Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations.

Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations. Research Abstract Details 

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Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations. Abstract Text:

Terumi Mizuno,Shoji Tokuoka,Masao Kishikawa,Eiji Nakashima,Kiyohiko Mabuchi,Keisuke S Iwamoto,

Epidemiological studies suggest that UV exposure from sunlight is the major etiology for skin cancers, both melanocytic and non-melanocytic. However, the radiation-related risk for skin cancer among atomic bomb survivors of Hiroshima and Nagasaki is primarily derived from the excess risk of basal cell carcinoma (BCC), with no demonstrable excess in squamous cell carcinoma or melanoma. The BCCs in this cohort are therefore unusual in being potentially attributable to two types of radiation-UV and ionizing (IR). BCCs have been associated with PTCH and/or p53 tumor suppressor gene alterations. To investigate the roles of these genes in relation to IR and UV exposures, we analyzed both genes in BCC samples from atomic bomb survivors. We examined 47 tumors, of which 70% had non-silent base-substitution p53 mutations independent of IR or UV exposure. However, the distribution of mutation type depends on UV and/or IR exposure. For example, C-to-T transitions at CpG sites adjacent to pyrimidine-pyrimidine (PyPy) sequences were more prevalent in tumors from UV-exposed than UV-shielded body areas and CpG-mutations at non-PyPy sequences were more prevalent in tumors from UV-shielded body areas with high-IR (>or=1 Gy) than low-IR (<0.2 Gy) exposure. And notably, although p53 deletion-frequencies demonstrated no IR-dose associations, deletions at the PTCH locus were more frequent (79% versus 44%) in tumors with high-IR than low-IR exposure. Moreover, 60% of high-IR tumors harbored both p53 and PTCH abnormalities compared with 23% of low-IR tumors. Therefore, alteration of both genes is likely to play a role in radiation-induced basal cell carcinogenesis.

Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations. Publishing Authors By Initials

T Mizuno,S Tokuoka,M Kishikawa,E Nakashima,K Mabuchi,KS Iwamoto,

For similar environment and public health: environment: meteorological factors: atmosphere: weather: sunlight: ultraviolet rays research abstracts see: environment and public health: environment: meteorological factors: atmosphere: weather: sunlight: ultraviolet rays research

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Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: Carcinogenesis

VOLUME: 27

Page Numbers: 2286-94

Journal Abbreviation: Carcinogenesis

ISSN: 0143-3334

DAY: 15

MONTH: 06

YEAR: 2006

Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8008055

Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations. Keywords Mesh Terms:

KEYWORDS: Ultraviolet Rays

MESH TERMS: genetics

Chemical & Substance for Abstract: Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations. Information

Substance Name: patched receptors

Registry Number: 0

Grant and Affiliation Information for Molecular basis of basal cell carcinogenesis in the atomic-bomb survivor population: p53 and PTCH gene alterations.

AFFILIATION: Department of Radiobiology/Molecular Epidemiology Hiroshima 732-0815, Japan.

Country: England

AGENCY: United States NCI

GRANT: N01-CP-71015

ACRONYM: CP

MEDLINETA: Carcinogenesis

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