ArticleMolecular cancer research : MCR2019
Mitotic DNA Synthesis Is Differentially Regulated between Cancer and Noncancerous Cells.
Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 29 citations in OpenAlex.
- The FANCD2-FANCI heterodimer coordinates chromatin openness and cell cycle progression throughout DNA double-strand break repair.Cell reports · 2026Article
- TopBP1 coordinates DNA repair synthesis in mitosis via recruitment of the nuclease scaffold SLX4.Communications biology · 2025Article
- Replication stress induces POLQ-mediated structural variant formation throughout common fragile sites after entry into mitosis.Nature communications · 2024Article
- RAD52 and ERCC6L/PICH have a compensatory relationship for genome stability in mitosis.PLoS genetics · 2024Article
- FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation.Functional & integrative genomics · 2024Article
- FANCD2-dependent mitotic DNA synthesis relies on PCNA K164 ubiquitination.Cell reports · 2023Article
- Mitotic DNA Synthesis in Untransformed Human Cells Preserves Common Fragile Site Stability via a FANCD2-Driven Mechanism That Requires HELQ.Journal of molecular biology · 2023Article
- UBE2T resolves transcription-replication conflicts and protects common fragile sites in primordial germ cells.Cellular and molecular life sciences : CMLS · 2023Article
- Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells.Nature communications · 2023Article
- Review
- Regulator of telomere elongation helicase 1 gene and its association with malignancy.Cancer reports (Hoboken, N.J.) · 2023Review
- FANCD2 promotes mitotic rescue from transcription-mediated replication stress in SETX-deficient cancer cells.Communications biology · 2022Article
- A moving target for drug discovery: Structure activity relationship and many genome (de)stabilizing functions of the RAD52 protein.DNA repair · 2022Review
- Processing DNA lesions during mitosis to prevent genomic instability.Biochemical Society transactions · 2022Review
- Consequences of telomere replication failure: the other end-replication problem.Trends in biochemical sciences · 2022Review
- DNA replication is highly resilient and persistent under the challenge of mild replication stress.Cell reports · 2022Article
- Expression of SnoRNA U50A Is Associated with Better Prognosis and Prolonged Mitosis in Breast Cancer.Cancers · 2021Article
- Mind the replication gap.Royal Society open science · 2021Review
- SMC5/6 is required for replication fork stability and faithful chromosome segregation during neurogenesis.eLife · 2020Article
- High-resolution mapping of mitotic DNA synthesis regions and common fragile sites in the human genome through direct sequencing.Cell research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitotic DNA synthesis is a recently discovered mechanism that resolves late replication intermediates, thereby supporting cell proliferation under replication stress. This unusual form of DNA synthesis occurs in the absence of RAD51 or BRCA2, which led to the identification of RAD52 as a key player in this process. Notably, mitotic DNA synthesis is predominantly observed at chromosome loci that colocalize with FANCD2 foci. However, the role of this protein in mitotic DNA synthesis remains largely unknown. In this study, we investigated the role of FANCD2 and its interplay with RAD52 in mitotic DNA synthesis using aphidicolin as a universal inducer of this process. After examining eight human cell lines, we provide evidence for FANCD2 rather than RAD52 as a fundamental supporter of mitotic DNA synthesis. In cancer cell lines, FANCD2 exerts this role independently of RAD52. Surprisingly, RAD52 is dispensable for mitotic DNA synthesis in noncancerous cell lines, but these cells strongly depend on FANCD2 for this process. Therefore, RAD52 functions selectively in cancer cells as a secondary regulator in addition to FANCD2 to facilitate mitotic DNA synthesis. As an alternative to aphidicolin, we found partial inhibition of origin licensing as an effective way to induce mitotic DNA synthesis preferentially in cancer cells. Importantly, cancer cells still perform mitotic DNA synthesis by dual regulation of FANCD2 and RAD52 under such conditions. IMPLICATIONS: These key differences in mitotic DNA synthesis between cancer and noncancerous cells advance our understanding of this mechanism and can be exploited for cancer therapies.
Indexed as
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.