Chemoprevention of Nonmelanoma Skin Cancer With Celecoxib: A Randomized, Double-Blind, Placebo-Controlled Trial
Background Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonme...
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| Published in | JNCI : Journal of the National Cancer Institute Vol. 102; no. 24; pp. 1835 - 1844 |
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| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Cary, NC
Oxford University Press
15.12.2010
Oxford Publishing Limited (England) |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonmelanoma skin cancers, and for nonmelanoma skin cancers, including cutaneous squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs). Methods A double-blind placebo-controlled randomized trial involving 240 subjects aged 37–87 years with 10–40 actinic keratoses was conducted at eight US academic medical centers. Patients were randomly assigned to receive 200 mg of celecoxib or placebo administered orally twice daily for 9 months. Subjects were evaluated at 3, 6, 9 (ie, completion of treatment), and 11 months after randomization. The primary endpoint was the number of new actinic keratoses at the 9-month visit as a percentage of the number at the time of randomization. In an intent-to-treat analysis, the incidence of actinic keratoses was compared between the two groups using t tests. In exploratory analyses, we evaluated the number of nonmelanoma skin cancers combined and SCCs and BCCs separately per patient at 11 months after randomization using Poisson regression, after adjustment for patient characteristics and time on study. The numbers of adverse events in the two treatment arms were compared using χ2 or Fisher exact tests. All statistical tests were two-sided. Results There was no difference in the incidence of actinic keratoses between the two groups at 9 months after randomization. However, at 11 months after randomization, there were fewer nonmelanoma skin cancers in the celecoxib arm than in the placebo arm (mean cumulative tumor number per patient 0.14 vs 0.35; rate ratio [RR] = .43, 95% confidence interval [CI] = 0.24 to 0.75; P = .003). After adjusting for age, sex, Fitzpatrick skin type, history of actinic keratosis at randomization, nonmelanoma skin cancer history, and patient time on study, the number of nonmelanoma skin cancers was lower in the celecoxib arm than in the placebo arm (RR = 0.41, 95% CI = 0.23 to 0.72, P = .002) as were the numbers of BCCs (RR = 0.40, 95% CI = 0.18 to 0.93, P = .032) and SCCs (RR = 0.42, 95% CI = 0.19 to 0.93, P = .032). Serious and cardiovascular adverse events were similar in the two groups. Conclusions Celecoxib may be effective for prevention of SCCs and BCCs in individuals who have extensive actinic damage and are at high risk for development of nonmelanoma skin cancers. |
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| AbstractList | Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonmelanoma skin cancers, and for nonmelanoma skin cancers, including cutaneous squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs).BACKGROUNDPreclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonmelanoma skin cancers, and for nonmelanoma skin cancers, including cutaneous squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs).A double-blind placebo-controlled randomized trial involving 240 subjects aged 37-87 years with 10-40 actinic keratoses was conducted at eight US academic medical centers. Patients were randomly assigned to receive 200 mg of celecoxib or placebo administered orally twice daily for 9 months. Subjects were evaluated at 3, 6, 9 (ie, completion of treatment), and 11 months after randomization. The primary endpoint was the number of new actinic keratoses at the 9-month visit as a percentage of the number at the time of randomization. In an intent-to-treat analysis, the incidence of actinic keratoses was compared between the two groups using t tests. In exploratory analyses, we evaluated the number of nonmelanoma skin cancers combined and SCCs and BCCs separately per patient at 11 months after randomization using Poisson regression, after adjustment for patient characteristics and time on study. The numbers of adverse events in the two treatment arms were compared using χ(2) or Fisher exact tests. All statistical tests were two-sided.METHODSA double-blind placebo-controlled randomized trial involving 240 subjects aged 37-87 years with 10-40 actinic keratoses was conducted at eight US academic medical centers. Patients were randomly assigned to receive 200 mg of celecoxib or placebo administered orally twice daily for 9 months. Subjects were evaluated at 3, 6, 9 (ie, completion of treatment), and 11 months after randomization. The primary endpoint was the number of new actinic keratoses at the 9-month visit as a percentage of the number at the time of randomization. In an intent-to-treat analysis, the incidence of actinic keratoses was compared between the two groups using t tests. In exploratory analyses, we evaluated the number of nonmelanoma skin cancers combined and SCCs and BCCs separately per patient at 11 months after randomization using Poisson regression, after adjustment for patient characteristics and time on study. The numbers of adverse events in the two treatment arms were compared using χ(2) or Fisher exact tests. All statistical tests were two-sided.There was no difference in the incidence of actinic keratoses between the two groups at 9 months after randomization. However, at 11 months after randomization, there were fewer nonmelanoma skin cancers in the celecoxib arm than in the placebo arm (mean cumulative tumor number per patient 0.14 vs 0.35; rate ratio [RR] = .43, 95% confidence interval [CI] = 0.24 to 0.75; P = .003). After adjusting for age, sex, Fitzpatrick skin type, history of actinic keratosis at randomization, nonmelanoma skin cancer history, and patient time on study, the number of nonmelanoma skin cancers was lower in the celecoxib arm than in the placebo arm (RR = 0.41, 95% CI = 0.23 to 0.72, P = .002) as were the numbers of BCCs (RR = 0.40, 95% CI = 0.18 to 0.93, P = .032) and SCCs (RR = 0.42, 95% CI = 0.19 to 0.93, P = .032). Serious and cardiovascular adverse events were similar in the two groups.RESULTSThere was no difference in the incidence of actinic keratoses between the two groups at 9 months after randomization. However, at 11 months after randomization, there were fewer nonmelanoma skin cancers in the celecoxib arm than in the placebo arm (mean cumulative tumor number per patient 0.14 vs 0.35; rate ratio [RR] = .43, 95% confidence interval [CI] = 0.24 to 0.75; P = .003). After adjusting for age, sex, Fitzpatrick skin type, history of actinic keratosis at randomization, nonmelanoma skin cancer history, and patient time on study, the number of nonmelanoma skin cancers was lower in the celecoxib arm than in the placebo arm (RR = 0.41, 95% CI = 0.23 to 0.72, P = .002) as were the numbers of BCCs (RR = 0.40, 95% CI = 0.18 to 0.93, P = .032) and SCCs (RR = 0.42, 95% CI = 0.19 to 0.93, P = .032). Serious and cardiovascular adverse events were similar in the two groups.Celecoxib may be effective for prevention of SCCs and BCCs in individuals who have extensive actinic damage and are at high risk for development of nonmelanoma skin cancers.CONCLUSIONSCelecoxib may be effective for prevention of SCCs and BCCs in individuals who have extensive actinic damage and are at high risk for development of nonmelanoma skin cancers. Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonmelanoma skin cancers, and for nonmelanoma skin cancers, including cutaneous squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs). A double-blind placebo-controlled randomized trial involving 240 subjects aged 37-87 years with 10-40 actinic keratoses was conducted at eight US academic medical centers. Patients were randomly assigned to receive 200 mg of celecoxib or placebo administered orally twice daily for 9 months. Subjects were evaluated at 3, 6, 9 (ie, completion of treatment), and 11 months after randomization. The primary endpoint was the number of new actinic keratoses at the 9-month visit as a percentage of the number at the time of randomization. In an intent-to-treat analysis, the incidence of actinic keratoses was compared between the two groups using t tests. In exploratory analyses, we evaluated the number of nonmelanoma skin cancers combined and SCCs and BCCs separately per patient at 11 months after randomization using Poisson regression, after adjustment for patient characteristics and time on study. The numbers of adverse events in the two treatment arms were compared using χ(2) or Fisher exact tests. All statistical tests were two-sided. There was no difference in the incidence of actinic keratoses between the two groups at 9 months after randomization. However, at 11 months after randomization, there were fewer nonmelanoma skin cancers in the celecoxib arm than in the placebo arm (mean cumulative tumor number per patient 0.14 vs 0.35; rate ratio [RR] = .43, 95% confidence interval [CI] = 0.24 to 0.75; P = .003). After adjusting for age, sex, Fitzpatrick skin type, history of actinic keratosis at randomization, nonmelanoma skin cancer history, and patient time on study, the number of nonmelanoma skin cancers was lower in the celecoxib arm than in the placebo arm (RR = 0.41, 95% CI = 0.23 to 0.72, P = .002) as were the numbers of BCCs (RR = 0.40, 95% CI = 0.18 to 0.93, P = .032) and SCCs (RR = 0.42, 95% CI = 0.19 to 0.93, P = .032). Serious and cardiovascular adverse events were similar in the two groups. Celecoxib may be effective for prevention of SCCs and BCCs in individuals who have extensive actinic damage and are at high risk for development of nonmelanoma skin cancers. Viner et al evaluate the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonmelanoma skin cancers, and for nonmelanoma skin cancers, including cutaneous squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs). At 11 months after randomization, there were fewer nonmelanoma skin cancers in the celecoxib arm than in the placebo arm (mean cumulative tumor number per patient 0.14 vs 0.35; rate ratio [RR] = .43, 95% confidence interval [CI] = 0.24 to 0.75; P= .003). After adjusting for age, sex, Fitzpatrick skin type, history of actinic keratosis at randomization, nonmelanoma skin cancer history, and patient time on study, the number of nonmelanoma skin cancers was lower in the celecoxib arm than in the placebo arm (RR = 0.41, 95% CI = 0.23 to 0.72, P = .002) as were the numbers of BCCs (RR = 0.40, 95% CI = 0.18 to 0.93, P = .032) and SCCs (RR = 0.42, 95% CI = 0.19 to 0.93, P = .032). Serious and cardiovascular adverse events were similar in the two groups. Background Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonmelanoma skin cancers, and for nonmelanoma skin cancers, including cutaneous squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs). Methods A double-blind placebo-controlled randomized trial involving 240 subjects aged 37-87 years with 10-40 actinic keratoses was conducted at eight US academic medical centers. Patients were randomly assigned to receive 200 mg of celecoxib or placebo administered orally twice daily for 9 months. Subjects were evaluated at 3, 6, 9 (ie, completion of treatment), and 11 months after randomization. The primary endpoint was the number of new actinic keratoses at the 9-month visit as a percentage of the number at the time of randomization. In an intent-to-treat analysis, the incidence of actinic keratoses was compared between the two groups using t tests. In exploratory analyses, we evaluated the number of nonmelanoma skin cancers combined and SCCs and BCCs separately per patient at 11 months after randomization using Poisson regression, after adjustment for patient characteristics and time on study. The numbers of adverse events in the two treatment arms were compared using chi super(2) or Fisher exact tests. All statistical tests were two-sided. Results There was no difference in the incidence of actinic keratoses between the two groups at 9 months after randomization. However, at 11 months after randomization, there were fewer nonmelanoma skin cancers in the celecoxib arm than in the placebo arm (mean cumulative tumor number per patient 0.14 vs 0.35; rate ratio [RR] = .43, 95% confidence interval [CI] = 0.24 to 0.75; P = .003). After adjusting for age, sex, Fitzpatrick skin type, history of actinic keratosis at randomization, nonmelanoma skin cancer history, and patient time on study, the number of nonmelanoma skin cancers was lower in the celecoxib arm than in the placebo arm (RR = 0.41, 95% CI = 0.23 to 0.72, P = .002) as were the numbers of BCCs (RR = 0.40, 95% CI = 0.18 to 0.93, P = .032) and SCCs (RR = 0.42, 95% CI = 0.19 to 0.93, P = .032). Serious and cardiovascular adverse events were similar in the two groups. Conclusions Celecoxib may be effective for prevention of SCCs and BCCs in individuals who have extensive actinic damage and are at high risk for development of nonmelanoma skin cancers. Background Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant precursor of nonmelanoma skin cancers, and for nonmelanoma skin cancers, including cutaneous squamous cell carcinomas (SCCs) and basal cell carcinomas (BCCs). Methods A double-blind placebo-controlled randomized trial involving 240 subjects aged 37–87 years with 10–40 actinic keratoses was conducted at eight US academic medical centers. Patients were randomly assigned to receive 200 mg of celecoxib or placebo administered orally twice daily for 9 months. Subjects were evaluated at 3, 6, 9 (ie, completion of treatment), and 11 months after randomization. The primary endpoint was the number of new actinic keratoses at the 9-month visit as a percentage of the number at the time of randomization. In an intent-to-treat analysis, the incidence of actinic keratoses was compared between the two groups using t tests. In exploratory analyses, we evaluated the number of nonmelanoma skin cancers combined and SCCs and BCCs separately per patient at 11 months after randomization using Poisson regression, after adjustment for patient characteristics and time on study. The numbers of adverse events in the two treatment arms were compared using χ2 or Fisher exact tests. All statistical tests were two-sided. Results There was no difference in the incidence of actinic keratoses between the two groups at 9 months after randomization. However, at 11 months after randomization, there were fewer nonmelanoma skin cancers in the celecoxib arm than in the placebo arm (mean cumulative tumor number per patient 0.14 vs 0.35; rate ratio [RR] = .43, 95% confidence interval [CI] = 0.24 to 0.75; P = .003). After adjusting for age, sex, Fitzpatrick skin type, history of actinic keratosis at randomization, nonmelanoma skin cancer history, and patient time on study, the number of nonmelanoma skin cancers was lower in the celecoxib arm than in the placebo arm (RR = 0.41, 95% CI = 0.23 to 0.72, P = .002) as were the numbers of BCCs (RR = 0.40, 95% CI = 0.18 to 0.93, P = .032) and SCCs (RR = 0.42, 95% CI = 0.19 to 0.93, P = .032). Serious and cardiovascular adverse events were similar in the two groups. Conclusions Celecoxib may be effective for prevention of SCCs and BCCs in individuals who have extensive actinic damage and are at high risk for development of nonmelanoma skin cancers. |
| Author | Kang, Sewon Lin, Hui-Yi Bailey, Howard Pentland, Alice P. Umar, Asad Bell, Walter Elewski, Boni E. Linden, Kenneth G. Elmets, Craig A. Viner, Jaye L. Heffernan, Michael Cantrell, Wendy Richmond, Ellen Duvic, Madeleine Gordon, Gary B. |
| AuthorAffiliation | Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madis |
| AuthorAffiliation_xml | – name: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) |
| Author_xml | – sequence: 1 givenname: Craig A. surname: Elmets fullname: Elmets, Craig A. email: celmets@uab.edu organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 2 givenname: Jaye L. surname: Viner fullname: Viner, Jaye L. organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 3 givenname: Alice P. surname: Pentland fullname: Pentland, Alice P. organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 4 givenname: Wendy surname: Cantrell fullname: Cantrell, Wendy organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 5 givenname: Hui-Yi surname: Lin fullname: Lin, Hui-Yi email: celmets@uab.edu organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 6 givenname: Howard surname: Bailey fullname: Bailey, Howard organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 7 givenname: Sewon surname: Kang fullname: Kang, Sewon organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 8 givenname: Kenneth G. surname: Linden fullname: Linden, Kenneth G. organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 9 givenname: Michael surname: Heffernan fullname: Heffernan, Michael organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 10 givenname: Madeleine surname: Duvic fullname: Duvic, Madeleine organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 11 givenname: Ellen surname: Richmond fullname: Richmond, Ellen organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 12 givenname: Boni E. surname: Elewski fullname: Elewski, Boni E. organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 13 givenname: Asad surname: Umar fullname: Umar, Asad organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 14 givenname: Walter surname: Bell fullname: Bell, Walter organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) – sequence: 15 givenname: Gary B. surname: Gordon fullname: Gordon, Gary B. organization: Affiliations of authors: Moffitt Cancer Center and Research Institute, Tampa, FL (H-YL); Formerly of Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (H-YL); Department of Dermatology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (CAE, WC, BEE); Veteran Affairs Medical Center, Birmingham, AL (CAE); Department of Pathology, Skin Diseases Research Center and the Comprehensive Cancer Center, University of Alabama at Birmingham, Birmingham, AL (WB); MedImmune, Inc, Gaithersburg, MD (JLV); Formerly of Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (JLV); Division of Cancer Prevention, National Cancer Institute, Bethesda, MD (ER, AU); Department of Dermatology, University of Rochester School of Medicine and Dentistry, Rochester, NY (APP), Department of Medicine, University of Wisconsin–Madison, Madison, WI (HB); Johns Hopkins University, Baltimore, MD (SK); Formerly of Department of Dermatology, University of Michigan, Ann Arbor, MI (SK); Department of Dermatology, University of California, Irvine, CA (KGL); Wright State University, Dayton, OH (MH); Formerly of Department of Medicine, Washington University School of Medicine, St Louis, MO (MH); Department of Dermatology, University of Texas M.D. Anderson Cancer Center, Houston, TX (MD); Abbott Laboratories, Abbott Park, IL (GBG); Formerly of Oncology/Immunodeficiency Research and Development, G.D. Searle, Skokie, IL (GBG) |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23715510$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/21115882$$D View this record in MEDLINE/PubMed |
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| Copyright | 2015 INIST-CNRS Copyright Oxford Publishing Limited(England) Dec 15, 2010 The Author 2010. Published by Oxford University Press. 2010 |
| Copyright_xml | – notice: 2015 INIST-CNRS – notice: Copyright Oxford Publishing Limited(England) Dec 15, 2010 – notice: The Author 2010. Published by Oxford University Press. 2010 |
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| Keywords | Human Prostaglandin-endoperoxide synthase Skin disease Chemoprophylaxis Enzyme Enzyme inhibitor Cyclooxygenase 2 inhibitor Malignant tumor Celecoxib Randomized controlled trial Skin cancer Prevention Cancerology Double blind study Oxidoreductases Public health Cancer |
| Language | English |
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| Snippet | Background Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy... Preclinical studies indicate that the enzyme cyclooxygenase 2 plays an important role in ultraviolet-induced skin cancers. We evaluated the efficacy and safety... Viner et al evaluate the efficacy and safety of celecoxib, a cyclooxygenase 2 inhibitor, as a chemopreventive agent for actinic keratoses, the premalignant... |
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| SubjectTerms | Adult Aged Aged, 80 and over Anticarcinogenic Agents - administration & dosage Anticarcinogenic Agents - adverse effects Anticarcinogenic Agents - therapeutic use Biological and medical sciences Carcinoma, Basal Cell - prevention & control Carcinoma, Squamous Cell - prevention & control Celecoxib Cell Transformation, Neoplastic Chemotherapy Clinical trials Cyclooxygenase 2 Inhibitors - therapeutic use Dermatology Double-Blind Method Female Humans Inhibitor drugs Keratosis, Actinic - drug therapy Keratosis, Actinic - pathology Male Medical sciences Middle Aged Oncology Pyrazoles - administration & dosage Pyrazoles - adverse effects Pyrazoles - therapeutic use Skin cancer Skin Neoplasms - etiology Skin Neoplasms - prevention & control Sulfonamides - administration & dosage Sulfonamides - adverse effects Sulfonamides - therapeutic use Treatment Outcome Tumors Tumors of the skin and soft tissue. Premalignant lesions |
| Title | Chemoprevention of Nonmelanoma Skin Cancer With Celecoxib: A Randomized, Double-Blind, Placebo-Controlled Trial |
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