ReviewTranslational pediatrics2014
Fanconi anemia pathway defects in inherited and sporadic cancers.
Review in Translational pediatrics, 2014. 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
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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
22 citing papers in PubMed, 28 citations in OpenAlex.
- Multi-omics analysis in suspected hereditary breast and ovarian cancer cases reveals novel candidate susceptibility factors.NPJ breast cancer · 2026Article
- X chromosome inactivation, X-linked disorders, and cancer.Frontiers in genetics · 2026Review
- The Fanconi Anemia Pathway Inhibits mTOR Signaling and Prevents Accelerated Translation in Head and Neck Cancer Cells.Cancers · 2025Article
- PLK1 Inhibition Induces Synthetic Lethality in Fanconi Anemia Pathway-Deficient Acute Myeloid Leukemia.Cancer research communications · 2025Article
- STIL facilitates the development and malignant progression of triple-negative breast cancer through activation of Fanconi anemia pathway via interacting with KLF16.Translational oncology · 2024Article
- Complex Interplay between DNA Damage and Autophagy in Disease and Therapy.Biomolecules · 2024Review
- Gene-Environment Analyses in a UK Biobank Skin Cancer Cohort Identifies Important SNPs in DNA Repair Genes That May Help Prognosticate Disease Risk.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2023Article
- FAAP100 is required for the resolution of transcription-replication conflicts in primordial germ cells.BMC biology · 2023Article
- Metastasising ameloblastoma or ameloblastic carcinoma? A case report with mutation analyses.BMC oral health · 2023Review
- Study on the role of SLC14A1 gene in biochemical recurrence of prostate cancer.Scientific reports · 2022Article
- [Research progress of Fanconi anemia and DNA interstrand crosslink repair].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2022Article
- SIK2 kinase synthetic lethality is driven by spindle assembly defects in FANCA-deficient cells.Molecular oncology · 2022Article
- Prevalence of cancer susceptibility variants in patients with multiple Lynch syndrome related cancers.Scientific reports · 2021Article
- A comprehensive analysis of candidate genes in familial pancreatic cancer families reveals a high frequency of potentially pathogenic germline variants.EBioMedicine · 2020Article
- A Multiple Primary Malignancy Patient With FANCA Gene Mutation: A Case Report and Literature Review.Frontiers in oncology · 2020Article
- Fanconi Anemia Pathway: Mechanisms of Breast Cancer Predisposition Development and Potential Therapeutic Targets.Frontiers in cell and developmental biology · 2020Review
- Targeted sequencing identifies the mutational signature of double primary and metastatic malignancies: a case report.Diagnostic pathology · 2019Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fanconi anemia (FA) is a recessive chromosomal instability syndrome. It is a hereditary disorder with defects in DNA repair characterized by progressive bone marrow failure, variable congenital malformations and predisposition to develop hematological or solid tumors. Bi-allelic gene mutations in FA cause not only the FA phenotype but also genome instability and additional mutations in their somatic cells resulting in a high predisposition to many different types of cancers. Mono-allelic mutation in FA genes increases the susceptibility to several types of cancers in a sporadic manner in non-FA patients. The strong link between cancer from bi-allelic and mono-allelic FA gene mutations has been well established. Studies have demonstrated a link between FA and cancer due to gene defects which cause the disruption of the FA pathways in a proportion of familial and sporadic cancers. The convincing evidence is that one of the FA genes, FANCD1 is identical to the well-known breast cancer susceptibility gene, BRCA2. Another three FA genes were found to be associated with genes mutated from breast cancer and other types of cancers such as prostate cancer as well. Studies on FA's biological function in genome instability maintenance, DNA damage/repair and its complex regulation pathways have become the main focus within the genetic cancer research field because of many unique features of FA. The lessons learnt from FA studies provided invaluable information towards the understanding of cancer pathogenesis to be translated into targeting cancer therapies. Studies also demonstrated that FA is a paradigm of cancer-prone inherited monogenic disease, offering insights into the pathogenesis of many types of human diseases, particularly in bone marrow failure, cancer and aging. In this review, brief FA clinical characteristics, identification of FA genes and their protein pathways, the pathogenic linking between cancers from bi-allelic and mono-allelic mutated FA genes will be discussed.
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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.