ArticleExperimental hematology2015
FANCA safeguards interphase and mitosis during hematopoiesis in vivo.
Article in Experimental hematology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Integrative proteomics defines FANCA as a multifunctional hub linking DNA repair to translation.iScience · 2026Article
- The periphery of nuclear speckles defines a spatially and temporally regulated compartment of long-lived intron-retained RNAs that resolves during mitosis.Nature cell biology · 2026Article
- Development of translational read-through-inducing drugs as novel therapeutic options for patients with Fanconi anemia.Cell death discovery · 2025Article
- Oncogenic properties of wild-type DNA repair gene FANCA in breast cancer.Cell reports · 2025Article
- PLK1 Inhibition Induces Synthetic Lethality in Fanconi Anemia Pathway-Deficient Acute Myeloid Leukemia.Cancer research communications · 2025Article
- MAT2A inhibitor AG-270/S095033 in patients with advanced malignancies: a phase I trial.Nature communications · 2025Article
- Intravesical BCG in patients with non-muscle invasive bladder cancer induces trained immunity and decreases respiratory infections.Journal for immunotherapy of cancer · 2023Observational
- Cytogenetics in Fanconi Anemia: The Importance of Follow-Up and the Search for New Biomarkers of Genomic Instability.International journal of molecular sciences · 2022Review
- SIK2 kinase synthetic lethality is driven by spindle assembly defects in FANCA-deficient cells.Molecular oncology · 2022Article
- Numbers of long-term hematopoietic stem cells from bone marrow of fanca and fancc knockout mice can be greatly enhanced by their collection and processing in physioxia conditions.Blood cells, molecules & diseases · 2021Article
- Review
- Fanconi Anemia Pathway: Mechanisms of Breast Cancer Predisposition Development and Potential Therapeutic Targets.Frontiers in cell and developmental biology · 2020Review
- Does FANCA Assist CENP-E in Architectural Organization of Chromosomes at Spindle Equator?Balkan medical journal · 2018Article
- Fanconi anaemia and cancer: an intricate relationship.Nature reviews. Cancer · 2018Review
- INPP5E Preserves Genomic Stability through Regulation of Mitosis.Molecular and cellular biology · 2017Article
- Maintenance of genome stability by Fanconi anemia proteins.Cell & bioscience · 2017Review
- Leukemia and chromosomal instability in aged Fancc-/- mice.Experimental hematology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The Fanconi anemia (FA/BRCA) signaling network controls multiple genome-housekeeping checkpoints, from interphase DNA repair to mitosis. The in vivo role of abnormal cell division in FA remains unknown. Here, we quantified the origins of genomic instability in FA patients and mice in vivo and ex vivo. We found that both mitotic errors and interphase DNA damage significantly contribute to genomic instability during FA-deficient hematopoiesis and in nonhematopoietic human and murine FA primary cells. Super-resolution microscopy coupled with functional assays revealed that FANCA shuttles to the pericentriolar material to regulate spindle assembly at mitotic entry. Loss of FA signaling rendered cells hypersensitive to spindle chemotherapeutics and allowed escape from the chemotherapy-induced spindle assembly checkpoint. In support of these findings, direct comparison of DNA crosslinking and anti-mitotic chemotherapeutics in primary FANCA-/- cells revealed genomic instability originating through divergent cell cycle checkpoint aberrations. Our data indicate that FA/BRCA signaling functions as an in vivo gatekeeper of genomic integrity throughout interphase and mitosis, which may have implications for future targeted therapies in FA and FA-deficient cancers.
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.