Elevations of serum alpha-fetoprotein (sAFP) have been reported in fetal and infant states of anemia. Fanconi anemia (FA) belongs to a family of genetic instability disorders which lack the capability to repair DNA breaks. The lesion occurs at a checkpoint regulatory step of the G2 to mitotic transition, allowing FA cells to override cell-cycle arrest. FA DNA repair pathways contain complementation groups known as FANC proteins. FANC proteins form multi-protein complexes with BRCA proteins and are involved in homologous DNA repair. An impaired cascade in these events imparts an increased breast cancer susceptibility to female FA patients. Elevations of sAFP have availed this fetal protein to serve as a biomarker for FA disease. However, the origin of the synthesis of sAFA has not been determined in FA patients. We hypothesize that hematopoietic multipotent progenitor stem cells in the bone marrow are the source of sAFP production in FA patients.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1080/15513815.2016.1225873 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Modulation of biological activities in adipose derived stem cells by histone deacetylation.
Sci Rep
January 2025
The Department of Biomedical and Clinical Sciences (BKV), Linköping University, Linköping, Sweden.
Difficult-to-heal wounds management accounts for about 4% of healthcare costs, highlighting the need for innovative solutions. Extracellular signals drive cell proliferation during tissue regeneration, while epigenetic mechanisms regulate stem cell homeostasis, differentiation, and skin repair. Exploring epigenetic regulation in adipose-derived stem cells (ADSCs) holds promise for improving skin injury treatments.
View Article and Find Full Text PDFConstruction of a Multiple Cyclic Ligation-Promoted Exponential Recombinase Polymerase Amplification Platform for Sensitive and Simultaneous Monitoring of Cancer Biomarkers Fpg and FEN1.
Anal Chem
January 2025
School of Chemistry and Chemical Engineering, State Key Laboratory of Digital Medical Engineering, Southeast University, Nanjing 211189, China.
Formamidopyrimidine DNA glycosylase (Fpg) and flap endonuclease 1 (FEN1) are essential to sustaining genomic stability and integrity, while the abnormal activities of Fpg and FEN1 may lead to various diseases and cancers. The development of simple methods for simultaneously monitoring Fpg and FEN1 is highly desirable. Herein, we construct a multiple cyclic ligation-promoted exponential recombinase polymerase amplification (RPA) platform for sensitive and simultaneous monitoring of Fpg and FEN1 in cells and clinical tissues.
View Article and Find Full Text PDFThe yeast checkpoint kinase Dun1p represses transcription of RNR genes independently of catalytic activity or Rad53p during respiratory growth.
J Biol Chem
January 2025
Department of Biological Sciences, St. John's University, Queens, New York, USA. Electronic address:
One of the key events in DNA damage response (DDR) is activation of checkpoint kinases leading to activation of ribonucleotide reductase (RNR) and increased synthesis of deoxyribonucleotide triphosphates (dNTPs), required for DNA repair. Among other mechanisms, the activation of dNTP synthesis is driven by derepression of genes encoding RNR subunits RNR2, RNR3, and RNR4, following checkpoint activation and checkpoint kinase Dun1p-mediated phosphorylation and inactivation of transcriptional repressor Crt1p. We report here that in the absence of genotoxic stress during respiratory growth on nonfermentable carbon source acetate, inactivation of checkpoint kinases results in significant growth defect and alters transcriptional regulation of RNR2-4 genes and genes encoding enzymes of the tricarboxylic acid (TCA) and glyoxylate cycles and gluconeogenesis.
View Article and Find Full Text PDFSmall-molecule activator of SMUG1 enhances repair of pyrimidine lesions in DNA.
DNA Repair (Amst)
January 2025
Department of Chemistry and Stanford University, Stanford, CA 94305, United States. Electronic address:
A potentially promising approach to targeted cancer prevention in genetically at-risk populations is the pharmacological upregulation of DNA repair pathways. SMUG1 is a base excision repair enzyme that ameliorates adverse genotoxic and mutagenic effects of hydrolytic and oxidative damage to pyrimidines. Here we describe the discovery and initial cellular activity of a small-molecule activator of SMUG1.
View Article and Find Full Text PDFReplication-Poison Treatment in BRCA1-Deficient Breast Cancer Causes MRE11 Over-Resection that Induces Single-Stranded DNA Accumulation and Mitotic Catastrophe.
Cancer Res
January 2025
INSERM U1194, Montpellier Cedex 05, Occitanie, France.
BRCA1 deficiency is observed in approximately 25% of triple-negative breast cancer (TNBC). BRCA1, a key player of homologous recombination (HR) repair, is also involved in stalled DNA replication fork protection and repair. Here, we investigated the sensitivity of BRCA1-deficient TNBC models to the frequently used replication chain terminator gemcitabine, which does not directly induce DNA breaks.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!