fanconi anemia/hypoxia

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Hypoxia disrupts the Fanconi anemia pathway and sensitizes cells to chemotherapy through regulation of UBE2T.

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OBJECTIVE Hypoxia is a common feature of the microenvironment of solid tumors which has been shown to promote malignancy and poor patient outcome through multiple mechanisms. The association of hypoxia with more aggressive disease may be due in part to recently identified links between hypoxia and

Hypoxia-reoxygenation induces premature senescence in FA bone marrow hematopoietic cells.

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Hematopoietic cells are often exposed to transient hypoxia and reoxygenation as they develop and migrate. Given that bone marrow (BM) failure occurred in patients with Fanconi anemia (FA), we reason that hypoxia-then-reoxygenation represents a physiologically relevant stress for FA hematopoietic

Hypoxic stress facilitates acute activation and chronic downregulation of fanconi anemia proteins.

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Hypoxia induces genomic instability through replication stress and dysregulation of vital DNA repair pathways. The Fanconi anemia (FA) proteins, FANCD2 and FANCI, are key members of a DNA repair pathway that responds to replicative stress, suggesting that they undergo regulation by hypoxic

Preclinical correction of human Fanconi anemia complementation group A bone marrow cells using a safety-modified lentiviral vector.

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One of the major hurdles for the development of gene therapy for Fanconi anemia (FA) is the increased sensitivity of FA stem cells to free radical-induced DNA damage during ex vivo culture and manipulation. To minimize this damage, we have developed a brief transduction procedure for lentivirus

Expression of the Fanconi anemia gene FAC in human cell lines: lack of effect of oxygen tension.

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Fanconi anemia (FA) is a recessively inherited disease characterized by bone marrow failure, congenital anomalies, chromosomal instability and hypersensitivity to crosslinking agents. Some of the cellular defects of FA are known to be responsive to the ambient oxygen concentration. We examined the

Prospects for nutritional interventions in the clinical management of Fanconi anemia.

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The evidence associating Fanconi anemia (FA) phenotype to in-vitro and ex-vivo oxidative stress is reviewed. A cancer-prone genetic disease, FA is characterized by delayed bone marrow failure with a progression to aplastic anemia. It is diagnosed by excess chromosomal instability induced by two

Pregnancy outcomes in mothers of offspring with inherited bone marrow failure syndromes.

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BACKGROUND Children with inherited bone marrow failure syndromes (IBMFSs) may be symptomatic in utero, resulting in maternal and fetal problems during the pregnancy. Subsequent pregnancies by their mothers should be considered "high risk". METHODS We retrospectively analyzed outcomes of 575

CXCR4 induction in hematopoietic progenitor cells from Fanca(-/-), -c(-/-), and -d2(-/-) mice.

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OBJECTIVE Bone marrow failure is a near-universal occurrence in patients with Fanconi anemia (FA) and is thought to result from exhaustion of the hematopoietic stem cell (HSC) pool. Retrovirus-mediated expression of the deficient protein corrects this phenotype and makes FA a candidate disease for

Preclinical evaluation of Laromustine for use in combination with radiation therapy in the treatment of solid tumors.

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OBJECTIVE These studies explored questions related to the potential use of Laromustine in the treatment of solid tumors and in combination with radiotherapy. METHODS The studies used mouse EMT6 cells (both parental and transfected with genes for O(6)-alkylguanine-DNA transferase [AGT]),

DNA Repair Deficient Chinese Hamster Ovary Cells Exhibiting Differential Sensitivity to Charged Particle Radiation under Aerobic and Hypoxic Conditions.

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It has been well established that hypoxia significantly increases both cellular and tumor resistance to ionizing radiation. Hypoxia associated radiation resistance has been known for some time but there has been limited success in sensitizing cells to radiation under hypoxic conditions. These

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