Detection of the major DNA adducts of benzo[b]fluoranthene in mouse skin: Role of phenolic dihydrodiols

1993 ◽  
Vol 6 (4) ◽  
pp. 568-577 ◽  
Author(s):  
Eric H. Weyand ◽  
Zhen Wei Cai ◽  
Yun Wu ◽  
Joseph E. Rice ◽  
Zhen Min He ◽  
...  
Keyword(s):  
Dna Adducts ◽  
Mouse Skin

scholarly journals The role of polycyclic aromatic hydrocarbon–DNA adducts in inducing mutations in mouse skin

2008 ◽  
Vol 649 (1-2) ◽  
pp. 161-178 ◽  
Author(s):  
Dhrubajyoti Chakravarti ◽  
Divya Venugopal ◽  
Paula C. Mailander ◽  
Jane L. Meza ◽  
Sheila Higginbotham ◽  
...  
Keyword(s):  
Polycyclic Aromatic Hydrocarbon ◽  
Aromatic Hydrocarbon ◽  
Dna Adducts ◽  
Mouse Skin ◽  
Polycyclic Aromatic

The Nude Mouse Skin Phenotype: The Role of Foxn1 in Hair Follicle Development and Cycling

2001 ◽  
Vol 71 (2) ◽  
pp. 171-178 ◽  
Author(s):  
Lars Mecklenburg ◽  
Motonobu Nakamura ◽  
John P. Sundberg ◽  
Ralf Paus
Keyword(s):  
Hair Follicle ◽  
Nude Mouse ◽  
Mouse Skin ◽  
Follicle Development ◽  
Hair Follicle Development

scholarly journals Differential Role of Basal Keratinocytes in UV-Induced Immunosuppression and Skin Cancer

2006 ◽  
Vol 26 (22) ◽  
pp. 8515-8526 ◽  
Author(s):  
Judith Jans ◽  
George A. Garinis ◽  
Wouter Schul ◽  
Adri van Oudenaren ◽  
Michael Moorhouse ◽  
...  
Keyword(s):  
Skin Cancer ◽  
Biological Effects ◽  
Mouse Skin ◽  
Cell Type ◽  
Cell Type Specificity ◽  
Basal Keratinocytes ◽  
Expression Of Genes ◽  
Pyrimidine Dimers ◽  
Response To Stress

ABSTRACT Cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs) comprise major UV-induced photolesions. If left unrepaired, these lesions can induce mutations and skin cancer, which is facilitated by UV-induced immunosuppression. Yet the contribution of lesion and cell type specificity to the harmful biological effects of UV exposure remains currently unclear. Using a series of photolyase-transgenic mice to ubiquitously remove either CPDs or 6-4PPs from all cells in the mouse skin or selectively from basal keratinocytes, we show that the majority of UV-induced acute effects to require the presence of CPDs in basal keratinocytes in the mouse skin. At the fundamental level of gene expression, CPDs induce the expression of genes associated with repair and recombinational processing of DNA damage, as well as apoptosis and a response to stress. At the organismal level, photolyase-mediated removal of CPDs, but not 6-4PPs, from the genome of only basal keratinocytes substantially diminishes the incidence of skin tumors; however, it does not affect the UVB-mediated immunosuppression. Taken together, these findings reveal a differential role of basal keratinocytes in these processes, providing novel insights into the skin's acute and chronic responses to UV in a lesion- and cell-type-specific manner.

scholarly journals Immunohistochemical Detection of Carcinogen-DNA Adducts and DNA Repair in Mouse Skin

1989 ◽  
Vol 92 (5) ◽  
pp. S275-S279 ◽  
Author(s):  
Kazuhiko Nakagawa ◽  
Yoko Nakatsuru ◽  
Takatoshi Ishikawa
Keyword(s):  
Dna Repair ◽  
Dna Adducts ◽  
Mouse Skin ◽  
Immunohistochemical Detection

scholarly journals 084 The role of interferon and retroelements in lupus-prone Ro60 knockout mouse skin

2018 ◽  
Vol 138 (5) ◽  
pp. S14
Author(s):  
D. Rokunohe ◽  
E. Chiou ◽  
X. Sun ◽  
L. Tanaka ◽  
S.L. Wolin ◽  
...  
Keyword(s):  
Knockout Mouse ◽  
Mouse Skin

scholarly journals MicroRNA-24 Modulates Aflatoxin B1-Related Hepatocellular Carcinoma Prognosis and Tumorigenesis

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Yi-Xiao Liu ◽  
Xi-Dai Long ◽  
Zhi-Feng Xi ◽  
Yun Ma ◽  
Xiao-Ying Huang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Dna Adducts ◽  
Aflatoxin B1 ◽  
Tissue Samples ◽  
Noncancerous Tissue ◽  
Free Survival ◽  
Tumor Tissues ◽  
Neoplastic Process ◽  
First Time

MicroRNA-24 (miR-24) may be involved in neoplastic process; however, the role of this microRNA in the hepatocellular carcinoma (HCC) related to aflatoxin B1 (AFB1) has not been well elaborated. Here, we tested miR-24 expression in 207 pathology-diagnosed HCC cases from high AFB1 exposure areas and HCC cells. We found that miR-24 was upregulated in HCC tumor tissues relative to adjacent noncancerous tissue samples, and that the high expression of miR-24 was significantly correlated with larger tumor size, higher microvessel density, and tumor dedifferentiation. Additionally, this microRNA overexpression modified the recurrence-free survival (relative hazard ratio [HR], 4.75; 95% confidence interval [CI], 2.66–8.47) and overall survival (HR=3.58, 95% CI = 2.34–5.46) of HCC patients. Furthermore, we observed some evidence of joint effects between miR-24 and AFB1 exposure on HCC prognosis. Functionally, miR-24 overexpression progressed tumor cells proliferation, inhibited cell apoptosis, and developed the formation of AFB1-DNA adducts. These results indicate for the first time that miR-24 may modify AFB1-related HCC prognosis and tumorigenesis.

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