ReviewCold Spring Harbor perspectives in medicine2014
Synthetic lethal screens as a means to understand and treat MYC-driven cancers.
Review in Cold Spring Harbor perspectives in medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 49 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
49 citing papers in PubMed, 71 citations in OpenAlex.
- Impaired mitochondrial metabolism is a critical cancer vulnerability for MYC inhibitors.Science advances · 2025Article
- Targeting the undruggable MYC in cancer: the rationale of using XPO1 inhibitors.Molecular biology reports · 2025Review
- CRISPR/Cas9 screen for genome-wide interrogation of essential MYC-bound E-boxes in cancer cells.Molecular oncology · 2023Article
- Strategies to target the cancer driver MYC in tumor cells.Frontiers in oncology · 2023Review
- Cyclin-Dependent Kinase Synthetic Lethality Partners in DNA Damage Response.International journal of molecular sciences · 2022Review
- Development of Metabolic Synthetic Lethality and Its Implications for Thyroid Cancer.Endocrinology and metabolism (Seoul, Korea) · 2022Article
- Tilting MYC toward cancer cell death.Trends in cancer · 2021Review
- Role of ARK5 in cancer and other diseases (Review).Experimental and therapeutic medicine · 2021Review
- Review
- Metabolic Control by DNA Tumor Virus-Encoded Proteins.Pathogens (Basel, Switzerland) · 2021Review
- Cyclin-Dependent Kinases (CDK) and Their Role in Diseases Development-Review.International journal of molecular sciences · 2021Review
- The SUMO pathway in pancreatic cancer: insights and inhibition.British journal of cancer · 2021Review
- The UVSSA complex alleviates MYC-driven transcription stress.The Journal of cell biology · 2021Article
- Targeting the MYC Ubiquitination-Proteasome Degradation Pathway for Cancer Therapy.Frontiers in oncology · 2021Review
- Methods for Determining Myc-Induced Apoptosis.Methods in molecular biology (Clifton, N.J.) · 2021Article
- The Molecular 'Myc-anisms' Behind Myc-Driven Tumorigenesis and the Relevant Myc-Directed Therapeutics.International journal of molecular sciences · 2020Review
- Targeting the ubiquitin-proteasome system in a pancreatic cancer subtype with hyperactive MYC.Molecular oncology · 2020Article
- Article
- Article
- Molecular Crosstalk Between MYC and HIF in Cancer.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Although therapeutics against MYC could potentially be used against a wide range of human cancers, MYC-targeted therapies have proven difficult to develop. The convergence of breakthroughs in human genomics and in gene silencing using RNA interference (RNAi) have recently allowed functional interrogation of the genome and systematic identification of synthetic lethal interactions with hyperactive MYC. Here, we focus on the pathways that have emerged through RNAi screens and present evidence that a subset of genes showing synthetic lethality with MYC are significantly interconnected and linked to chromatin and transcriptional processes, as well as to DNA repair and cell cycle checkpoints. Other synthetic lethal interactions with MYC point to novel pathways and potentially broaden the repertoire of targeted therapies. The elucidation of MYC synthetic lethal interactions is still in its infancy, and how these interactions may be influenced by tissue-specific programs and by concurrent genetic change will require further investigation. Nevertheless, we predict that these studies may lead the way to novel therapeutic approaches and new insights into the role of MYC in cancer.
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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.