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Medline ® Abstracts for References 103-105

of '化疗引起的脱发'

103
TI
Protection from 1-beta-D-arabinofuranosylcytosine-induced alopecia by epidermal growth factor and fibroblast growth factor in the rat model.
AU
Jimenez JJ, Yunis AA
SO
Cancer Res. 1992;52(2):413.
 
The present study was designed to examine the effect of epidermal growth factor (EGF) and fibroblast growth factor (FGF) on 1-beta-D-arabinofuranosylcytosine (ARA-C)- and cyclophosphamide-induced alopecia in the young rat model. Seven-day-old rats were given ARA-C with or without human or murine EGF daily for 7 days. Alopecia was scored on the 12th day of the experiment. Both human and murine EGF protected rats from ARA-C-induced alopecia. The topical application of murine EFG in dimethyl sulfoxide offered significant protection limited to the treated area. In other experiments the administration of acidic FGF (aFGF) with ARA-C resulted in protection from alopecia limited to the site of FGF injection. Neither EGF nor FGF had any influence on alopecia from cyclophosphamide. It is concluded that both EGF and FGF are effective in protecting against ARA-C-induced alopecia in the rat model.
AD
Department of Medicine, University of Miami School of Medicine, Florida 33101.
PMID
104
TI
Epidermal growth factor receptor inhibition induces trichomegaly.
AU
Dueland S, Sauer T, Lund-Johansen F, Ostenstad B, Tveit KM
SO
Acta Oncol. 2003;42(4):345.
 
AD
Department of Oncology, Ullevaal University Hospital, Oslo, Norway. svein.dueland@labmed.uio.no
PMID
105
TI
Role for the epidermal growth factor receptor in chemotherapy-induced alopecia.
AU
Bichsel KJ, Gogia N, Malouff T, Pena Z, Forney E, Hammiller B, Watson P, Hansen LA
SO
PLoS One. 2013;8(7):e69368. Epub 2013 Jul 19.
 
Treatment of cancer patients with chemotherapeutics like cyclophosphamide often causes alopecia as a result of premature and aberrant catagen. Because the epidermal growth factor receptor (EGFR) signals anagen hair follicles to enter catagen, we hypothesized that EGFR signaling may be involved in cyclophosphamide-induced alopecia. To test this hypothesis, skin-targeted Egfr mutant mice were generated by crossing floxed Egfr and Keratin 14 promoter-driven Cre recombinase mice. Cyclophosphamide treatment of control mice resulted in alopecia while Egfr mutant skin was resistant to cyclophosphamide-induced alopecia. Egfr mutant skin entered catagen normally, as indicated by dermal papilla condensation and decreased follicular proliferation, but did not progress to telogen as did Egfr wild type follicles. Egfr mutant follicles responded with less proliferation, apoptosis, and fewer p53-positive cells after cyclophosphamide. Treatment of control mice with the EGFR inhibitors erlotinib or gefitinib similarly suppressed alopecia and catagen progression by cyclophosphamide. Secondary analysis of clinical trials utilizing EGFR-targeted therapies and alopecia-inducing chemotherapy also revealed evidence for involvement of EGFR in chemotherapy-induced alopecia. Taken together, our results demonstrated the involvement of EGFR signaling in chemotherapy-induced alopecia, which will help in the design of novel therapeutic regimens to minimize chemotherapy-induced alopecia.
AD
Department of Biomedical Sciences, School of Medicine, Creighton University, Omaha, Nebraska, United States of America.
PMID