ULTRAVIOLET RADIATION INDUCED SKIN CANCER

紫外线辐射诱发的皮肤癌

基本信息

项目摘要

UV radiation suppresses the induction and elicitation of delayed-type hypersensitivity (DTH) in some individuals, but not all. We have developed a quantitative method using laser Doppler perfusion imaging analysis of UV-AB induced suppression of DTH using the elicitation response in previously tuberculin-PPD sensitized individuals in order to investigate the dose response relationship between UV dose and induction of suppression or resistance to UV induced suppression. Nineteen healthy volunteers were irradiated daily for four days on delineated areas on the upper back with UV-AB radiation. UV-AB dose levels were adjusted to deliver 60 or 120 mJ/ cm2 UV-B radiation. On the fourth day, one irradiated and one unirradiated test site for each UV-dose were chosen at random on each individual and injected intradermally with tuberculin. Test reactions were analyzed and quantified at j96 h clinically and with laser Doppler perfusion imaging. The results indicate that UV-AB radiation can suppress the elicitation phase of tuberculin delayed type hypersensitivity immune reaction and that there are dose dependent and individual differences in the immune suppressive effect of the UV- radiation. at low dose (UV-B), both the susceptible and resistant phenotypes were observed at an approximate ratio of 1:1. However, doubling the dose of UV-B increased the suppression in some individuals, induced suppression in others that were resistant, or induced a resistance or tolerance in others that were susceptible at the lower dose of UV. We hypothesize that the thresholds for UV induced suppression of DTH and the induction of T suppressor cells that may block elicitation vary considerably. Thus, characterization of both the UVR and the UVR dose response relationship for induction of susceptibility or resistance must be determined in order to adequately phenotype for these traits. These phenotypic differences in the human population may be used to determine if increased risks to skin cancer occurs in individuals who are suppressed.
紫外线辐射抑制延迟型的诱导和激发

项目成果

期刊论文数量(0)
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J E FRENCH其他文献

J E FRENCH的其他文献

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{{ truncateString('J E FRENCH', 18)}}的其他基金

MOLECULAR GENETICS OF AROMATIC AMINE INDUCED BLADDER CANCER
芳香胺诱发膀胱癌的分子遗传学
  • 批准号:
    6162134
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
DEVELOPMENT OF AN IN VIVO MODEL OF GENOMIC INSTABILITY (LACI--P53(+/-)MICE)
基因组不稳定性体内模型的开发(LACI--P53(/-)小鼠)
  • 批准号:
    6162130
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
GENETIC SUSCEPTIBILITY TO ULTRAVIOLET RADIATION AND CHEMICAL INDUCED SKIN CANCER
对紫外线辐射和化学诱发皮肤癌的遗传易感性
  • 批准号:
    3755399
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
IDENTIFICATION AND ISOLATION OF C-FMS PROTOONCOGEN FROM F344/N RAT LEUKEMIA
F344/N 大鼠白血病 C-FMS 原癌原的鉴定和分离
  • 批准号:
    3876855
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
ENVIRONMENTAL CHEMICAL AND OXIDATIVE STRESS INDUCED DNA DAMAGE & CARCINOGENESIS
环境化学和氧化应激引起的 DNA 损伤
  • 批准号:
    3841038
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
KARYOTYPIC ANALYSIS OF MALIGNANT SKIN TUMORS OF TG-AG (V-HA-RAS) AND FVB MICE
TG-AG (V-HA-RAS) 和 FVB 小鼠恶性皮肤肿瘤的核型分析
  • 批准号:
    3841046
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
MUTAGENESIS AND CARCINOGENESIS STUDIES IN P53 (+/-) OR LACI:P53 (+/-) MICE
P53 ( /-) 或 LACI:P53 ( /-) 小鼠的突变和致癌研究
  • 批准号:
    5202144
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
DEVELOPMENT OF IN VITRO PROPAGATED F344/N MONONUCLEAR CELL LINK
体外增殖的 F344/N 单核细胞链接的开发
  • 批准号:
    3918637
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
MOLECULAR GENETICS OF AROMATIC AMINE INDUCED BLADDER CANCER
芳香胺诱发膀胱癌的分子遗传学
  • 批准号:
    2452842
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:
IDENTIFICATION AND ISOLATION OF C-FMS PROTOONCOGEN FROM F344/N RAT LEUKEMIA
F344/N 大鼠白血病 C-FMS 原癌原的鉴定和分离
  • 批准号:
    3941497
  • 财政年份:
  • 资助金额:
    --
  • 项目类别:

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