TLDR Inhibiting ODC can prevent UV-induced skin cancer.
The study from September 2001 demonstrated that ornithine decarboxylase (ODC) played a crucial role in UVB-induced skin carcinogenesis. Using K5/ODC transgenic mice, researchers found that UVB exposure significantly increased ODC activity, leading to the development of epidermal tumors in 40% of the mice, while nontransgenic mice did not develop tumors. The study concluded that inhibiting ODC with α-difluoromethylornithine (DFMO) completely prevented tumor formation, suggesting that ODC inhibitors could be a potential therapeutic strategy for preventing UV-induced skin cancer.
88 citations
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August 1998 in “Carcinogenesis” High levels of ODC and a mutant Ha-ras gene cause tumors in mice.
16 citations
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January 1998 in “PubMed” Sun exposure and genetics increase skin cancer risk from precancerous lesions.
233 citations
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July 1997 in “PubMed” High levels of ornithine decarboxylase can cause tumors in mouse skin.
71 citations
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May 1996 in “Journal of Investigative Dermatology” Ornithine decarboxylase is crucial for hair growth regulation in mice.
January 2017 in “Jikken doubutsu ihou/Jikken doubutsu/Experimental animals/Jikken Dobutsu” Mice with a changed Hr gene lose and regrow hair due to changes in the gene's activity.
67 citations
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September 2001 in “American Journal Of Pathology” Inhibiting ODC can prevent UV-induced skin cancer.
233 citations
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July 1997 in “PubMed” High levels of ornithine decarboxylase can cause tumors in mouse skin.
25 citations
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September 1995 in “Biochemistry and Cell Biology” High levels of human keratin 16 in mice cause skin lesions and abnormal skin development.
