In:
Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 19, No. 11 ( 2010-11-01), p. 2833-2838
Abstract:
Background: Vitamin B12, holo-haptocorrin, and the folate-pathway single-nucleotide polymorphisms MTR 2756A & gt;G and SHMT1 1420C & gt;T have been associated with an increased risk of prostate cancer. We investigated whether these and other elements of folate metabolism were associated with prostate-specific antigen (PSA) velocity (PSAV) as a proxy measure of prostate cancer progression in men with localized prostate cancer. Methods: We measured plasma folate, B12, holo-haptocorrin, holo-transcobalamin, total transcobalamin, and total homocysteine at diagnosis in 424 men (ages 45-70 years) with localized prostate cancer in a U.K.-wide population-based cohort. Thirteen folate-pathway single-nucleotide polymorphisms were genotyped for 311 of these men. Postdiagnosis PSAV (continuous measure and with a threshold set a priori at 2 ng/mL/y) was estimated from repeat PSA measurements. Results: Median follow-up time was 2.5 (range, 0.8-5.6) years. Vitamin B12, holo-haptocorrin, holo-transcobalamin, total transcobalamin, and total homocysteine were not associated with postdiagnosis PSAV. Folate was associated with an increased risk of PSAV & gt;2 ng/mL/y [odds ratio (OR) per unit increase in loge concentration, 1.57; 95% confidence interval (95% CI), 0.98-2.51; P = 0.06]. MTRR 66A & gt;G (rs1801394) was associated with a reduced risk (recessive model OR, 0.33; 95% CI, 0.11-0.97; P = 0.04), and SHMT1 1420C & gt;T (rs1979277) with an increased risk (per-allele OR, 1.49; 95% CI, 0.93-2.37; P = 0.09) of PSAV & gt;2 ng/mL/y. Conclusions: We found weak evidence that higher folate levels may be associated with faster progression of localized prostate cancer. Impact: Long-term follow-up is needed to test associations with metastases and mortality, and the observed genetic effects require replication. Cancer Epidemiol Biomarkers Prev; 19(11); 2833–8. ©2010 AACR.
Type of Medium:
Online Resource
ISSN:
1055-9965
,
1538-7755
DOI:
10.1158/1055-9965.EPI-10-0582
Language:
English
Publisher:
American Association for Cancer Research (AACR)
Publication Date:
2010
detail.hit.zdb_id:
2036781-8
detail.hit.zdb_id:
1153420-5
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