ReviewNucleus (Austin, Tex.)2019
ALT control, delete: FANCM as an anti-cancer target in Alternative Lengthening of Telomeres.
Review in Nucleus (Austin, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 32 citations in OpenAlex.
- Twisting the End Game: How Telomere Chromatin Modifications Shape Telomere Maintenance.Aging cell · 2026Review
- SLX4IP limits replication stress globally and at ALT telomeres.The EMBO journal · 2026Article
- Structural Studies of βTrCP Reveal Plasticity in Binding Modes of Consensus and Nonconsensus Degrons.ACS chemical biology · 2026Article
- CHAMP1 complex promotes heterochromatin assembly and reduces replication stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- Targeting FANCM by antisense oligonucleotides in ALT-positive cancers.Molecular therapy. Nucleic acids · 2025Article
- SLX4IP acts in parallel to FANCM to limit BLM-dependent replication stress at ALT telomeres.bioRxiv : the preprint server for biology · 2025Article
- The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.bioRxiv : the preprint server for biology · 2025Article
- Mechanism of structure-specific DNA binding by the FANCM branchpoint translocase.Nucleic acids research · 2024Article
- FANCM Gene Variants in a Male Diagnosed with Sertoli Cell-Only Syndrome and Diffuse Astrocytoma.Genes · 2024Article
- Genome maintenance meets mechanobiology.Chromosoma · 2024Review
- Analyses of Genes Critical to Tumor Survival Reveal Potential 'Supertargets': Focus on Transcription.Cancers · 2023Article
- The Molecular Mechanisms and Therapeutic Prospects of Alternative Lengthening of Telomeres (ALT).Cancers · 2023Review
- Alternative lengthening of telomeres in primary hepatic neoplasms.Human pathology · 2023Article
- Telomeric replication stress: the beginning and the end for alternative lengthening of telomeres cancers.Open biology · 2022Review
- Regulation of Replication Stress in Alternative Lengthening of Telomeres by Fanconi Anaemia Protein.Genes · 2022Review
- Review
- Novel Bi-Allelic Variants ofFrontiers in genetics · 2021Article
- Long interspersed element-1 ribonucleoprotein particles protect telomeric ends in alternative lengthening of telomeres dependent cells.Neoplasia (New York, N.Y.) · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Break-induced replication is a specific type of DNA repair that has a co-opted role in telomere extension by telomerase-negative cancer cells. This Alternative Lengthening of Telomeres (or 'ALT') is required for viability in approximately 10% of all carcinomas, but up to 50% of the soft-tissue derived sarcomas. In several recent studies, we and others demonstrate that expression and activity of FANCM, a DNA translocase protein, is essential for the viability of ALT-associated cancers. Here we provide a summary of how and why FANCM depletion leads to deletion of ALT-controlled cancers, predominantly through a hyper-activation of break-induced replication. We also discuss how FANCM can and has been targeted in cancer cell killing, including potential opportunities in ALT and other genetic backgrounds.
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What Socratic 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 Socratic graph.