ArticleCancer research2022
A Novel Synthetic Lethal Approach to Target MYC-Driven Cancers.
Article in Cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 8 citations in OpenAlex.
- MYC in Oncogenesis and Therapeutic Implications.MedComm · 2026Review
- CTPS1 modulates mitophagy to propel diffuse large B-cell lymphoma via reshaping CEPT1-mediated phospholipid metabolism.Redox biology · 2026Article
- c-MYC enhances transcription of the type 1 diabetes mellitus associated gene BATF3 via promoter binding.Scientific reports · 2026Article
- Impaired mitochondrial metabolism is a critical cancer vulnerability for MYC inhibitors.Science advances · 2025Article
- Untangling the Role of MYC in Sarcomas and Its Potential as a Promising Therapeutic Target.International journal of molecular sciences · 2025Review
- A Small Molecule Selectively Targets N-Myc to Suppress Neuroblastoma Cancer Progression.International journal of biological sciences · 2025Article
- A comprehensive prognostic score for head and neck squamous cancer driver genes and phenotype traits.Discover oncology · 2023Article
- Identifying key transcription factors and immune infiltration in non-small-cell lung cancer using weighted correlation network and Cox regression analyses.Frontiers in oncology · 2023Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MYC proto-oncogene family encompasses three related transcription factors (MYC, MYCL, and MYCN), which are master regulators of cellular programs orchestrating multiple hallmarks of cancer, including proliferation, metabolism, invasiveness, and immune surveillance. MYC activation is one of the most frequent alterations in cancer, induced by genetic, epigenetic, or posttranslational alterations of MYC itself, or of MYC-related proteins or pathways. Sun and colleagues found a unique function of the rate-limiting nucleotide synthesis enzyme CTP synthase 1 (CTPS1) in the survival of MYC-driven cancer cells. They further identified a novel synthetic lethal strategy to combat MYC-driven cancers by combining CTPS1 inhibitors with ataxia telangiectasia and Rad3-related protein inhibitors, which exploits the inherent vulnerability of MYC-driven tumors to nucleotide shortage and DNA replication stress. These findings open novel therapeutic avenues for targeting the traditionally "undruggable" MYC-driven cancers, which represent one of the highest unmet clinical needs in cancer. See related article by Sun et al. p. 1013.
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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.