Treatment with 1-alpha,25-dihydroxyvitamin D3 (vitamin D 3) to inhibit carcinogenesis in the hamster buccal pouch model

Jeremy D. Meier, Danny J. Enepekides, Brian Poirier, Christopher A. Bradley, Joanna S. Albala, D Gregory Farwell

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Objective: To investigate whether systemic therapy with 1-alpha,25-dihydroxyvitamin D3 (vitamin D3 [hereinafter, VD3]) prevents tumor formation in a hamster buccal pouch model of carcinogenesis. Design: Randomized trial in which a known carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), was applied to the buccal pouch of 40 hamsters. Animals were randomized to receive systemic VD3 or no treatment and killed at 2, 6, and 14 weeks after the initiation of DMBA exposure. Setting: Academic medical center. Subjects: Forty male golden Syrian hamsters, aged 5 to 6 weeks, were used. Interventions: A dose of 0.25 μg/kg of VD3 via intraperitoneal injection was given to 20 animals 3 times per week. Of the remaining 20 control animals, 5 received placebo vehicle injection, and 15 received no further treatment. Main Outcome Measures: Timing, size, and number of tumors that developed in the 2 groups. Results: Only 1 hamster treated with VD3 developed a confirmed neoplasm compared with 7 of the control animals (P<.01). The mean±SD total diameter of gross lesions per animal in the VD3-treated group was 1.2±1.9 mm compared with 6.8±6.6mm in the control group (P=.03). The time to onset of lesion formation was significantly delayed in those animals treated with VD 3, with a mean±SD time to development of 13.4±0.9 weeks, while the control animals developed lesions at 11.2±1.7 weeks (P=.02). Conclusions: Systemic VD3 therapy delays carcinogenesis in the hamster buccal pouch model. Further investigation into the mechanisms through which VD3 inhibits carcinogenesis may lead to development of effective chemopreventive agents to combat head and neck cancer.

Original languageEnglish (US)
Pages (from-to)1149-1152
Number of pages4
JournalArchives of Otolaryngology - Head and Neck Surgery
Volume133
Issue number11
DOIs
StatePublished - Nov 2007

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Cheek
Cricetinae
Carcinogenesis
9,10-Dimethyl-1,2-benzanthracene
Cholecalciferol
Therapeutics
Neoplasms
Dihydroxycholecalciferols
Mesocricetus
Head and Neck Neoplasms
Intraperitoneal Injections
Vitamins
Carcinogens
Placebos
Outcome Assessment (Health Care)
Control Groups
Injections

ASJC Scopus subject areas

  • Otorhinolaryngology

Cite this

Treatment with 1-alpha,25-dihydroxyvitamin D3 (vitamin D 3) to inhibit carcinogenesis in the hamster buccal pouch model. / Meier, Jeremy D.; Enepekides, Danny J.; Poirier, Brian; Bradley, Christopher A.; Albala, Joanna S.; Farwell, D Gregory.

In: Archives of Otolaryngology - Head and Neck Surgery, Vol. 133, No. 11, 11.2007, p. 1149-1152.

Research output: Contribution to journalArticle

Meier, Jeremy D. ; Enepekides, Danny J. ; Poirier, Brian ; Bradley, Christopher A. ; Albala, Joanna S. ; Farwell, D Gregory. / Treatment with 1-alpha,25-dihydroxyvitamin D3 (vitamin D 3) to inhibit carcinogenesis in the hamster buccal pouch model. In: Archives of Otolaryngology - Head and Neck Surgery. 2007 ; Vol. 133, No. 11. pp. 1149-1152.
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abstract = "Objective: To investigate whether systemic therapy with 1-alpha,25-dihydroxyvitamin D3 (vitamin D3 [hereinafter, VD3]) prevents tumor formation in a hamster buccal pouch model of carcinogenesis. Design: Randomized trial in which a known carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), was applied to the buccal pouch of 40 hamsters. Animals were randomized to receive systemic VD3 or no treatment and killed at 2, 6, and 14 weeks after the initiation of DMBA exposure. Setting: Academic medical center. Subjects: Forty male golden Syrian hamsters, aged 5 to 6 weeks, were used. Interventions: A dose of 0.25 μg/kg of VD3 via intraperitoneal injection was given to 20 animals 3 times per week. Of the remaining 20 control animals, 5 received placebo vehicle injection, and 15 received no further treatment. Main Outcome Measures: Timing, size, and number of tumors that developed in the 2 groups. Results: Only 1 hamster treated with VD3 developed a confirmed neoplasm compared with 7 of the control animals (P<.01). The mean±SD total diameter of gross lesions per animal in the VD3-treated group was 1.2±1.9 mm compared with 6.8±6.6mm in the control group (P=.03). The time to onset of lesion formation was significantly delayed in those animals treated with VD 3, with a mean±SD time to development of 13.4±0.9 weeks, while the control animals developed lesions at 11.2±1.7 weeks (P=.02). Conclusions: Systemic VD3 therapy delays carcinogenesis in the hamster buccal pouch model. Further investigation into the mechanisms through which VD3 inhibits carcinogenesis may lead to development of effective chemopreventive agents to combat head and neck cancer.",
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AU - Enepekides, Danny J.

AU - Poirier, Brian

AU - Bradley, Christopher A.

AU - Albala, Joanna S.

AU - Farwell, D Gregory

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AB - Objective: To investigate whether systemic therapy with 1-alpha,25-dihydroxyvitamin D3 (vitamin D3 [hereinafter, VD3]) prevents tumor formation in a hamster buccal pouch model of carcinogenesis. Design: Randomized trial in which a known carcinogen, 7,12-dimethylbenz[a]anthracene (DMBA), was applied to the buccal pouch of 40 hamsters. Animals were randomized to receive systemic VD3 or no treatment and killed at 2, 6, and 14 weeks after the initiation of DMBA exposure. Setting: Academic medical center. Subjects: Forty male golden Syrian hamsters, aged 5 to 6 weeks, were used. Interventions: A dose of 0.25 μg/kg of VD3 via intraperitoneal injection was given to 20 animals 3 times per week. Of the remaining 20 control animals, 5 received placebo vehicle injection, and 15 received no further treatment. Main Outcome Measures: Timing, size, and number of tumors that developed in the 2 groups. Results: Only 1 hamster treated with VD3 developed a confirmed neoplasm compared with 7 of the control animals (P<.01). The mean±SD total diameter of gross lesions per animal in the VD3-treated group was 1.2±1.9 mm compared with 6.8±6.6mm in the control group (P=.03). The time to onset of lesion formation was significantly delayed in those animals treated with VD 3, with a mean±SD time to development of 13.4±0.9 weeks, while the control animals developed lesions at 11.2±1.7 weeks (P=.02). Conclusions: Systemic VD3 therapy delays carcinogenesis in the hamster buccal pouch model. Further investigation into the mechanisms through which VD3 inhibits carcinogenesis may lead to development of effective chemopreventive agents to combat head and neck cancer.

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