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Protection against cyclophosphamide‐induced alopecia and inhibition of mammary tumor growth by topical 1,25‐dihydroxyvitamin D 3 in mice
Author(s) -
Chen Guan,
Baechle Alec,
Nevins Thomas D.,
Oh Susan,
Harmon Charles,
Stacey Dennis W.
Publication year - 1998
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19980119)75:2<303::aid-ijc21>3.0.co;2-c
Subject(s) - cyclophosphamide , hair growth , medicine , mammary tumor , mammary gland , endocrinology , cancer research , pharmacology , chemotherapy , physiology , cancer , breast cancer
Twenty‐one‐day‐old BALB/c mice were shaved on the back to synchronize hair growth. On day 30 or 31, when at least 90% of mice exhibited hair regrowth in the shaved area, 1,25(OH) 2 D 3 was applied topically to the shaved area daily for 5 days. On the 6th day, cyclophosphamide (Cytoxan, CTX) was injected i.p. to induce hair loss in the shaved area. Alopecia was induced in a dose‐dependent manner by CTX treatment within 1 to 2 weeks. This effect was reduced significantly if mice were pre‐treated with 1,25(OH) 2 D 3 , though only slight protection was observed in female mice. Interestingly, this 1,25(OH) 2 D 3 ‐mediated protection against hair loss was attenuated in male mice but became more significant in female mice when they were inoculated with the EMT‐6 murine mammary tumor prior to treatment. More importantly, topical treatment with 1,25(OH) 2 D 3 alone was able to inhibit EMT‐6 tumor growth in both male and female BALB/c mice. Furthermore, 1,25(OH) 2 D 3 pre‐treatment also augmented the anti‐tumor effect of CTX. Our results demonstrate that topical application of 1,25(OH) 2 D 3 can protect against CTX‐induced alopecia both in tumor‐free and in tumor‐bearing mice in a sex‐dependent manner. Moreover, 1,25(OH) 2 D 3 was shown, either alone or in combination with CTX, to inhibit tumor growth. Int. J. Cancer 75:303–309, 1998. © 1998 Wiley‐Liss, Inc.