Relevant bibliographies by topics / DMBA/TPA-induced skin cancer

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

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

Author: Grafiati
Published: 9 March 2023

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

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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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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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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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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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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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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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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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Dao, Vinh, Srilakshmi Pandeswara, Yang Liu, Vincent Hurez, Aijie Liu, and Tyler Curiel. "Oral rapamycin (eRapa) requires IFN-γ and promotes γδ T cell cytotoxicity to prevent carcinogen and inflammation-induced dermal cancer (TUM9P.1003)." Journal of Immunology 194, no. 1_Supplement (May 1, 2015): 210.5. http://dx.doi.org/10.4049/jimmunol.194.supp.210.5.

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Abstract Rapamycin, a mammalian target of rapamycin (mTOR) inhibitor, prevents distinct cancers in mice and prolongs life, making it a candidate cancer prevention (and life extension) agent. We hypothesized that eRapa cancer prevention includes immune effects, as mTOR is pivotal in immunity. We tested immune effects in carcinogen (DMBA) and inflammation (TPA)-induced dermal carcinogenesis with eRapa daily at 14 ppm, which protected 100% from skin cancer in wild type (WT) mice. Tumor mTORC1 was not suppressed, supporting eRapa immune effects. γδ T cells and IFN-γ are protective in this model. In δ TCR KO (no γδ T cells) and IFN-γ KO mice, eRapa cancer protection was lost, confirming immune mechanisms. IFN-γ KO mice had significantly reduced CD69+Lamp1+GzB+CXCR3+ epidermal γδ T cells and CXCL10, suggesting IFN-γ is required for epidermal γδ T cell migration (via CXCR3/CXCL10), activation and cytolysis. Bone marrow (BM) chimeras showed eRapa skin cancer protection and maximum γδ T cell epidermal infiltration requires IFN-γ signals in BM (e.g., γδ T cells) and non-BM (e.g., epidermal) cells. Intratumor injections of WT but not Prf1 (perforin) KO γδ T cells regressed DMBA/TPA tumors in δ TCR KO mice on eRapa but not control, showing eRapa boosts anti-tumor γδ T cell cytotoxicity. Our data confirm eRapa cancer prevention through immune mechanisms, challenging the paradigm of mTOR effects solely on cancer cells for prevention, and suggesting novel immune-mediated life extension mechanisms.
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Ramovs, Veronika, Ana Krotenberg Garcia, Ji-Ying Song, Iris de Rink, Maaike Kreft, Roel Goldschmeding, and Arnoud Sonnenberg. "Integrin α3β1 in hair bulge stem cells modulates CCN2 expression and promotes skin tumorigenesis." Life Science Alliance 3, no. 7 (May 18, 2020): e202000645. http://dx.doi.org/10.26508/lsa.202000645.

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Epidermal-specific deletion of integrin α3β1 almost completely prevents the formation of papillomas during 7,12-Dimethylbenz[a]anthracene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA) two-stage skin carcinogenesis. This dramatic decrease in tumorigenesis was thought to be due to an egress and premature differentiation of α3β1-depleted hair bulge (HB) stem cells (SCs), previously considered to be the cancer cells-of-origin in the DMBA/TPA model. Using a reporter mouse line with inducible deletion of α3β1 in HBs, we show that HB SCs remain confined to their niche regardless of the presence of α3β1 and are largely absent from skin tumors. However, tumor formation was significantly decreased in mice deficient for α3β1 in HB SCs. RNA sequencing of HB SCs isolated from short-term DMBA/TPA–treated skin showed α3β1-dependent expression of the matricellular protein connective tissue growth factor (CCN2), which was confirmed in vitro, where CCN2 promoted colony formation and 3D growth of transformed keratinocytes. Together, these findings show that HBs contribute to skin tumorigenesis in an α3β1-dependent manner and suggest a role of HB SCs in creating a permissive environment for tumor growth through the modulation of CCN2 secretion.
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Chang, Soo, Chen, and Shyur. "Essential Oil of Mentha aquatica var. Kenting Water Mint Suppresses Two-Stage Skin Carcinogenesis Accelerated by BRAF Inhibitor Vemurafenib." Molecules 24, no. 12 (June 25, 2019): 2344. http://dx.doi.org/10.3390/molecules24122344.

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The v-raf murine sarcoma viral homolog B1 (BRAF) inhibitor drug vemurafenib (PLX4032) is used to treat melanoma; however, epidemiological evidence reveals that it could cause cutaneous keratoacanthomas and squamous cell carcinoma in cancer patients with the most prevalent HRASQ61L mutation. In a two-stage skin carcinogenesis mouse model, the skin papillomas induced by 7,12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA) (DT) resemble the lesions in BRAF inhibitor-treated patients. In this study, we investigated the bioactivity of Mentha aquatica var. Kenting Water Mint essential oil (KWM-EO) against PDV cells, mouse keratinocytes bearing HRASQ61L mutation, and its effect on inhibiting papilloma formation in a two-stage skin carcinogenesis mouse model with or without PLX4032 co-treatment. Our results revealed that KWM-EO effectively attenuated cell viability, colony formation, and the invasive and migratory abilities of PDV cells. Induction of G2/M cell-cycle arrest and apoptosis in PDV cells was also observed. KWM-EO treatment significantly decreased the formation of cutaneous papilloma further induced by PLX4032 in DT mice (DTP). Immunohistochemistry analyses showed overexpression of keratin14 and COX-2 in DT and DTP skin were profoundly suppressed by KWM-EO treatment. This study demonstrates that KWM-EO has chemopreventive effects against PLX4032-induced cutaneous side-effects in a DMBA/TPA-induced two-stage carcinogenesis model and will be worth further exploration for possible application in melanoma patients.
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Dissertations / Theses on the topic "DMBA/TPA-induced skin cancer"

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Wu, Xuemei. "Genetic control of tumour susceptibility in mouse skin carcinogenesis." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312688.

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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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Rosa, Paola Vendramini Ferreira. "Caracterização da resposta inflamatória na tumorigênese cutânea induzida quimicamente em camundongos selvagens e deficientes para componentes da resposta imune adaptativa." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42133/tde-11072014-131858/.

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O câncer representa desequilíbrio na homeostase do organismo e os mecanismos de defesa para controlar as células tumorais envolvem respostas do sistema imune inato e adaptativo, sendo que a primeira reação do organismo é a inflamação. O objetivo deste estudo foi caracterizar a resposta inflamatória em linhagens de camundongos C57BL/6, CD4KO, CD8KO, RAG e NUDE. Os animais foram tratados com o carcinógeno DMBA e o agente de promoção tumoral TPA. Os animais foram acompanhados e avaliados por 100 dias, após este período a pele tratada foi retirada e processada para análise de citocinas pró- e anti-inflamatórias e enzima mieloperoxidase (MPO). As citocinas pró e anti-inflamatórias e a enzima MPO foram maiores nos animais CD4KO quando comparados aos outros grupos de animais. As linhagens C57BL/6 WT, CD4KO e NUDE foram avaliadas 48 horas após tratamento com DMBA. Os animais CD4KO apresentaram maior número de neutrófilos e citocinas pró-inflamatórias quando comparados aos grupos C57BL/6 WT e NUDE, enquanto que as citocinas anti-inflamatórias não mostraram diferenças nos 3 grupos tratados. Estes resultados sugerem que os linfócitos TCD4 participam do controle da inflamação causada pelo DMBA e TPA.
Cancer represents imbalance in homeostasis and defense mechanisms to control the tumor cells involving the innate and adaptive immune responses, and the first reaction of the body is inflammation. The aim of this study was to characterize the inflammatory response in the following strains: C57BL/6 WT, CD4KO, CD8KO, RAG and NUDE mice. We treated the animals with the carcinogen DMBA as well as with TPA tumor promoting agent. The animals were followed for 100 days and evaluated after this period, the treated skin was removed and processed for analysis of pro-and anti-inflammatory and enzyme myeloperoxidase (MPO). The pro-and anti-inflammatory cytokines and MPO enzyme were higher in animals CD4KO than the other groups of animals. The C57BL/6 WT and CD4KO NUDE lines were evaluated 48 hours after treatment with DMBA. The CD4KO animals had greater numbers of neutrophils and proinflammatory cytokine than the C57BL/6 WT and NUDE mice, while anti-inflammatory cytokines showed no differences in the three treated groups. These results suggest that CD4 + T lymphocytes participate in the control of the induced by DMBA and TPA.
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Jiang, Wen-Ru, and 蔣宛儒. "The effects of Se-allylselenocysteine (ASC), an analogue of garlic compound, on DMBA/TPA-induced skin tumorigenesis." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/25954993166279458241.

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碩士
國立臺灣大學
食品科技研究所
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Se-allylselenocysteine (ASC), an analogue of garlic compound, has been shown to inhibit mammary carcinogenesis in vivo and cell growth in vitro. However, the function of ASC on anti-inflammatory effect remains largely unknown. Therefore, we investigated whether ASC has anti-inflammatory on LPS-induced inflammation in vitro or anti-tumor promoting on 7, 12-dimethylbenz[a]anthracene (DMBA)/12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin tumorigenesis in vivo and tried to elucidate the mechanisms involved. In in vitro study, the result showed that ASC inhibited lipopolysaccharide (LPS)-induced production of nitric oxide (NO) with decreased protein level of inducible nitric oxide synthase (iNOS) in RAW 264.7 cells. ASC also reduced nuclear factor-B (NF-B) luciferase activity. On the other hand, ASC can enhance LPS-induced COX-2 protein level and mRNA expression in RAW 264.7 cells. In in vivo study, topical application of ASC on the dorsal skin of DMBA-initiated and TPA-promoted mice could significantly accelerate skin tumorigenesis and raise tumor multiplicity than positive control group (DMBA+TPA). The number of tumors that were 1–3 mm, 3–5 mm and >5 mm in size per mouse was increased in a dose-dependent manner in the ASC-pretreated groups. Pretreatment with ASC showed significant increment on the expression of COX-2 compared with positive control group. In summary, the present results speculate that COX-2 played a crucial role in tumor-promoting effect of ASC on DMBA/TPA-induced skin cancer in mice.
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Book chapters on the topic "DMBA/TPA-induced skin cancer"

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"DMBA/TPA Mouse Skin Carcinogenesis Model." In Encyclopedia of Cancer, 1128. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1661.

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Conference papers on the topic "DMBA/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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Singh, Manju, and Raosaheb K. Kale. "Abstract A64: Chemopreventive potential ofBauhinia variegataagainst DMBA‐induced skin papillomagenesis in Swiss albino mice." In Abstracts: AACR International Conference on Frontiers in Cancer Prevention Research‐‐ Dec 6–9, 2009; Houston, TX. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1940-6207.prev-09-a64.

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Das, Ila, Asha Acharya, Archana Sengupta, Shukta Das, Sudin Bhattacharya, and Tapas Saha. "Abstract 2880: Spices suppress oxidative stress during DMBA induced skin carcinogenesis in mice, mimicking human non-melanoma skin cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2880.

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Singh, M., S. Singh, and R. K. Kale. "Abstract B68: Chemomodulatory potential of aloe vera gel on DMBA-induced skin papillomagenesis, drug metabolizing and antioxidant enzymes." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-b68.

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Barman, Provaboti, Katherine Marie DeAzambuja, Joy Ai Toyama, Deborah Lee, Kristopher Chua, David Elashoff, and Dorothy J. Wiley. "Abstract C31: DMBA-induced skin tumors in HPV16 E7 transgenic mice are affected by bovine α-lactalbumin made lethal to tumor cells (BAMLET)." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-c31.

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Diagaradjane, Parmeswaran, Mohammed A. Yaseen, Jie Yu, Michael S. Wong, and Bahman Anvari. "Autofluorescence characterization of DMBA-TPA-induced two-stage carcinogenesis in mouse skin for the early detection of tissue transformation." In Biomedical Optics 2005, edited by Kenneth E. Bartels, Lawrence S. Bass, Werner T. W. de Riese, Kenton W. Gregory, Henry Hirschberg, Abraham Katzir, Nikiforos Kollias, et al. SPIE, 2005. http://dx.doi.org/10.1117/12.589328.

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