ArticleBritish journal of cancer1997
Loss of heterozygosity at the 5,10-methylenetetrahydrofolate reductase locus in human ovarian carcinomas.
Article in British journal of cancer, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- A systematic review and meta-analysis expounding the relationship between methylene tetrahydrofolate reductase gene polymorphism and the risk of intracerebral hemorrhage among populations.Frontiers in genetics · 2022Pooled it
- Targeting purine metabolism in ovarian cancer.Journal of ovarian research · 2022Review
- A hidden cause of infertility in hypothyroid patients.Clinical case reports · 2020Article
- Correlation Between Methylenetetrahydrofolate Reductase (MTHFR) C677T Polymorphisms and Pemetrexed Chemotherapy Efficacy/Toxicity in Non-Squamous Non-Small Cell Lung Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Flavin-dependent enzymes in cancer prevention.International journal of molecular sciences · 2012Review
- Genetic polymorphism of MTHFR G1793A in Chinese populations.European journal of epidemiology · 2008Article
- Analysis of the MTHFR 1298A-->C and 677C-->T polymorphisms as risk factors for neural tube defects.Journal of human genetics · 2003Article
- Antisense inhibition of methylenetetrahydrofolate reductase reduces survival of methionine-dependent tumour lines.British journal of cancer · 2002Article
- The methylenetetrahydrofolate reductase (MTHFR) gene in colorectal cancer: role in tumor development and significance of allelic loss in tumor progression.International journal of gastrointestinal cancer · 2001Article
- A second common mutation in the methylenetetrahydrofolate reductase gene: an additional risk factor for neural-tube defects?American journal of human genetics · 1998Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high-affinity folate-binding protein (FBP) is primarily involved in the uptake of the 5-methyltetrahydrofolate, and its expression may be physiologically regulated by the intracellular folate content. The overexpression of FBP on the cell surface of ovarian carcinoma cells may be responsible for an increased folate uptake. We tested the hypothesis of the existence of a defect in the 5, 10-methylenetetrahydrofolate reductase (MTHFR) in ovarian tumours that could cause reduced intracellular regeneration of the 5-methyltetrahydrofolate and induce increased FBP expression. No sequence mutations were found in the MTHFR gene, but allelic deletions of this gene were frequently detected in ovarian tumours (59%). Chromosomal losses appeared to be confined to the 1p36.3 region to which the MTHFR gene maps. Although it cannot be stated that MTHFR is the target gene of the chromosomal loss involving the 1p36.3 region, a correlation between loss of heterozygosity at this locus and decrease in MTHFR activity was shown, suggesting a role of these allelic deletions in generating a biochemical defect in folate metabolism. Further studies are needed to assess further the relationship between MTHFR and FBP overexpression, but the demonstration of the alteration of a key metabolic enzyme of the folate cycle in a subset of human ovarian tumours is in accordance with the hypothesis of an altered folate metabolism in these neoplasias and might be exploited for therapeutic purposes.
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