The Hair Cycle of the Mouse and Its Importance in the Study of Sequences of Experimental Carcinogenesis

Wolbach, S. B.

doi:10.1111/j.1749-6632.1951.tb31954.x

Cited by 101 publications

(23 citation statements)

References 15 publications

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“…In agreem ent with the findings obtained in different previous in vestigations, including our own [2][3][4][5][6], the tum or incidence was higher in the mice exposed to the carcinogen during the resting phase than in those exposed during the growing phase of the hair cycle. It was also higher in the females than in males except for the mice exposed during anagen VI, i. c. on the day of the emergence of new hair on the skin surface (group 2).…”

Section: Discussionsupporting

confidence: 82%

“…[4], Borum [5] and Wolbach [6] that a single application of a potent carcinogen to the skin of the mouse causes more animals to develop tum ors when the application is perform ed during the resting phase of the hair cycle than when it is performed during the growing phase. This difference in tum or yield has been explained by Wolbacli [6] and Berenblum [4] on an anatomic and " m echanistic" basis. The former pointed out that during the resting phase of the hair cycle (telogen), the hair canal is open so that the cells of the bulb are exposed to the carcinogen, while Berenblum el al.…”

mentioning

confidence: 99%

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The Phase of the Hair Cycle at the Time of Chemical Carcinogen Exposure and Epidermal Tumor Development in Mice

Weidenreich-Sherwin¹,

Herrmann²

1964

Dermatology

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Section: Discussionsupporting

confidence: 82%

mentioning

confidence: 99%

The Phase of the Hair Cycle at the Time of Chemical Carcinogen Exposure and Epidermal Tumor Development in Mice

Weidenreich-Sherwin¹,

Herrmann²

1964

Dermatology

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“…As reviewed above, few of these mouse mutations have been used consistently in cutaneous carcinogenesis studies. The lesions induced by various carcinogenesis protocols in some of the mice with hair mutations are different from the papillomas and squamous cell carcinomas commonly reported or implied by studies of mice with a normal pelage [22,23]. This may reflect the effects of the carcinogen on defective follicular structures, of endogenous or environmental cocarcinogens, or of differences in genetic background of the host.…”

Section: Introductionmentioning

confidence: 77%

Comparison of chemical carcinogen skin tumor induction efficacy in inbred, mutant, and hybrid strains of mice: Morphologic variations of induced tumors and absence of a papillomavirus cocarcinogen

Sundberg¹,

Sundberg²,

Beamer³

1997

Mol. Carcinog.

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Chemical carcinogen induction of skin tumors in mice was investigated to determine (i) if tumor induction efficacy was modified by single gene mutations, (ii) if the histologic types of the tumors varied with these mutations, and (iii) if a novel papillomavirus was involved as a cocarcinogen. A two-stage carcinogenesis protocol (7,12-dimethylbenz[a]anthracene followed by 12-O-tetradecanoylphorbol-13-acetate) was used to induce papillomas in 14 inbred, two hybrid, and 15 other genetic stocks of mice with inherited, single-gene mutations causing skin abnormalities. Histopathological, immunohistochemical, and Southern blot analyses were performed to determine tumor type and to detect the presence of papillomaviruses. The histologic types of tumors induced included early follicular papillomas, mixed papillomas, exophytic papillomas, hyperplastic papillomas, fibropapillomas, squamous cell carcinomas, and mast cell tumors. The efficacy of tumor induction was influenced by strain background, as seen by the clustering of mice into high-, intermediate-, and nonresponding groups. Similarly, tumor induction efficacy was affected by specific mutant genes that cause skin abnormalities. No evidence of papillomavirus structural antigens or viral genomic DNA was identified in 547 induced tumors. These observations indicate that numerous modifier genes but not papillomaviruses are involved in cutaneous chemical carcinogenesis.

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“…One major difference between these two pigmentary processes is that epidermal pigmentation is continuous, whereas hair pigmentation is coupled with the hair cycle. The hair cycle, first described in [16], consists of phases of growth (anagen), regression (catagen) and resting (telogen), which are controlled in part by apoptotic processes. Follicular melanocytes proliferate during early anagen, mature in mid-late anagen and undergo apoptosis during early catagen [17].…”

Section: Hair Pigmentation and The Hair Cyclementioning

confidence: 99%

Age‐induced hair greying – the multiple effects of oxidative stress

Seiberg¹

2013

Intern J of Cosmetic Sci

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SynopsisAn obvious sign of ageing is hair greying, or the loss of pigment production and deposition within the hair shafts. Numerous mechanisms, acting at different levels and follicular locations, contribute to hair greying, ranging from melanocyte stem cells defects to follicular melanocyte death. One key issue that is in common to these processes is oxidative damage. At the hair follicle stem cells niche, oxidative stress, accelerated by B-cell lymphoma 2 gene (BCL-2) depletion, leads to selective apoptosis and diminution of melanocyte stem cells, reducing the repopulation of newly formed anagen follicles. Melanotic bulbar melanocytes express high levels of BCL-2 to enable survival from melanogenesis-and ultraviolet A (UVA)-induced reactive oxygen species (ROS) attacks. With ageing, the bulbar melanocyte expression of anti-oxidant proteins such as BCL-2, and possibly TRP-2, is reduced, and the dedicated enzymatic anti-oxidant defence system throughout the follicle weakens, resulting in enhanced oxidative stress. A marked reduction in catalase expression and activity results in millimolar accumulation of hydrogen peroxide, contributing to bulbar melanocyte malfunction and death. Interestingly, amelanotic melanocytes at the outer root sheath (ORS) are somewhat less affected by these processes and survive for longer time even within the white, ageing hair follicles. Better understanding of the overtime susceptibility of melanocytes to oxidative stress at the different follicular locations might yield clues to possible therapies for the prevention and reversal of hair greying.R esum e Un signe evident du vieillissement est le grisonnement des cheveux ou la perte de la production de pigment et de son d epôt dans les follicules pileux. De nombreux m ecanismes, agissant a diff erents niveaux et endroits folliculaires, contribuent aux cheveux grisonnants, allant des dommages aux cellules souches m elanocytaires a la mort des m elanocytes folliculaires. Une question cl e qui est commune a ces processus concerne le dommage oxydatif. Au niveau de la niche des cellules souches du follicule, le stress oxydatif, acc el er e par l'appauvrissement de BCL-2, conduit a l'apoptose et a une diminution s elective des cellules souches des m elanocytes, ce qui r eduit le repeuplement des follicules anag enes nouvellement form es. Les m elanocytes bulbaires m elaniques expriment des niveaux elev es de Bcl-2 pour permettre la survie suite a l'attaque par les esp eces r eactives de l'oxyg ene (ROS) induites par la m elanog en ese et les ultraviolets A (UVA). Avec le vieillissement, l'expression dans m elanocytes du bulbe des prot eines anti-oxydantes comme BCL-2, et peut-être TRP-2, est r eduite, et la d efense sp ecifique du syst eme antioxydant enzymatique faiblit a travers le follicule, r esultant en un plus grand stress oxydatif. Une r eduction marqu ee de l'expression catalase et les r esultats de l'activit e de l'accumulation millimolaire de peroxyde d'hydrog ene contribuent a un dysfonctionnement et a la mort des m elanocytes b...

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The Hair Cycle of the Mouse and Its Importance in the Study of Sequences of Experimental Carcinogenesis

Cited by 101 publications

References 15 publications

The Phase of the Hair Cycle at the Time of Chemical Carcinogen Exposure and Epidermal Tumor Development in Mice

The Phase of the Hair Cycle at the Time of Chemical Carcinogen Exposure and Epidermal Tumor Development in Mice

Comparison of chemical carcinogen skin tumor induction efficacy in inbred, mutant, and hybrid strains of mice: Morphologic variations of induced tumors and absence of a papillomavirus cocarcinogen

Age‐induced hair greying – the multiple effects of oxidative stress

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