Der Einfluß des Endoxans auf die Haarmelanogenese und das Haarwachstum bei Mäusen

Kostanecki, W; E, Kwiatkowska; R, Zák

doi:10.1007/bf00496389

Cited by 4 publications

(3 citation statements)

References 9 publications

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“…at the beginning of anagen VI (Fig. 1, 4B, 5B), the hair follicles react by acute dystrophy (Braun-Falco, 1961;Kostanecki et al, 1967;Paus et al, 1994a;Slominski et al, 1996). The whole population of multiplying melanocytes and keratinocytes undergo abrupt apoptosis (Hendrix et al, 2005), resulting in alopecia (Fig.…”

Section: Hair Cycle and Melanogenesismentioning

confidence: 98%

“…Impairment of the hair cycle and of the related melanin production is often associated with ectopic deposition of the pigment in the hair follicle outside the hair shaft. Such pathological melanization is a side-effect of cancer chemotherapy with cyclophosphamide (CYP) in humans (Braun-Falco, 1961), and in model mice (Kostanecki et al, 1967). This is a rationale to suppose that in such a case a particular increase in splenic melanin deposition can be expected.…”

Section: Introductionmentioning

confidence: 99%

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Splenic melanosis during normal murine C57BL/6 hair cycle and after chemotherapy.

et al. 2013

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Cancer chemotherapy is associated with serious side effects, including temporary hair loss and impairment of pigmentation. We suspect that ectopic melanin deposition occurring due to chemotherapy may add to these effects worsening the already unpleasant symptoms. We associated the ectopic occurrence of follicular melanin after chemotherapy with splenic melanosis - an interesting example of extradermal melanin localization - and we expected an increase in splenic melanin deposition after chemotherapy. Using the C57BL/6 murine model of synchronized hair cycle induced by depilation, we visualized splenic melanin by means of several histological and histochemical protocols of staining: hematoxylin and eosin, May-Grünwald-Giemsa and Fontana-Masson. Unexpectedly, the splenic deposition of melanin decreased due to application of cyclophosphamide (i.p. 120 mg/ kg body weight on day 9 post depilation). The drop was abrupt and lasted for at least 5 days (day 13-18 post depilation), as compared with normal hair cycle. Moreover, in mice with normal, depilation-induced hair cycle we observed a similar drop shortly before entering catagen (day 15 post depilation), followed by a slow and partial increase in splenic melanization up to day 27 post depilation in both groups. We conclude that cyclophosphamide negatively affects splenic melanization and/or extradermal transfer of ectopic melanin from the dystrophic hair follicles, but the most powerful down-regulator of splenic melanosis is normal and dystrophic catagen - the phase of hair follicle involution and re-modelling.

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Section: Hair Cycle and Melanogenesismentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Splenic melanosis during normal murine C57BL/6 hair cycle and after chemotherapy.

et al. 2013

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“…His observations lead him to pass his professorial qualifying exam ‘Habilitation’ in 1970. Kostanecki published several papers in Archiv für klinische und experimentelle Dermatologie, two of which concerned chemotherapy‐induced hair pigmentation disorders: the first reported the observations of human chemotherapy‐induced alopecia, and the second was devoted to a suitable mouse model . This parallel approach to dissect the problem at hand was crucial and exemplary, because it generated translationally relevant research by combing the advantages of the murine model with observations of human hair follicles .…”

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confidence: 99%

Hair pigmentation disorders or 50 years of German‐Polish alliance for study on a severe side effect of chemotherapy: Kostanecki's legacy

Płonka

2014

Experimental Dermatology

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Pharmacological Disruption of Hair Follicle Pigmentation by Cyclophosphamide as a Model for Studying the Melanocyte Response to and Recovery from Cytotoxic Drug Damage In Situ

Słomiński

Paus

Płonka

et al. 1996

Journal of Investigative Dermatology

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Here we show that cyclophosphamide induces disruption of follicular melanogenesis, which is characterized by abnormal transfer of pigment granules to ectopic hair bulb locations, extrafollicular melanin incontinence, disordered formation of melanosomes, and inhibition of melanosome transfer into precortical keratinocytes. This is in contrast to dexamethasone-induced termination of follicle melanogenesis, which activates premature but predominantly normal catagen development. Cyclophosphamide-induced pigmentation disruption was accompanied by significant alterations of biochemical and biophysical markers of melanogenesis, compared to control mice treated either with vehicle or with topical dexamethasone. Electron paramagnetic resonance spectroscopy shows a decline in the melanin signal and predominant eumelanin production. Tyrosine hydroxylase activity of tyrosinase and dihydroxyphenylalanine oxidation drop rapidly, while DOPAchrome tautomerase activity increases and dihydroxyindole carboxylic acid conversion factor activity remains unchanged in cyclophosphamide-treated mice compared to controls. These observations emphasize the key role of tyrosinase as opposed to postdihydroxyphenylalanine oxidase steps in normal and pathological termination of melanogenesis and shows that tyrosinase is the most sensitive target of the melanogenic apparatus for pharmacological regulation. Follicle pigmentation recovers only during the subsequent hair cycle, i.e., after a new anagen hair bulb has been constructed, which points to the existence of a relatively chemoresistant melanoblast-like cell population residing in the noncycling part of the hair follicle.

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Der Einfluß des Endoxans auf die Haarmelanogenese und das Haarwachstum bei Mäusen

Cited by 4 publications

References 9 publications

Splenic melanosis during normal murine C57BL/6 hair cycle and after chemotherapy.

Splenic melanosis during normal murine C57BL/6 hair cycle and after chemotherapy.

Hair pigmentation disorders or 50 years of German‐Polish alliance for study on a severe side effect of chemotherapy: Kostanecki's legacy

Pharmacological Disruption of Hair Follicle Pigmentation by Cyclophosphamide as a Model for Studying the Melanocyte Response to and Recovery from Cytotoxic Drug Damage In Situ

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