(Q23914668)

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Deficient nucleotide excision repair capacity enhances human prostate cancer risk

journal article published in 2004

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19 July 2017

Deficient nucleotide excision repair capacity enhances human prostate cancer risk (English)

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12 July 2017

National Institute for Occupational Safety and Health

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29 March 2020

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29 March 2020

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29 March 2020

J. J. Hu

1

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language of work or name

English

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publication date

1 February 2004

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published in

Cancer Research

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volume

64

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issue

3

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page(s)

1197-1201

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performing organization

Johns Hopkins University

object named as

Johns Hopkins University

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stated in

NIOSHTIC-2

retrieved

2 February 2024

on focus list of Wikimedia project

Wikimedia–NIOSH collaboration

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1 reference

25 September 2023

Cancer statistics, 2003.

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Symposium overview: genetic polymorphisms in DNA repair and cancer risk

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DNA repair and aging in basal cell carcinoma: a molecular epidemiology study

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DNA adducts from a tumorigenic metabolite of benzo[a]pyrene block human RNA polymerase II elongation in a sequence- and stereochemistry-dependent manner

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Prostate cancer is part of the hereditary non-polyposis colorectal cancer (HNPCC) tumor spectrum

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Human DNA repair genes

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Mortality in relation to smoking history: 13 years' follow-up of 68,000 Norwegian men and women 35-49 years.

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Modulation of repair of ultraviolet damage in the host-cell reactivation assay by polymorphic XPC and XPD/ERCC2 genotypes

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Mutations in CHEK2 associated with prostate cancer risk

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Effect of DNA repair gene polymorphisms on BPDE-DNA adducts in human lymphocytes

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Smoking and prostate cancer

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Rapid assessment of repair of ultraviolet DNA damage with a modified host-cell reactivation assay using a luciferase reporter gene and correlation with polymorphisms of DNA repair genes in normal human lymphocytes.

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Primary cultures of prostate cells and their ability to activate carcinogens

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(Q23914668)

Deficient nucleotide excision repair capacity enhances human prostate cancer risk

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