Safety and Efficacy of Dose-Intensive Oral Vitamin A in Subjects with Sun-Damaged Skin

Alberts, David S.; Ranger‐Moore, James; Einspahr, Janine G.; Saboda, Kathylynn; Bozzo, Paul; Liu, Yun; Xu, Xiao Chun; Lotan, Reuben; Warneke, James; Salasche, Stuart J.; Stratton, Suzanne; Levine, Norman; Goldman, Rayna; Islas, Marcy; Duckett, Laura; Thompson, Deborah; Bartels, Peter H.

doi:10.1158/1078-0432.ccr-03-0188

Cited by 42 publications

(29 citation statements)

References 13 publications

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“…RAR-b 2 expression is frequently and progressively lost in premalignant and malignant tissues of different human cancers (see review in Xu and Lotan, 1999). Induction of RAR-b 2 in vivo has been used as a biomarker in several clinical chemoprevention trials by researchers at our institution and by other groups (Lotan et al, 1995Ayoub et al, 1999;Berg et al, 1999;Xu et al, 1999a;Kurie et al, 2000Kurie et al, , 2003Lam et al, 2003;Alberts et al, 2004). Taken together, all these data support that RAR-b 2 plays important roles in suppressing human cancer development.…”

Section: Introductionsupporting

confidence: 60%

Induction of cyclooxygenase-2 by benzo[a]pyrene diol epoxide through inhibition of retinoic acid receptor-β2 expression

et al. 2005

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Benzo [a]pyrene diol epoxide (BPDE, a carcinogen present in tobacco smoke and environmental pollution) has been shown to suppress retinoic acid receptor-beta2 (RAR-b 2 ) and induce cyclooxygenase-2 (COX-2) expression. Restoration of RAR-b 2 inhibited growth and colony formation of esophageal cancer cells, which was correlated with COX-2 suppression. In this study, we investigated the molecular mechanisms for RAR-b 2 -mediated suppression of COX-2 expression using BPDE as a tool. We found that BPDE-induced COX-2 expression was through inhibition of RAR-b 2 and consequently, induction of epidermal growth factor receptor (EGFR), extracellular signal-regulated protein kinases 1/2 (Erk1/2) phosphorylation, and c-Jun expression. Esophageal cancer cells that do not express RAR-b 2 did not respond to BPDE for induction of COX-2. BPDE was also unable to induce COX-2 expression after RAR-b 2 expression was manipulated in these esophageal cancer cells. Furthermore, BPDE induced time-dependent methylation of RAR-b 2 gene promoter in esophageal cancer cells. Transfection of RAR-b 2 expression vector into esophageal cancer cells suppressed expression of EGFR, Erk1/2 phosphorylation, c-Jun, and COX-2. In addition, co-treatment of RAR-b 2 -positive cells with BPDE and the MEK1/2 inhibitor U0126 caused little change in c-Jun and COX-2 expression. This study demonstrated that BPDE-suppressed expression of RAR-b 2 results in COX-2 induction and restoration of RAR-b 2 expression reduces COX-2 protein in esophageal cancer cells, thereby further supporting our previous finding that RAR-b 2 plays an important role in suppressing esophageal carcinogenesis.

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Section: Introductionsupporting

confidence: 60%

Induction of cyclooxygenase-2 by benzo[a]pyrene diol epoxide through inhibition of retinoic acid receptor-β2 expression

et al. 2005

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“…Study design is another important consideration. Although some skin cancer chemoprevention trials have used subjects as their own control (48,49), others have relied on separate control groups (50). Both designs have utility with the goal to show clinical improvement, as well as a change in the biomarker as a result of an intervention.…”

Section: Discussionmentioning

confidence: 99%

Reproducibility and Expression of Skin Biomarkers in Sun-Damaged Skin and Actinic Keratoses

Einspahr

Warneke³

et al. 2006

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Objectives: To explore p53 and proliferating cell nuclear antigen (PCNA) expression and polyamine content as biomarkers in skin cancer chemoprevention trials, we evaluated their expression in early stages of UV-induced squamous cell tumorigenesis. Methods: Biopsies were collected from three groups: 78 subjects with sun damage on forearms, 33 with actinic keratosis (AK) on forearms, and 32 with previous squamous cell carcinoma. Participants with sun damage were randomized to sunscreen or no sunscreen. Results: We found significant differences in p53 and polyamines in forearms from the sun-damaged group (11.5 F 1.2% for p53, 65.5 F 1.9 nmol/g for putrescine, and 187.7 F 3.3 nmol/g for spermidine) compared with the group with sun damage plus AK (20.9 F 2.3% for p53, P = 0.0001; 81.7 F 3.9 nmol/g for putrescine, P = 0.0001; 209.4 F 8.2 nmol/g for spermidine, P < 0.06). PCNA was not different. When lesion histology was considered, there was a stepwise significant increase in p53 in biopsies without characteristics of AK compared with early AK (P = 0.02) and AK (P = 0.0006) and a similar pattern for PCNA with the only significant difference between early AK and AK. There was a stepwise increase in putrescine and spermidine in normal, sun-damaged forearm, forearm from subjects with AK, and the AK lesion itself (P < 0.0001). No significant differences in p53 or polyamines were seen in 3-month biopsies or, as a result of sunscreen use, although PCNA in the sun-damaged group not using sunscreen decreased significantly. Conclusions: p53 expression and polyamines in skin were elevated in early stages of skin tumorigenesis and were not affected by sunscreen, adding validity to their use as biomarkers in skin cancer chemoprevention trials. (Cancer Epidemiol Biomarkers Prev 2006;15(10):1841 -8)

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“…Crude LG was then coupled with CNBr-activated Sepharose-4B (Pharmacia, Uppsala, Sweden) according to the manufacturer's instructions with some modifications [39]. Briefly, 3.33 g of freeze-dried Sepharose was resuspended in 20 mL of 1 mM HCl and then immediately washed with 20x volume of the same solution.…”

Section: Methodsmentioning

confidence: 99%

β-Lactoglobulin Influences Human Immunity and Promotes Cell Proliferation

Tai

Chen

2016

BioMed Research International

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β-Lactoglobulin (LG) is suspected to enhance or modulate human immune responses. Moreover, LG is also hypothesized to increase human cell proliferation. However, these potential functions of LG have not been directly or thoroughly addressed. In this study, we demonstrated that LG is a potent stimulator of cell proliferation using a hybridoma cell (a splenocyte fused with a myeloma cell) model. LG's ability to promote cell proliferation was lost when the protein is denatured. To further investigate the influence of LG's conformation on cell proliferation, we chemically modified LG by either carboxymethylation (CM) or acetylation and observed significantly reduced cell proliferation when the protein structure was altered. Furthermore, we proved that LG enhances cell proliferation via receptor-mediated membrane IgM receptor. These data indicated that nondenatured LG is the major component in milk that modulates cell proliferation. Collectively, our study showed that LG plays a key role in enhancing immune responses by promoting cell proliferation through IgM receptor.

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Safety and Efficacy of Dose-Intensive Oral Vitamin A in Subjects with Sun-Damaged Skin

Cited by 42 publications

References 13 publications

Induction of cyclooxygenase-2 by benzo[a]pyrene diol epoxide through inhibition of retinoic acid receptor-β2 expression

Induction of cyclooxygenase-2 by benzo[a]pyrene diol epoxide through inhibition of retinoic acid receptor-β2 expression

Reproducibility and Expression of Skin Biomarkers in Sun-Damaged Skin and Actinic Keratoses

β-Lactoglobulin Influences Human Immunity and Promotes Cell Proliferation

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