Relevant bibliographies by topics / TPA-induced skin cancer

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Academic literature on the topic 'TPA-induced skin cancer'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "TPA-induced skin cancer"

1

Xiu, Dianhui, Min Cheng, Wenlei Zhang, Xibo Ma, and Lin Liu. "Pseudomonas aeruginosa-mannose-sensitive hemagglutinin inhibits chemical-induced skin cancer through suppressing hedgehog signaling." Experimental Biology and Medicine 245, no. 3 (January 5, 2020): 213–20. http://dx.doi.org/10.1177/1535370219897240.

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Pseudomonas aeruginosa-mannose-sensitive hemagglutinin (PAM) is an inactivate P. aeruginosa with mannose-sensitive hemagglutinin. Recently, the anticancer properties of PAM against many cancers have been reported across a range of studies. However, the exact mechanism through which PAM prevents skin cancer remains unclear. The aim of this study is to show to what extent PAM could inhibit the dimethylbenzanthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin cancer. JB6 cells were treated by TPA so as to establish an in vitro model. The effects of PAM on proliferation of the cells were analyzed using cell counting kit-8 assays. Effects on epithelial–mesenchymal transition (EMT) were assayed by real-time PCR and Western blotting. A DMBA/TPA-induced skin cancer mouse model was also established. The results showed that TPA promoted EMT changes through the activation of the hedgehog (Hh) pathway, which was reversed by PAM. Moreover, PAM inhibited the cancer growth and Hh pathway in vivo. These data indicate that PAM may serve as a potential anticancer agent for the treatment of skin cancer. Impact statement Pseudomonas aeruginosa-mannose-sensitive hemagglutinin (PAM) restrained the chemical-induced skin cancer cells in vitro and in vivo partly through suppressing the Hh signaling pathway, indicating that PAM may be a promising anticancer agent for treating skin cancer.
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Dao, Vinh, Vincent Hurez, Sri Lakshmi Pandeswara, Kim Cardenas, Lishi Sun, Aijie Liu, Paul Hasty, Z. Dave Sharp, and Tyler Curiel. "Oral rapamycin (eRapa) safely prevents carcinogen-induced dermal carcinogenesis through an interferon-γ-dependent mechanism (TUM7P.931)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 203.13. http://dx.doi.org/10.4049/jimmunol.192.supp.203.13.

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Abstract eRapa extends life in mice and cancer prevention could be a mechanism. Rapamycin inhibits mTOR, which has significant immune effects that are surprisingly unstudied in cancer therapy or prevention. We hypothesize that cancer prevention by eRapa is mediated by improved cancer immune surveillance, which we tested in the well-established DMBA/TPA carcinogen-induced skin cancer model. Mice got eRapa or control chow, and skin tumors were induced with DMBA/TPA over 24 weeks. eRapa reduced benign (p=.001) and malignant (p=.05) tumors in WT mice. T cells and IFN-γ mediate cancer immune surveillance. eRapa reduced skin tumors in βδ KO mice lacking all T cells (p=.04), but not in IFN-γ KO mice (p=.13), consistent with loss of beneficial eRapa-induced, non-T cell IFN-γ. In support, WT or IFN-γ KO T cell transfer into IFN-γ KO mice did not alter eRapa cancer prevention in DMBA/TPA. In WT mice on DMBA/TPA, eRapa increased IFN-γ-producing natural killer cells (p=.01) that could mediate skin cancer immune surveillance, and decreased CD34+CD49fint skin cancer stem cells (p=.01) and CXCR3+ T cells (p<.001) that contribute to cancer in this model. eRapa reduced skin pAKT with divergent mTORC1/2 effects needing more study. eRapa appeared safe (no increased Tregs or reduced protection in infection and autoimmunity models). A widely applicable, safe and tolerable cancer prevention agent would be highly useful. Understanding its immune mechanisms could improve efficacy and widen applications.
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Koul, Ashwani, Mohinder Pal Bansal, Aniqa Aniqa, Harsh Chaudhary, and Neha Arora Chugh. "Lycopene enriched tomato extract suppresses chemically induced skin tumorigenesis in mice." International Journal for Vitamin and Nutrition Research 90, no. 5-6 (October 2020): 493–513. http://dx.doi.org/10.1024/0300-9831/a000597.

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Abstract. The present study revealed the effects of Lycopene enriched tomato extract (LycT) on chemically induced skin cancer in mice. Skin tumors were induced by topical application of 7,12-Dimethylbenz(a)anthracene (DMBA) [500 nmol/100 ul of acetone, twice a week for two weeks] and 12-O-tetradecanoyl phorbol-13-acetate (TPA) [1.7 nmol/100 ul of acetone, twice a week for eighteen weeks] and LycT (5 mg/kg b.w.) was administered orally. Male Balb/c mice were divided into four groups (n = 15 per group): control, DMBA/TPA, LycT and LycT + DMBA/TPA. The chemopreventive response of LycT to skin tumorigenesis was evident by inhibition in tumor incidence, number, size, burden and volume in LycT + DMBA/TPA group when compared to DMBA/TPA group. This was associated with inhibition of cell proliferation in LycT + DMBA/TPA group as observed by the decrease in epidermal morphometric parameters and mRNA and protein expression of proliferating cell nuclear antigen when compared to DMBA/TPA group (p ≤ 0.05). LycT decreased (p ≤ 0.05) the mRNA and protein expression of angiogenic genes (vascular endothelial growth factor, angiopoietin-2, basic fibroblast growth factor) in LycT + DMBA/TPA group, suggesting its anti-angiogenic effects. The increase (p ≤ 0.05) in protein expression of connexin-32 and 43 in LycT + DMBA/TPA group suggests improved inter cellular communication when compared to DMBA/TPA group. Histochemical studies demonstrated that the components of extracellular matrix (fibrous proteins and mucopolysaccharides) were also modulated during skin carcinogenesis and its chemoprevention by LycT. The decrease in cell proliferation parameters and expression of angiogenesis associated genes, modulation of ECM components and increase in expression of connexins suggest that LycT improved multiple dysregulated processes during chemoprevention of skin cancer.
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Cho, Hae-Ra, Yingchun Wang, Xiaohui Bai, Yun-Yan Xiang, Christina Lu, Alexander Post, Ayman Al Habeeb, and Mingyao Liu. "XB130 deficiency enhances carcinogen-induced skin tumorigenesis." Carcinogenesis 40, no. 11 (March 1, 2019): 1363–75. http://dx.doi.org/10.1093/carcin/bgz042.

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AbstractXB130 is an adaptor protein that functions as a mediator of multiple tyrosine kinases important for regulating cell proliferation, survival, migration and invasion. Formerly predicted as an oncogene, alterations of its expression are documented in various human cancers. However, the exact role of XB130 in tumorigenesis is unknown. To address its function in skin tumorigenesis, a two-stage dimethylbenzanthracene (DMBA)/12-O-tetradecanoylphorbol 13-acetate (TPA) study was performed on XB130 knockout (KO), heterozygous (HZ) and wild-type (WT) littermate mice. DMBA/TPA-treated XB130 KO and HZ males developed a significantly higher number of epidermal tumors that were notably larger in size than did WT mice. Interestingly, DMBA/TPA-treated female mice did not show any difference in tumor multiplicity regardless of the genotypes. The skin tumor lesions of XB130 KO males were more progressed with an increased frequency of keratoacanthoma. Deficiency of XB130 dramatically increased epidermal tumor cell proliferation. The responses to DMBA and TPA stimuli were also individually investigated to elucidate the mechanistic role of XB130 at different stages of tumorigenesis. DMBA-treated male XB130 KO mice showed compensatory p53-mediated stress response. TPA-treated XB130 KO males demonstrated more skin ulceration with more severe edema, enhanced cell proliferation, accumulation of infiltrating neutrophils and increased production of pro-inflammatory cytokine genes compared with WT mice. Enhanced activities of nuclear factor-kappa B pathway, increased protein expression of metalloproteinase-9 and ERK1/2 phosphorylation were found in these KO mice. These findings demonstrate that XB130 acts as a tumor suppressor in carcinogen-induced skin tumorigenesis that may be mediated through inhibiting inflammation.
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Arora, Reena, Mohammed Samim, and Chander Parkash. "Evaluation of Anti-inflammatory and Anti-cancer Activity of Calcium Phosphate Encapsulated Resveratrol in Mouse Skin Cancer Model." Biomedical and Pharmacology Journal 14, no. 1 (March 28, 2021): 113–22. http://dx.doi.org/10.13005/bpj/2105.

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Resveratrol, a non-flavonoid phenolic phytochemical present in red grapes and berries, has been reported to have significant health benefits. Resveratrol is known for its chemopreventive and chemotherapeutic effects in multiple cancers as well as cardiovascular and inflammatory diseases. But its higher lipophilicity, poor aqueous solubility and bioavailability remains a challenge for its usage as an effective chemopreventive and chemotherapeutic agent. To overcome this,we have prepared a biocompatible calcium phosphate encapsulated resveratrol (Nanoresveratrol; NRV) and studied its antioxidant, anti-inflammatory and anti-cancer activities in the present study.Nanoresveratrol, unlike resveratrol, readily dispersed in aqueous media and showed a sustained release. Nanoresveratrol (NRV) and resveratrol (RV) showed comparable antioxidant activities. The anti-inflammatory and anticancer activities of nanoresveratrol were studied for its inhibitory effect on 7, 12-dimethylbenz[a]anthracene (DMBA)-induced/12-O-tetradecanoylphorbol-13-acetate (TPA) promoted skin inflammation and tumorigenesis mouse model. Nanoresveratrol showed a significant decrease of TPA-induced skin edema, ODC activity and thymidine incorporation when compared to resveratrol. Nanoresveratrol also inhibited chemical-induced tumorigenesis.Overall, the study results support that nanoresveratrol may represent a potential anti-cancer agent and warrants further investigations for the treatment of skin cancer.
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Rahman, Shakilur, Rizwan Ahmed Ansari, Hasibur Rehman, Suhel Parvez, and Sheikh Raisuddin. "Nordihydroguaiaretic Acid from Creosote Bush (Larrea tridentata) Mitigates 12-O-Tetradecanoylphorbol-13-Acetate-Induced Inflammatory and Oxidative Stress Responses of Tumor Promotion Cascade in Mouse Skin." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–10. http://dx.doi.org/10.1093/ecam/nep076.

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Nordihydroguaiaretic acid (NDGA) is a phenolic antioxidant found in the leaves and twigs of the evergreen desert shrub,Larrea tridentata(Sesse and Moc. ex DC) Coville (creosote bush). It has a long history of traditional medicinal use by the Native Americans and Mexicans. The modulatory effects of topically applied NDGA was studied on acute inflammatory and oxidative stress responses in mouse skin induced by stage I tumor promoting agent, 12-O-tetradecanoylphorbol-13-acetate (TPA). Double TPA treatment adversely altered many of the marker responses of stage I skin tumor promotion cascade. Pretreatment of NDGA in TPA-treated mice mitigated cutaneous lipid peroxidation and inhibited production of hydrogen peroxide. NDGA treatment also restored reduced glutathione level and activities of antioxidant enzymes. Elevated activities of myeloperoxidase, xanthine oxidase and skin edema formation in TPA-treated mice were also lowered by NDGA indicating a restrained inflammatory response. Furthermore, results of histological study demonstrated inhibitory effect of NDGA on cellular inflammatory responses. This study provides a direct evidence of antioxidative and anti-inflammatory properties of NDGA against TPA-induced cutaneous inflammation and oxidative stress corroborating its chemopreventive potential against skin cancer.
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7

Loprinzi, C. L., A. K. Verma, R. K. Boutwell, and P. P. Carbone. "Inhibition of phorbol ester--induced human epidermal ornithine decarboxylase activity by oral compounds: a possible role in human chemoprevention studies." Journal of Clinical Oncology 3, no. 6 (June 1985): 751–57. http://dx.doi.org/10.1200/jco.1985.3.6.751.

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Extensive animal data have suggested that, in some systems, the induction of ornithine decarboxylase (ODC) is an essential, although not sufficient, aspect of tumor promotion and that compounds that inhibit ODC can inhibit tumor formation. Using fasting human volunteers, we report that human epidermal and dermal ODC are consistently induced by the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) in a manner similar to that seen in mouse skin. There is a marked intersubject variation in TPA-induced epidermal ODC activity levels. Orally administered compounds significantly inhibited TPA-caused human epidermal ODC induction. These data may be useful in the further development of drugs, doses, and dose schedules for use in human cancer chemoprevention studies.
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Vähätupa, Maria, Saara Aittomäki, Zuzet Martinez Cordova, Ulrike May, Stuart Prince, Hannele Uusitalo-Järvinen, Tero A. Järvinen, and Marko Pesu. "T-cell-expressed proprotein convertase FURIN inhibits DMBA/TPA-induced skin cancer development." OncoImmunology 5, no. 12 (October 14, 2016): e1245266. http://dx.doi.org/10.1080/2162402x.2016.1245266.

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9

Pandey, Chhaya, Rashmi Arnold, and Rahasya Mani Mishra. "Modulation of p21, DAPK1 and COX-2 during the DMBA/TPA-induced mouse skin tumorigenesis and its prevention by phytic acid." Indian Journal of Pharmaceutical and Biological Research 2, no. 04 (December 31, 2014): 61–67. http://dx.doi.org/10.30750/ijpbr.2.4.11.

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Chemoprevention by naturally occurring agents is gaining much attention as a newer dimension in the management of cancer. Many naturally occurring agents have shown cancer chemopreventive potential in a variety of bioassay systems and animal models, having relevance to human disease. Phytic acid or Inositol hexaphosphate (IP6), an antioxidant, is a naturally occurring polyphosphorylated carbohydrate that has shown a strong anticancer activity in several experimental models. We assessed the protective effects of Phytic acid against the 7, 12-dimethylbenz [a] anthracene (DMBA)/ 12-O-tetradecanoylphorbol-13- acetate (TPA) induced mouse skin tumorigenesis at 4 and 16 weeks, the time before and after the tumor development. At molecular level we studied expression and promoter CpG methylation status of p21, DAPK1 and COX-2. Our data suggests exposure of DMBA/TPA methylated the promoter region of p21 and DAPK1 genes in time dependent manner that could be the cause of down regulation of their expression with time, which were reversed by administration of phytic acid. But we did not observe methylation in COX-2 whereas upregulation of COX-2 was observed at protein level in mice treated with DMBA followed by TPA in time dependent manner. Administration of phytic acid prevented theses DMBA/TPA induced molecular changes. Study provides a rationale for cancer chemoprevention by natural occurring compounds like Phytic acid.
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Surien, Omchit, Siti Fathiah Masre, Dayang Fredalina Basri, and Ahmad Rohi Ghazali. "Chemopreventive Effects of Oral Pterostilbene in Multistage Carcinogenesis of Skin Squamous Cell Carcinoma Mouse Model Induced by DMBA/TPA." Biomedicines 10, no. 11 (October 28, 2022): 2743. http://dx.doi.org/10.3390/biomedicines10112743.

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Skin squamous cell carcinoma (SCC) is a type of non-melanoma skin cancer. Pterostilbene is a natural compound proven to exhibit various pharmacological properties, including chemo-preventive effects. This study aimed to explore the chemo-preventive effect of oral pterostilbene during initiation, promotion or continuous on multistage skin SCC mouse models induced by 7,12-Dimethylbenz(a)anthracene (DMBA)/12-O-Tetradecanoylphorbol-13-acetate (TPA). The experimental design consists of five groups of female Institute of Cancer Research (ICR) mice, with two control groups of vehicle and cancer. Three oral pterostilbene groups consisted of orally administered pterostilbene during initiation, promotion, or continuously. Oral pterostilbene significantly reduced the number and volume of tumours. Oral pterostilbene demonstrated less severe skin histology changes compared to the cancer control group, with less pleomorphic in the cells and nuclei, and the basement membrane remained intact. Our results showed fewer invasive tumours in oral PT-treated groups than in cancer groups that displayed mitotic bodies, highly pleomorphic cells and nuclei, and basement membrane invasion. The cell proliferation marker (Ki-67) was reduced in oral pterostilbene-treated groups. Overall, oral pterostilbene is a promising chemo-preventive intervention due to its anti-initiation and anti-promotion on skin carcinogenesis. Thus, the potential molecular mechanisms of oral pterostilbene chemo-prevention agent should be explored.
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Dissertations / Theses on the topic "TPA-induced skin cancer"

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Gentile, S. "THE PROTECTIVE ROLE OF PTX3 IN MOUSE SKIN CARCINOGENESIS." Doctoral thesis, Università degli Studi di Milano, 2015. http://hdl.handle.net/2434/251045.

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Abstract The implication of the innate immune system on inflammatory carcinogenesis is a central topic in tumor biology. The humoral pattern recognition molecule PTX3 plays a fundamental role in the modulation of inflammation by regulating Complement cascade and P-selectin dependent neutrophil recruitment. Available information in human and murine 3-MCA induced sarcomas suggests a protective role of PTX3 in cancer-related inflammation. In this study we showed that PTX3-deficient mice were more susceptible to DMBA/TPA chemically-induced epithelial skin cancer than PTX3-competent mice, in term of incidence, multiplicity of papillomas and number of lesions evolving to skin carcinomas, suggesting a more aggressive behavior of PTX3-/- tumors. In the skin, PTX3 was strongly produced during the acute phase of carcinogenesis by infiltrating macrophages, neutrophils, and vessels. Immunohistochemical investigation of papillomas showed low presence of PTX3 in the extracellular matrix. The deficiency of PTX3 was associated with increased cancer-related inflammation in term of neutrophil infiltration, higher production of pro-inflammatory cytokines and chemokines, increased C3 and IgG deposition. In the effort to define the molecular mechanisms underlying this phenotype, we observed that P-selectin deficiency and in vivo neutrophil depletion reverted the tumor susceptibility of Ptx3-/- mice. All together, these results provide evidence that PTX3 is locally produced and plays a protective role in epithelial skin carcinogenesis acting as an extrinsic oncosuppressor. The mechanism of PTX3-mediated protection is explained by modulation of cancer-related inflammation regulating P-selectin dependent neutrophil recruitment and Complement activation.
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Conference papers on the topic "TPA-induced skin cancer"

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Lee, Jong Hun, Limin Shu, Mou-Tuan Huang, Allan H. Conney, and Ah-Ng Tony Kong. "Abstract 5371: Epigenetic regulation in skin cancer: global DNA methylation profiling in DMBA/TPA induced mice." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5371.

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Journal articles
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