality and Its Implications for Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2022Article
- Aberrant SKP1 Expression: Diverse Mechanisms Impacting Genome and Chromosome Stability.Frontiers in cell and developmental biology · 2022Review
- Article
- The SCF Complex Is Essential to Maintain Genome and Chromosome Stability.International journal of molecular sciences · 2021Review
- The tumor therapy landscape of synthetic lethality.Nature communications · 2021Article
- Chromosome Instability; Implications in Cancer Development, Progression, and Clinical Outcomes.Cancers · 2020Review
- Reduced Expression of Genes Regulating Cohesion Induces Chromosome Instability that May Promote Cancer and Impact Patient Outcomes.Scientific reports · 2020Article
- Humanized yeast genetic interaction mapping predicts synthetic lethal interactions of FBXW7 in breast cancer.BMC medical genomics · 2019Article
- Beyond Synthetic Lethality: Charting the Landscape of Pairwise Gene Expression States Associated with Survival in Cancer.Cell reports · 2019Article
- Role of RNF20 in cancer development and progression - a comprehensive review.Bioscience reports · 2018Review
- Synthetic lethal targeting of RNF20 through PARP1 silencing and inhibition.Cellular oncology (Dordrecht, Netherlands) · 2017Article
- The synthetic lethal killing of RAD54B-deficient colorectal cancer cells by PARP1 inhibition is enhanced with SOD1 inhibition.Oncotarget · 2016Article
- Predicting chemotherapeutic drug combinations through gene network profiling.Scientific reports · 2016Article
- Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition.Seminars in cancer biology · 2015Review
- Synthetic dosage lethality in the human metabolic network is highly predictive of tumor growth and cancer patient survival.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Targeting SOD1 induces synthetic lethal killing in BLM- and CHEK2-deficient colorectal cancer cells.Oncotarget · 2015Article
- Autoimmune response to PARP and BRCA1/BRCA2 in cancer.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer is a leading cause of death throughout the World. A limitation of many current chemotherapeutic approaches is that their cytotoxic effects are not restricted to cancer cells, and adverse side effects can occur within normal tissues. Consequently, novel strategies are urgently needed to better target cancer cells. As we approach the era of personalized medicine, targeting the specific molecular defect(s) within a given patient's tumor will become a more effective treatment strategy than traditional approaches that often target a given cancer type or sub-type. Synthetic genetic interactions are now being examined for their therapeutic potential and are designed to target the specific genetic and epigenetic phenomena associated with tumor formation, and thus are predicted to be highly selective. In general, two complementary approaches have been employed, including synthetic lethality and synthetic dosage lethality, to target aberrant expression and/or function associated with tumor suppressor genes and oncogenes, respectively. Here we discuss the concepts of synthetic lethality and synthetic dosage lethality, and explain three general experimental approaches designed to identify novel genetic interactors. We present examples and discuss the merits and caveats of each approach. Finally, we provide insight into the subsequent pre-clinical work required to validate novel candidate drug targets.
Identifiers
What 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.