hydroxyurea has been researched along with Fanconi Anemia in 13 studies
Fanconi Anemia: Congenital disorder affecting all bone marrow elements, resulting in ANEMIA; LEUKOPENIA; and THROMBOPENIA, and associated with cardiac, renal, and limb malformations as well as dermal pigmentary changes. Spontaneous CHROMOSOME BREAKAGE is a feature of this disease along with predisposition to LEUKEMIA. There are at least 7 complementation groups in Fanconi anemia: FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, and FANCL. (from Online Mendelian Inheritance in Man, http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=227650, August 20, 2004)
| Excerpt | Relevance | Reference |
|---|---|---|
| "Hydroxyurea (HU) is an agent that induces replicative stress by inhibiting ribonucleotide reductase (RNR), which synthesizes deoxyribonucleotide triphosphates (dNTPs) necessary for DNA replication and repair." | 5.42 | Hydroxyurea induces chromosomal damage in G2 and enhances the clastogenic effect of mitomycin C in Fanconi anemia cells. ( Altamirano-Lozano, M; Carnevale, A; Frias, S; Gómez, L; Marchetti, F; Molina, B; Ortiz, R; Ramos, S; Torres, L, 2015) |
| "Chromosomal aberrations were first measured after exposure to mitomicyn C (MMC) or hydroxyurea (HU)." | 5.35 | Differential expression of TP53 associated genes in Fanconi anemia cells after mitomycin C and hydroxyurea treatment. ( Acuña, H; Coleman, MA; Frias, S; Gómez, L; Hinz, JM; Jones, IM; Martinez, A; Molina, B, 2008) |
| "Hydroxyurea (HU) is an agent that induces replicative stress by inhibiting ribonucleotide reductase (RNR), which synthesizes deoxyribonucleotide triphosphates (dNTPs) necessary for DNA replication and repair." | 1.42 | Hydroxyurea induces chromosomal damage in G2 and enhances the clastogenic effect of mitomycin C in Fanconi anemia cells. ( Altamirano-Lozano, M; Carnevale, A; Frias, S; Gómez, L; Marchetti, F; Molina, B; Ortiz, R; Ramos, S; Torres, L, 2015) |
| "Chromosomal aberrations were first measured after exposure to mitomicyn C (MMC) or hydroxyurea (HU)." | 1.35 | Differential expression of TP53 associated genes in Fanconi anemia cells after mitomycin C and hydroxyurea treatment. ( Acuña, H; Coleman, MA; Frias, S; Gómez, L; Hinz, JM; Jones, IM; Martinez, A; Molina, B, 2008) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 3 (23.08) | 18.2507 |
| 2000's | 2 (15.38) | 29.6817 |
| 2010's | 5 (38.46) | 24.3611 |
| 2020's | 3 (23.08) | 2.80 |
| Authors | Studies |
|---|---|
| Voter, AF | 1 |
| Manthei, KA | 1 |
| Keck, JL | 1 |
| Rickman, KA | 1 |
| Noonan, RJ | 1 |
| Lach, FP | 1 |
| Sridhar, S | 1 |
| Wang, AT | 1 |
| Abhyankar, A | 1 |
| Huang, A | 1 |
| Kelly, M | 1 |
| Auerbach, AD | 1 |
| Smogorzewska, A | 1 |
| Nolan, M | 1 |
| Knudson, K | 1 |
| Holz, MK | 1 |
| Chaudhury, I | 1 |
| Xu, X | 1 |
| Xu, Y | 1 |
| Guo, R | 2 |
| Xu, R | 1 |
| Fu, C | 1 |
| Xing, M | 1 |
| Sasanuma, H | 1 |
| Li, Q | 1 |
| Takata, M | 1 |
| Takeda, S | 1 |
| Xu, D | 1 |
| Singh, S | 1 |
| Shemesh, K | 1 |
| Liefshitz, B | 1 |
| Kupiec, M | 1 |
| Molina, B | 3 |
| Marchetti, F | 1 |
| Gómez, L | 3 |
| Ramos, S | 1 |
| Torres, L | 1 |
| Ortiz, R | 1 |
| Altamirano-Lozano, M | 1 |
| Carnevale, A | 2 |
| Frias, S | 3 |
| Chen, X | 1 |
| Bosques, L | 1 |
| Sung, P | 1 |
| Kupfer, GM | 1 |
| Clark, DW | 1 |
| Tripathi, K | 1 |
| Dorsman, JC | 1 |
| Palle, K | 1 |
| Martinez, A | 1 |
| Hinz, JM | 1 |
| Acuña, H | 1 |
| Jones, IM | 1 |
| Coleman, MA | 1 |
| Howlett, NG | 1 |
| Taniguchi, T | 1 |
| Durkin, SG | 1 |
| D'Andrea, AD | 1 |
| Glover, TW | 1 |
| Rojas, E | 1 |
| Ostrosky-Wegman, P | 1 |
| Heinrich, MC | 1 |
| Hoatlin, ME | 1 |
| Zigler, AJ | 1 |
| Silvey, KV | 1 |
| Bakke, AC | 1 |
| Keeble, WW | 1 |
| Zhi, Y | 1 |
| Reifsteck, CA | 1 |
| Grompe, M | 1 |
| Brown, MG | 1 |
| Magenis, RE | 1 |
| Olson, SB | 1 |
| Bagby, GC | 1 |
| Johnstone, P | 1 |
| Reifsteck, C | 1 |
| Kohler, S | 1 |
| Worland, P | 1 |
| Olson, S | 1 |
| Moses, RE | 1 |
13 other studies available for hydroxyurea and Fanconi Anemia
| Article | Year |
|---|---|
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
Topics: Antineoplastic Agents; DNA Damage; DNA Helicases; DNA Repair; Drug Screening Assays, Antitumor; Fanc | 2016 |
Distinct roles of BRCA2 in replication fork protection in response to hydroxyurea and DNA interstrand cross-links.
Topics: BRCA2 Protein; Cell Line; DNA; DNA Repair; DNA Replication; Fanconi Anemia; Homologous Recombination | 2020 |
Fanconi anemia and mTOR pathways functionally interact during stalled replication fork recovery.
Topics: Aphidicolin; Cell Survival; DNA; DNA Repair; DNA Replication; Fanconi Anemia; Fanconi Anemia Complem | 2021 |
Fanconi anemia proteins participate in a break-induced-replication-like pathway to counter replication stress.
Topics: Aneuploidy; Animals; Bone Marrow Failure Disorders; Cell Line, Transformed; Chickens; Chromosome Bre | 2021 |
Genetic and physical interactions between the yeast ELG1 gene and orthologs of the Fanconi anemia pathway.
Topics: Carrier Proteins; Chromosomal Proteins, Non-Histone; DEAD-box RNA Helicases; DNA Damage; Fanconi Ane | 2013 |
Hydroxyurea induces chromosomal damage in G2 and enhances the clastogenic effect of mitomycin C in Fanconi anemia cells.
Topics: Cell Line; Chromosome Aberrations; Cytogenetic Analysis; Drug Synergism; Fanconi Anemia; G2 Phase; H | 2015 |
A novel role for non-ubiquitinated FANCD2 in response to hydroxyurea-induced DNA damage.
Topics: DNA Damage; DNA-Binding Proteins; DNA-Directed DNA Polymerase; Fanconi Anemia; Fanconi Anemia Comple | 2016 |
FANCJ protein is important for the stability of FANCD2/FANCI proteins and protects them from proteasome and caspase-3 dependent degradation.
Topics: Basic-Leucine Zipper Transcription Factors; Caspase 3; Cell Line, Tumor; DNA Damage; DNA Repair; Enz | 2015 |
Differential expression of TP53 associated genes in Fanconi anemia cells after mitomycin C and hydroxyurea treatment.
Topics: Cell Line; Chromosome Aberrations; Cross-Linking Reagents; DNA Damage; Fanconi Anemia; Gene Expressi | 2008 |
The Fanconi anemia pathway is required for the DNA replication stress response and for the regulation of common fragile site stability.
Topics: Aphidicolin; Chromosomal Instability; Chromosome Fragile Sites; DNA Replication; Fanconi Anemia; Fan | 2005 |
Effect of hydroxyurea and normal plasma on DNA synthesis in lymphocytes from Fanconi anemia patients.
Topics: Cells, Cultured; Culture Media; Deoxyribonucleotides; DNA; DNA Repair; Enzyme Inhibitors; Fanconi An | 1996 |
DNA cross-linker-induced G2/M arrest in group C Fanconi anemia lymphoblasts reflects normal checkpoint function.
Topics: Caffeine; Cell Line, Transformed; Cross-Linking Reagents; DNA; DNA Damage; DNA, Complementary; Fanco | 1998 |
Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation.
Topics: Antibiotics, Antineoplastic; Antineoplastic Agents, Alkylating; Caffeine; Cell Cycle; Cells, Culture | 1997 |