Journal articles: '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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Ko, J.-H., B.-G. Jung, Y.-S. Park, and B.-J. Lee. "Inhibitory effects of interferon-gamma plasmid DNA on DMBA-TPA induced mouse skin carcinogenesis." Cancer Gene Therapy 18, no. 9 (July 29, 2011): 646–54. http://dx.doi.org/10.1038/cgt.2011.36.

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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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Li, Hui, Simon Petersen, Alberto Garcia Mariscal, and Cord Brakebusch. "Negative Regulation of p53-Induced Senescence by N-WASP Is Crucial for DMBA/TPA-Induced Skin Tumor Formation." Cancer Research 79, no. 9 (March 20, 2019): 2167–81. http://dx.doi.org/10.1158/0008-5472.can-18-1253.

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Spurgeon, Megan E., Amy Liem, Darya Buehler, Jingwei Cheng, James A. DeCaprio, and Paul F. Lambert. "The Merkel Cell Polyomavirus T Antigens Function as Tumor Promoters in Murine Skin." Cancers 13, no. 2 (January 9, 2021): 222. http://dx.doi.org/10.3390/cancers13020222.

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Merkel cell polyomavirus (MCPyV) causes the majority of human Merkel cell carcinomas (MCC), a rare but highly aggressive form of skin cancer. We recently reported that constitutive expression of MCC tumor-derived MCPyV tumor (T) antigens in the skin of transgenic mice leads to hyperplasia, increased proliferation, and spontaneous epithelial tumor development. We sought to evaluate how the MCPyV T antigens contribute to tumor formation in vivo using a classical, multi-stage model for squamous cell carcinoma development. In this model, two chemical carcinogens, DMBA and TPA, contribute to two distinct phases of carcinogenesis—initiation and promotion, respectively—that are required for tumors to develop. By treating the MCPyV transgenic mice with each chemical carcinogen, we determined how the viral oncogenes contributed to carcinogenesis. We observed that the MCPyV T antigens synergized with the tumor initiator DMBA, but not with the tumor promoter TPA, cause tumors. Therefore, the MCPyV tumor antigens function primarily as tumor promoters, similar to that seen with human papillomavirus (HPV) oncoproteins. These studies provide insight into the role of MCPyV T antigen expression in tumor formation in vivo and contribute to our understanding of how MCPyV may function as a human DNA tumor virus.

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Spurgeon, Megan E., Amy Liem, Darya Buehler, Jingwei Cheng, James A. DeCaprio, and Paul F. Lambert. "The Merkel Cell Polyomavirus T Antigens Function as Tumor Promoters in Murine Skin." Cancers 13, no. 2 (January 9, 2021): 222. http://dx.doi.org/10.3390/cancers13020222.

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Merkel cell polyomavirus (MCPyV) causes the majority of human Merkel cell carcinomas (MCC), a rare but highly aggressive form of skin cancer. We recently reported that constitutive expression of MCC tumor-derived MCPyV tumor (T) antigens in the skin of transgenic mice leads to hyperplasia, increased proliferation, and spontaneous epithelial tumor development. We sought to evaluate how the MCPyV T antigens contribute to tumor formation in vivo using a classical, multi-stage model for squamous cell carcinoma development. In this model, two chemical carcinogens, DMBA and TPA, contribute to two distinct phases of carcinogenesis—initiation and promotion, respectively—that are required for tumors to develop. By treating the MCPyV transgenic mice with each chemical carcinogen, we determined how the viral oncogenes contributed to carcinogenesis. We observed that the MCPyV T antigens synergized with the tumor initiator DMBA, but not with the tumor promoter TPA, cause tumors. Therefore, the MCPyV tumor antigens function primarily as tumor promoters, similar to that seen with human papillomavirus (HPV) oncoproteins. These studies provide insight into the role of MCPyV T antigen expression in tumor formation in vivo and contribute to our understanding of how MCPyV may function as a human DNA tumor virus.

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Yang, Anne Yuqing, Jong Hun Lee, Limin Shu, Chengyue Zhang, Zheng-Yuan Su, Yaoping Lu, Mou-Tuan Huang, et al. "Genome-wide analysis of DNA methylation in UVB- and DMBA/TPA-induced mouse skin cancer models." Life Sciences 113, no. 1-2 (September 2014): 45–54. http://dx.doi.org/10.1016/j.lfs.2014.07.031.

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George, Jeneesha, A. Thabitha, N. Vignesh, V. Manigandan, R. Saravanan, Ghaji Daradkeh, and M. Walid Qoronfleh. "Antiskin Cancer and Antioxidant Activities of Formulated Agar from Brown Seaweed Laminaria digitata (Hudson) in Dimethyl Benzanthracene-Induced Swiss Albino Mice." International Journal of Polymer Science 2021 (June 15, 2021): 1–12. http://dx.doi.org/10.1155/2021/9930777.

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This study explores the antiskin cancer effect of formulated agar (FA) from Laminaria digitata on dimethyl benzanthracene- (DMBA-) induced skin cancer mice. The agar was extracted and formulated (emulgel), and FA was biochemically characterized. The in vitro cytotoxicity of FA was tested using NTT 3T3 mice fibroblast cells. The mice were divided into 5 groups: group 1 served as control mice, group 2 mice were considered as DMBA-induced cancer control, group 3 mice were FA pretreated (low dose) + DMBA-induced mice, group 4 mice were FA pretreated (high dose) + DMBA-induced mice, and group 5 were positive control + DMBA-induced mice. The behaviour and biochemical markers of cancer were significantly decreased in group 2 (DMBA-induced) mice, which were brought to near normalcy by FA pretreated mice (groups 3 and 4). The levels of p53 and keratin were significantly elevated in group 2 mice and these levels were decreased in 3 and 4 mice as well. The histopathological examination of DMBA-induced mice was shown degenerated cervical patches in the skin, cirrhosis in liver, oedema in the renal tissue, and swollen and damage in cardiac tissue, which were reduced for the mice applied with FA. This confirms that FA pretreatment offered potential antiskin cancer property.

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Gebhardt, Christoffer, Astrid Riehl, Moritz Durchdewald, Julia Németh, Gerhard Fürstenberger, Karin Müller-Decker, Alexander Enk, et al. "RAGE signaling sustains inflammation and promotes tumor development." Journal of Experimental Medicine 205, no. 2 (January 21, 2008): 275–85. http://dx.doi.org/10.1084/jem.20070679.

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A broad range of experimental and clinical evidence has highlighted the central role of chronic inflammation in promoting tumor development. However, the molecular mechanisms converting a transient inflammatory tissue reaction into a tumor-promoting microenvironment remain largely elusive. We show that mice deficient for the receptor for advanced glycation end-products (RAGE) are resistant to DMBA/TPA-induced skin carcinogenesis and exhibit a severe defect in sustaining inflammation during the promotion phase. Accordingly, RAGE is required for TPA-induced up-regulation of proinflammatory mediators, maintenance of immune cell infiltration, and epidermal hyperplasia. RAGE-dependent up-regulation of its potential ligands S100a8 and S100a9 supports the existence of an S100/RAGE-driven feed-forward loop in chronic inflammation and tumor promotion. Finally, bone marrow chimera experiments revealed that RAGE expression on immune cells, but not keratinocytes or endothelial cells, is essential for TPA-induced dermal infiltration and epidermal hyperplasia. We show that RAGE signaling drives the strength and maintenance of an inflammatory reaction during tumor promotion and provide direct genetic evidence for a novel role for RAGE in linking chronic inflammation and cancer.

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Konoshima, Takao, and Midori Takasaki. "Cancer-chemopreventive effects of natural sweeteners and related compounds." Pure and Applied Chemistry 74, no. 7 (January 1, 2002): 1309–16. http://dx.doi.org/10.1351/pac200274071309.

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To search for possible cancer-chemopreventive agents from natural resources, several natural sweeteners were screened by the in vitro assay indicated by the inhibitory effects of Epstein-Barr virus early antigen (EBV-EA) induction. Of active compounds that showed the remarkable inhibitory effects on the EBV-EA induction, stevioside, from the leaves of Stevia rebaudiana, and mogroside V, from the fruits of Momordica grosvenori, exhibited significant inhibitory effects on the two-stage mouse skin carcinogenesis in vivo induced by 7,12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoylphorbol-13-acetate (TPA). The inhibitory effect of stevioside is stronger than that of glycyrrhizin, which had been known as an antitumor-promoter in chemical carcinogenesis. Furthermore, stevioside also inhibited mouse skin carcinogenesis initiated by peroxynitrite. These results suggest that stevioside and mogroside V might be valuable as chemopreventive agents for chemical carcinogenesis.

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Sati, Jasmine, Biraja Prasad Mohanty, Mohan Lal Garg, and Ashwani Koul. "Pro-Oxidant Role of Silibinin in DMBA/TPA Induced Skin Cancer: 1H NMR Metabolomic and Biochemical Study." PLOS ONE 11, no. 7 (July 14, 2016): e0158955. http://dx.doi.org/10.1371/journal.pone.0158955.

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Das, Ila, Asha Acharya, Deborah L. Berry, Supti Sen, Elizabeth Williams, Eva Permaul, Archana Sengupta, Sudin Bhattacharya, and Tapas Saha. "Antioxidative effects of the spice cardamom against non-melanoma skin cancer by modulating nuclear factor erythroid-2-related factor 2 and NF-κB signalling pathways." British Journal of Nutrition 108, no. 6 (December 19, 2011): 984–97. http://dx.doi.org/10.1017/s0007114511006283.

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The role of dietary factors in inhibiting or delaying the development of non-melanoma skin cancer (NMSC) has been investigated for many years. Cardamom, which is a dietary phytoproduct, has been commonly used in cuisines for flavour and has numerous health benefits, such as improving digestion and stimulating metabolism and having antitumorigenic effects. We have investigated the efficacy of dietary cardamom against 7,12-dimethylbenz[a]anthracene (DMBA)-induced skin papillomatogenesis in Swiss albino mice that closely resembles human NMSC. Mice were grouped into normal wild type (untreated), vehicle-treated (acetone), carcinogen-treated (DMBA), and DMBA and cardamom-treated (DMBA+CARD) to delineate the role of cardamom against DMBA-induced papillomatogenesis. Oral administration of cardamom to DMBA-treated mice up-regulated the phase II detoxification enzymes, such as glutathione-S-transferase and glutathione peroxidase, probably via activation of nuclear factor erythroid-2-related factor 2 transcription factor in ‘DMBA+CARD’ mice. Furthermore, reduced glutathione, glutathione reductase, superoxide dismutase and catalase were also up-regulated by cardamom in the same ‘DMBA+CARD’ group of mice compared with DMBA-treated mice. Cardamom ingestion in DMBA-treated mice blocked NF-κB activation and down-regulated cyclo-oxygenase-2 expression. As a consequence, both the size and the number of skin papillomas generated on the skin due to the DMBA treatment were reduced in the ‘DMBA+CARD’ group. Thus, the results from the present study suggest that cardamom has a potential to become a pivotal chemopreventive agent to prevent papillomagenesis on the skin.

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Kim, Myoung Ok, Sung Hyun Kim, Mi Jung Shin, Dong Hoon Yu, Bong Soo Kim, Kyu Tae Chang, Sanggyu Lee, Yong Bok Park, Tae-Hoon Lee, and Zae Young Ryoo. "DMBA/TPA-Induced Tumor Formation Is Aggravated in Human Papillomavirus Type 16 E6/E7 Transgenic Mouse Skin." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 16, no. 7 (July 1, 2006): 325–32. http://dx.doi.org/10.3727/000000006783980964.

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Na Takuathung, Mingkwan, Kanjana Jaijoy, Noppamas Soonthornchareonnon, and Seewaboon Sireeratawong. "Anti-inflammatory, Antinociceptive, and Antitumorigenesis Activities of Terminalia Bellerica (Gaertn.) Roxb. in Animal Models." Natural Product Communications 17, no. 4 (April 2022): 1934578X2210899. http://dx.doi.org/10.1177/1934578x221089996.

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Previous pharmacological research has demonstrated that Terminalia bellerica (Gaertn.) Roxb. (TB) extract possesses several pharmacological activities. However, there is scant evidence documenting the therapeutic activities of TB extract on inflammation, pain, and cancers. Our study examined the in vivo anti-inflammation, antinociception, and antitumorigenesis effects of TB extract and investigated possible mechanisms for those effects. Anti-inflammation activities of TB extract were evaluated using ethyl phenylpropiolate (EPP)- and arachidonic acid (AA)-induced ear edema models, a cotton pellet-induced granulation formation model, and a carrageenan-induced hind paw edema model. An antinociceptive property of TB extract was assessed using a formalin-induced nociception test. An anticarcinogenesis effect was investigated using a 7,12-dimethylbenz( a) anthracene (DMBA) and 12- O-tetradecanoylphorbol-13-acetate (TPA)-induced tumorigenesis model. In the study, TB extract exhibited significant anti-inflammatory effects against EPP-induced ear edema and carrageenan-induced hind paw edema in rats. However, the TB extract showed insignificant inhibitory activity against AA-induced ear edema and cotton pellet-induced granuloma. A dose-dependent decrease in analgesic activity was observed with TB extract evidenced by decreased licking time in formalin-induced pain in mice in both the early and late phases. TB extract also significantly inhibited DMBA/TPA-induced mouse skin tumorigenesis. In conclusion, TB extract possesses anti-inflammatory, analgesic, and anticarcinogenesis properties which act, at least in part, through inhibitory effects of inflammatory mediator production.

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Singhal, Sharad S., Prakash Kulkarni, Jyotsana Singhal, David Horne, Sanjay Awasthi, and Ravi Salgia. "Abstract 5345: Novel approach to attenuate melanoma initiation and progression." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5345. http://dx.doi.org/10.1158/1538-7445.am2022-5345.

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Abstract Background and Purpose: Melanocytic nevi are benign proliferations of melanocytic cells that are positively correlated with susceptibility to melanoma. Polyaromatic hydrocarbons (PAH) are ubiquitous environmental pollutants that are potent mutagens and carcinogens, and the investigators have taken advantage of these properties to investigate the mechanisms by which chemicals cause cancer of the skin and other organs. In comparison to C57Bl/6 strain, C3H/HeN mice are more susceptible to the development of PAH induced tumors. Therefore, a mouse model of nevus initiation and progression was developed in C3H/HeN mice using a modified chemical carcinogenesis protocol. Experimental Design: In the traditional two-stage skin carcinogenesis model, initiation is accomplished by the application of a subcarcinogenic dose of a carcinogen. Subsequently, tumor development is elicited by repeated treatment with a tumor promoting agent. Nevi develop due to DNA damage initiated by 7, 12-dimethylbenz[a]anthracene (DMBA) followed by chronic promotion with 12-O-tetradecanoyl-phorbol-13-acetate (TPA). Results: Dysplastic pigmented skin lesions appeared in ~10 wk with 100% penetrance. Studies reported here demonstrating that inhibition or depletion of RLIP results in apoptosis and cancer regression in an exceptionally broad spectrum on neoplasia have suggested an intriguing possibility that RLIP is an anti-apoptotic mechanism required not only for the survival of cancer cells, but also for their very existence. In support of this assertion results presented here that the well-known carcinogens, DMBA and phorbol esters (PMA or TPA) are ineffective in causing neoplasia in C3H/HeN mice treated with RLIP-targeting agent’s (RLIP antibodies and RLIP antisense). Here we demonstrate that DMBA/PMA-induced skin carcinogenesis in C3H/HeN mouse was suppressed completely by depletion of RLIP by antisense or inhibition by antibodies. In addition, C3H/HeN mice treated with RLIP-targeting agent’s, p53, P38, and JNK activation did not occur in response to carcinogens. These findings demonstrate a fundamental role of RLIP in chemical carcinogenesis. Conclusions: We demonstrate that RLIP expression is significantly greater in cancer cells than in non-malignant cells, and RLIP-targeting agent’s (RLIP antibodies and RLIP antisense) treatment was significantly suppress the generation of melanocytic nevi and their progression to melanoma. (This work was supported in part by the Department of Defense grants W81XWH-16-1-0641 and W81XWH-20-1-0362. Funding from the Beckman Research Institute of City of Hope is also acknowledged). Citation Format: Sharad S. Singhal, Prakash Kulkarni, Jyotsana Singhal, David Horne, Sanjay Awasthi, Ravi Salgia. Novel approach to attenuate melanoma initiation and progression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5345.

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Ishikawa, Tomo-o., Indracanti Prem Kumar, Hidevaldo B. Machado, Koon-Pong Wong, Donna Kusewitt, Sung-Cheng Huang, Susan M. Fischer, and Harvey R. Herschman. "Positron emission tomography imaging of DMBA/TPA mouse skin multi-step tumorigenesis." Molecular Oncology 4, no. 2 (February 2, 2010): 119–25. http://dx.doi.org/10.1016/j.molonc.2010.01.005.

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Agame-Lagunes, B., M. Alegria-Rivadeneyra, A. Alexander-Aguilera, R. Quintana-Castro, C. Torres-Palacios, P. Grube-Pagola, C. Cano-Sarmiento, R. García-Varela, and H. S. García. "Bioactivity of betulinic acid nanoemulsions on skin carcinogenesis in transgenic mice K14E6." Grasas y Aceites 72, no. 4 (December 30, 2021): e433. http://dx.doi.org/10.3989/gya.0553201.

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Alternative therapies for cancer treatment have been developed using bioactive compounds such as betulinic acid (BA). The objective of this study was to investigate the bioactivity of BA in its free form and compare it with its nano-encapsulated form under a skin carcinogenesis protocol in a genetically modified murine model. K14E6 and FVB mice were divided into four groups to be treated with free BA and with betulinic acid nanoemulsion (BANE). Lecithin enriched with medium chain fatty acids (MCFAs) was employed as an emulsifier to prepare the nanoemulsions with a mean droplet size of 40 nm. Skin tumors were induced by exposure to DMBA and TPA directly to the transgenic mice. Tumor development was completely inhibited by BANE and by 70% with free BA. This was validated by histological sections and the gene expression of the Cdk4 and Casp8 genes.

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Thomas, Giju, Bastiaan Tuk, Ji-Ying Song, Hoa Truong, Hans C. Gerritsen, Frank R. de Gruijl, and Henricus J. C. M. Sterenborg. "Studying skin tumourigenesis and progression in immunocompetent hairless SKH1-hr mice using chronic 7,12-dimethylbenz(a)anthracene topical applications to develop a useful experimental skin cancer model." Laboratory Animals 51, no. 1 (July 10, 2016): 24–35. http://dx.doi.org/10.1177/0023677216637305.

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Previous studies have established that 7,12-dimethylbenz(a)anthracene (DMBA) can initiate skin tumourigenesis in conventional furred mouse models by acting on hair follicle stem cells. However, further cancer progression depends on repeated applications of tumour promoter agents. This study evaluated the timeline involved in skin tumourigenesis and progression in immunocompetent hairless SKH1-hr mice with dysfunctional hair follicles using only DMBA with no additional tumour promoter agents. The results showed that topical application of 30 µg (117 nmol) of DMBA over the back and flank regions of the mouse once a week and 15 µg (58.5 nmol) twice a week produced skin tumours after 7–8 weeks. However, by week 14 a heavy benign tumour load required the mice to be euthanized. Lowering the DMBA dose to 15 µg (58.5 nmol) once a week produced tumours more slowly and allowed the mice to be studied for a longer period to week 23. This low-dose DMBA regimen yielded a high percentage of malignant tumours (58.8%) after 23 weekly applications. Additionally DMBA-treated skin showed an increase in mean epidermal thickness in comparison to untreated and acetone-treated skin. Despite the aberrant hair follicles in SKH1-hr mice, this chemically driven skin cancer model in hairless mice can serve as a suitable alternative to the ultraviolet-induced skin cancer models and can be reliably replicated as demonstrated by both the pilot and main experiments.

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Liu, Zhaoguo, Pingting Zhu, Yu Tao, Cunsi Shen, Siliang Wang, Lingang Zhao, Hongyan Wu, et al. "Cancer-promoting effect of capsaicin on DMBA/TPA-induced skin tumorigenesis by modulating inflammation, Erk and p38 in mice." Food and Chemical Toxicology 81 (July 2015): 1–8. http://dx.doi.org/10.1016/j.fct.2015.04.002.

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Kim, Sung-Hyun, Myoung-Ok Kim, Peng Gao, Cheng-A. Youm, Hae-ryoung Park, Sang-Ryeul Lee, Kil-Soo Kim, et al. "Overexpression of Extracellular Superoxide Dismutase (EC-SOD) in Mouse Skin Plays a Protective Role in DMBA/TPA-Induced Tumor Formation." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 15, no. 7 (July 1, 2005): 333–41. http://dx.doi.org/10.3727/096504005776449725.

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Bhutia, Yangzom D., Mohini Saini, Anil K. Sharma, Bhaskar Sharma, and Devendra Swarup. "Efficacy ofCurcuma longaExtract Against DMBA Induced Skin Cancer in Rats." Journal of Applied Animal Research 36, no. 2 (December 2009): 291–96. http://dx.doi.org/10.1080/09712119.2009.9707079.

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Sherwani, Mohd Asif, Saba Tufail, Aijaz Ahmed Khan, and Mohammad Owais. "Dendrosome mediated topical gene silencing by PLK-1 specific siRNA: implication in treatment of skin cancer in mouse model." RSC Advances 6, no. 8 (2016): 6843–57. http://dx.doi.org/10.1039/c5ra15270d.

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Napalkov, N., A. Likhachev, V. Anisimov, A. Lokitonov, M. Zabezhinski, A. Ovsyannikov, J. Wahrendorf, H. Becher, and L. Tomatis. "Promotion of skin tumours by TPA in the progeny of mice exposed pre-natally to DMBA." Carcinogenesis 8, no. 3 (1987): 381–85. http://dx.doi.org/10.1093/carcin/8.3.381.

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Li, Yun Rose, Kyle Halliwill, Eve Kandyba, Reyno Delrosario, Quan Tran, Nora Bayani, Di Wu, et al. "Abstract 2198: The impact of carcinogens, obesity, and chronic inflammatory processes on mutational signatures and cancer risk in mouse tumor models." Cancer Research 82, no. 12_Supplement (June 15, 2022): 2198. http://dx.doi.org/10.1158/1538-7445.am2022-2198.

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Abstract An estimated 40% of all human cancers are suspected to be a result of modifiable risk factors such as obesity, high fat diet and chronic inflammation. Whole genome sequencing (WGS) of thousands of human tumors have revealed “mutational signatures” that provide a molecular footprint of cancer origins. Whether such signatures exist for modifiable cancer risk factors remains unclear. We studied the impact of lifestyle risk factors using a compendium of 107 mouse tumors that model obesity, high fat diet, wounding, chronic inflammation, or chemotherapy. We used a well-established 2-step skin carcinogenesis model composed of exposure to mutagen DMBA followed by tumor promoter TPA, generating squamous carcinomas that were analysed by WGS for identification of mutational signatures. In addition to recapitulating many COSMIC human signatures, we identified a novel SNV signature induced by a single treatment with DMBA (SBS.DMBA) which explains the majority of all detected mutations. While a single exposure of normal skin to DMBA induces a highly variable number of carcinogen-specific mutations, a very high mutation burden is insufficient for tumorigenesis. SNVs attributable to reactive oxygen species (ROS) are broadly found in about 25% of all mouse tumors, but are most prominent in tumors from mice that are exposed to DMBA in utero, suggesting that the developmental age of mutagen exposure may impact the repair of ROS generated mutations and that the timing of exposure is a poorly understudied component of carcinogenesis. In mouse tumor models of genetic and dietary obesity, the total mutational load and mutational signatures in tumors from obese mice were indistinguishable from those of lean mice despite dramatic differences in tumor latency and progression as well transcriptomic differences in immune activation. We found an enrichment in deleterious Tgfrb2 mutations in tumors from mice with low compared to high body mass index (BMI) (p<0.016). Using a conditionally activated RAS mouse model, we also show that a non-mutagenic inflammatory signal such as a chronic wound can act as the rate-limiting step for full tumor development. Surprisingly these tumors can be evoked even in somatic genomes with very few mutations apart from the initiating Ras driver. Finally, together with the Riva et al study, these chemically induced mouse tumors recapitulate >50% of established human cancer driver genes. DMBA caused 91% of all Hras/Kras mutations, but only a minority of other recurrent driver mutations in genes such as Trp53 and Tert, suggesting that these occur later during the process of carcinogenesis. Taken together, we have analyzed the largest compendium of WGS data from nearly 300 mouse tumors, showing that while exogenous promotional factors do not increase mutation burden or induce novel mutational patterns, they have a major rate-limiting role in determining cancer risk. Citation Format: Yun Rose Li, Kyle Halliwill, Eve Kandyba, Reyno Delrosario, Quan Tran, Nora Bayani, Di Wu, Olga Mirzoeva, Melissa McCreery Reeves, Mishu Islam, Laura Riva, Eric Bergstrom, John Digiovanni, Ludmil Alexandrov, Allan Balmain. The impact of carcinogens, obesity, and chronic inflammatory processes on mutational signatures and cancer risk in mouse tumor models [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2198.

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Zhou, Hong, Qi-xiang Zhao, Jia-dong Yu, Cheng-cheng Yue, Yan Hao, Hua-ping Zheng, Jing Hu, Zhen Wang, and Jiong Li. "Interleukin-38 promotes skin tumorigenesis via regulation of epidermal cell hyperplasia and pro-tumorigenic microenvironment in an IL-1Rrp2-dependent manner." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 22.01. http://dx.doi.org/10.4049/jimmunol.206.supp.22.01.

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Abstract As the newest member of the IL-1 family, interleukin-38 (IL-38) has strong associations with chronic inflammatory diseases. However, its roles in tumorigenesis and the underlying mechanism remain poorly understood. Here, we demonstrated that IL-38, which was highly expressed in skin, downregulated in human cutaneous squamous cell carcinomas (CSCC) and 7,12-dimethylbenzanthracene (DMBA)/12-O-tetradecanoyl phorbol-13-acetate (TPA) induced mouse skin tumorigenesis. IL-38 keratinocyte-specific knockout mice (IL-38 cKO) dramatically promoted skin tumor formation and their malignant progression. Mechanistically, IL-38 is dispensable for epidermal mutagenesis. IL-38 keratinocyte-specific deletion reduced proliferative gene expression along with epidermal cell proliferation and hyperplasia. Additionally, keratinocyte-specific deletion of IL-38 was associated with reduced secretion of inflammatory cytokines leading to a decreased infiltration of myeloid cells into the local tumor microenvironment, these inflammation-driven tumorigenesis are essential for carcinogenesis process. Furthermore, we first demonstrated that IL-38 activated the c-Jun N-terminal kinase (JNK)/activator protein 1 (AP-1) signal transduction pathway to promote proliferation and migration of tumor cells and expression of cancer-related inflammatory cytokines in an IL-1 receptor (IL-1R)-related protein 2 (IL-1Rrp2)-dependent manner. Together, our findings highlight the role of IL-38 in the regulation of epidermal cell hyperplasia and pro-tumorigenic microenvironment through IL-1Rrp2 /JNK and establish a new defined factor IL-38/ IL-1Rrp2 as therapeutic targets in skin cancer.

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Ali, Huma, and Savita Dixit. "Extraction Optimization ofTinospora cordifoliaand Assessment of the Anticancer Activity of Its Alkaloid Palmatine." Scientific World Journal 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/376216.

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Objective. To optimize the conditions for the extraction of alkaloid palmatine fromTinospora cordifoliaby using response surface methodology (RSM) and study its anticancerous property against 7,12-dimethylbenz(a)anthracene (DMBA) induced skin carcinogenesis in Swiss albino mice.Methods. The effect of three independent variables, namely, extraction temperature, time, and cycles was investigated by using central composite design. A single topical application of DMBA (100 μg/100 μL of acetone), followed 2 weeks later by repeated application of croton oil (1% in acetone three times a week) for 16 weeks, exhibited 100 percent tumor incidence (Group 2).Results. The highest yield of alkaloid fromTinospora cordifoliacould be achieved at 16 hours of extraction time under 40°C with 4 extraction cycles. Alkaloid administration significantly decreases tumor size, number, and the activity of serum enzyme when compared with the control (Group 2). In addition, depleted levels of reduced glutathione (GSH), superoxide dismutase (SOD), and catalase and increased DNA damage were restored in palmatine treated groups.Conclusion. The data of the present study clearly indicate the anticancer potential of palmatine alkaloid in DMBA induced skin cancer model in mice.

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Nicol, C. J. "PPAR influences susceptibility to DMBA-induced mammary, ovarian and skin carcinogenesis." Carcinogenesis 25, no. 9 (April 1, 2004): 1747–55. http://dx.doi.org/10.1093/carcin/bgh160.

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Sutapa Mukherjee, Archismaan Ghosh, and Madhumita Roy. "Co-Carcinogenicity of Arsenic: Probable Mechanisms." International Journal of Current Microbiology and Applied Sciences 10, no. 11 (November 10, 2021): 294–305. http://dx.doi.org/10.20546/ijcmas.2021.1011.033.

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Presence of carcinogens, like Polycyclic Aromatic Hydrocarbons (PAH), in the form of cigarette smoke, vehicular emission and industrial emissions in our immediate surroundings is a potent health hazard. Arsenic, a carcinogenic metalloid, omnipresent in the environment, can act as co-carcinogen, where it enhances the carcinogenicity of other carcinogens. In the present study, the co-carcinogenic effect of Arsenic has been investigated, upon the 7,12-dimethylbenz[a]-anthracene (DMBA), a PAH, induced skin cancer model, in Swiss albino mice. Histological analysis revealed earlier development of invasive carcinoma in the DMBA and arsenic treated group in comparison to the DMBA treated mice alone. To understand this phenomena, ROS generation, DNA damage, lipid peroxidation, protein carbonyl content, total antioxidant capacity and activity of pro-inflammatory cytokines (TNF-α, IL6, IL17a, IL22) and their downstream modulators (NF-κB) was assessed. The results suggested that arsenic in the presence of DMBA induced higher ROS generation, greater DNA damage, elevated lipid peroxidation, increased protein carbonyl content, upregulated activity of pro-inflammatory cytokines and their downstream regulators as well as down regulated the total antioxidant capacity in comparison to DMBA alone. These findings hint at the co-carcinogenic potential of arsenic, as it significantly enhances the carcinogenicity of DMBA and hastens carcinogenesis.

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Hayashi, K., Y. Momoi, N. Tanuma, A. Kishimoto, H. Ogoh, H. Kato, M. Suzuki, et al. "Abrogation of protein phosphatase 6 promotes skin carcinogenesis induced by DMBA." Oncogene 34, no. 35 (December 8, 2014): 4647–55. http://dx.doi.org/10.1038/onc.2014.398.

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Fischer, Wolfgang H., Peter E. Beland, and Werner K. Lutz. "DNA adducts, cell proliferation and papilloma latency time in mouse skin after repeated dermal application of DMBA and TPA." Carcinogenesis 14, no. 7 (1993): 1285–88. http://dx.doi.org/10.1093/carcin/14.7.1285.

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Etoh, Tadahiro, Yong P. Kim, Masahiko Hayashi, Michiko Suzawa, Shiming Li, Chi-Tang Ho, and Kanki Komiyama. "Inhibitory effect of a formulated extract from multiple citrus peels on LPS-induced inflammation in RAW 246.7 macrophages." Functional Foods in Health and Disease 3, no. 6 (June 26, 2013): 242. http://dx.doi.org/10.31989/ffhd.v3i6.50.

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Background: Formulated Citrus Peel Extract (GL) made from the peels of six citrus fruits available in Japan, namely navel oranges, citrus hassaku, citrus limon, citrus natsudaidai, citrus miyauchi and satsuma, was initially developed as a cosmetic product to protect skin from UV irradiation. Anecdotal evidences of anti-cancer property of GL have been reported by consumers based on the cases such as topical application for melanoma, and oral ingestion for prostate, lung and liver cancers. Those anecdotal reports stimulated us to investigate anti-tumorigenesis activity of GL. In the previous study, we reported that the topical application of GL inhibited DMBA/TPA-induced skin tumor formation by decreasing inflammatory gene parameters.Objective: In this study, we mainly investigated the effect of GL on translocation of NF-kB together with production of nitric-oxide and TNF-α induced by LPS in RAW 264.7 cells.Results: This investigation showed that GL decreased the release of TNF-α and nitric oxide from macrophage RAW264.7 cells stimulated by LPS in a dose-dependent manner. In addition, GL suppressed the expression of iNOS and nuclear translocation of NF-kB in RAW264.7 cells, inhibited the degradation of IκB-α, and scavenged hydroxyl radicals (DMPO/OH adduct) in vitro.Conclusions: Our findings suggest that GL suppresses the inflammation in vitro, and exerts chemopreventive activity through the inhibition of production of TNF-α and iNOS proteins due to the inhibition of nuclear translocation of NF-kB and oxidative stress. GL appears to be a novel functional natural product capable of preventing inflammation and inflammation-associated tumorigenesis. Keywords: GL, Citrus peel extract, anti-inflammation, Nitric oxide, iNOS, NF-kB, TNF-α

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chen, wanjiao, Vinh A. Dao, Kim Cardenas, Shunhua Lao, Álvaro Padrón, Edward P. Hasty, Zelton Dave Sharp, Vincent Hurez, and Tyler J. Curiel. "Microencapulated rapamycin prevents carcinogen and inflammation driven colon cancer through immune mechanisms." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 73.9. http://dx.doi.org/10.4049/jimmunol.196.supp.73.9.

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Abstract We tested microencapsulated rapamycin (eRapa, ~2.2 mg/kg rapamycin/mouse/day) in carcinogen (azoxymethane, AOM) + inflammatory agent (dextran sodium sulfate, DSS) colon cancer. WT BL6 mice fed eRapa before, and during AOM/DSS had significantly fewer colon tumors and tumor burden than control fed mice (empty microcapsules). eRapa prevented colon cancer in δ TCR KO mice lacking γδ T cells but not in IFN-γ KO mice. In carcinogen (DMBA) + inflammatory agent (TPA) skin cancer, IFN-γ and γδ T cells were both needed for eRapa cancer prevention, showing tumor-specific and common immune requirements for eRapa-mediated cancer prevention. In βδ TCR KO mice lacking all T cells, AOM/DSS induced no cancer or only few tumors, suggesting αβ T cells are required for colon neoplasia and cancer in the AOM/DSS model. Protection from acute colitis in this model usually predicts colon cancer protection. Strikingly, however, eRapa did not prevent acute clinical or histologic colitis induced by DSS, despite cancer protection, suggesting effects on chronic colitis, or induction of cancer-protective but not acute colitis-protective mechanisms. In acute colitis, eRapa significantly decreased spleen and colon weights and CD3+CD4+ T cells, and increased mesenteric lymph node γδ T cells (with decreased Vγ1.1+ and increased Vγ2+ subsets) consistent with altered inflammation and reduced CD4-CXCR3+ and CD4-α4β7 T cells (likely γδ T cells) consistent with altered trafficking but did not affect CCR9+ T cells. In chronic colitis, eRapa significantly increased γδ T cells (with no changes in Vγ1.1+ or Vγ2+ subsets) that could mediate cancer protection. These novel immune effects of rapamycin help define its cancer prevention mechanisms and define novel clinical uses.

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Barresi, Caterina, Heidemarie Rossiter, Maria Buchberger, Johannes Pammer, Supawadee Sukseree, Maria Sibilia, Erwin Tschachler, and Leopold Eckhart. "Inactivation of Autophagy in Keratinocytes Reduces Tumor Growth in Mouse Models of Epithelial Skin Cancer." Cells 11, no. 22 (November 21, 2022): 3691. http://dx.doi.org/10.3390/cells11223691.

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Autophagy is a ubiquitous degradation mechanism, which plays a critical role in cellular homeostasis. To test whether autophagy suppresses or supports the growth of tumors in the epidermis of the skin, we inactivated the essential autophagy gene Atg7 specifically in the epidermal keratinocytes of mice (Atg7∆ep) and subjected such mutant mice and fully autophagy-competent mice to tumorigenesis. The lack of epithelial Atg7 did not prevent tumor formation in response to 7, 12-dimethylbenz(a)anthracene (DMBA) as the initiator and 12-O tetradecanoylphorbol-13-acetate (TPA) as the promoter of tumor growth. However, the number of tumors per mouse was reduced in mice with epithelial Atg7 deficiency. In the K5-SOS EGFRwa2/wa2 mouse model, epithelial tumors were initiated by Son of sevenless (SOS) in response to wounding. Within 12 weeks after tumor initiation, 60% of the autophagy-competent K5-SOS EGFRwa2/wa2 mice had tumors of 1 cm diameter and had to be sacrificed, whereas none of the Atg7∆ep K5-SOS EGFRwa2/wa2 mice formed tumors of this size. In summary, the deletion of Atg7 reduced the growth of epithelial tumors in these two mouse models of skin cancer. Thus, our data show that the inhibition of autophagy limits the growth of epithelial skin tumors.

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Nafz, J., M. Ohnesorge, E. Stockfleth, F. Rösl, and I. Nindl. "Imiquimod treatment of papilloma virus and DMBA /TPA-induced cutaneous skin cancer in Mastomys coucha: an unique animal model system useful for preclinical studies." British Journal of Dermatology 157 (December 7, 2007): 14–17. http://dx.doi.org/10.1111/j.1365-2133.2007.08266.x.

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Majed, Ferial, Summya Rashid, Abdul Quaiyoom Khan, Sana Nafees, Nemat Ali, Rashid Ali, Rehan Khan, Syed Kazim Hasan, Syed Jafar Mehdi, and Sarwat Sultana. "Tannic acid mitigates the DMBA/croton oil-induced skin cancer progression in mice." Molecular and Cellular Biochemistry 399, no. 1-2 (November 16, 2014): 217–28. http://dx.doi.org/10.1007/s11010-014-2248-3.

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Arora, Annu, Imtiaz A. Siddiqui, and Yogeshwer Shukla. "Modulation of p53 in 7,12-dimethylbenz[a]anthracene–induced skin tumors by diallyl sulfide in Swiss albino mice." Molecular Cancer Therapeutics 3, no. 11 (November 1, 2004): 1459–66. http://dx.doi.org/10.1158/1535-7163.1459.3.11.

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Abstract Allium vegetables have been shown to have beneficial health effects against several chronic diseases including cancer. Diallyl sulfide (DAS), an organosulfur compound present in garlic, is well known for its chemopreventive properties in several tumor models. The pharmacologic role of DAS in prevention and treatment of cancer is well documented in the literature, but its molecular mechanism of action is not yet well defined. In the present study, modulation in p53 expression by topical application of DAS was recorded in 7,12-dimethylbenz[a]anthracene (DMBA)–induced skin tumors in Swiss albino mice. Western blot analysis and immunohistochemical protein detection, combined with multivariable flow cytometry, show that DAS application induces the expression of the wild-type (wt) p53 and down-regulates the expression of mutant (mut) p53. Immunoblotting analysis of tumors showed significant increase in levels of wtp53 by DAS application, whereas for mutp53 the DMBA-induced levels of protein were found to reduce to near normal levels with DAS application. The quantitative analysis of immunostained skin/tumor sections using image analysis and quantitative stereology showed 66.6% and 54.2% increases in wtp53 levels and 53.4% and 44.3% decreases in mutp53 levels in animals where DAS was applied 1 hour prior to or 1 hour after DMBA application, respectively. Flow cytometric analysis further confirmed modulation of wtp53 and mutp53 protein in DAS-supplemented tumors. The increase in the expression of wt tumor suppressor gene protein p53 was accompanied by elevation of the levels of cyclin-dependent kinase inhibitor p21/waf1. The percentage increase in the levels of p21/waf1 was found to be 72.9% and 61.3%, respectively, in DAS-supplemented groups before and after administration. These results thus show that DAS is a potential chemopreventive agent capable of modulating and regulating the tumor suppressor p53 along with its downstream effective molecule, p21/waf1. Thus, DAS can be a potential chemopreventive agent against skin tumor development.

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Wang, Fei, Hongxia Ma, Zhaoguo Liu, Wei Huang, Xiaojing Xu, and Xuemei Zhang. "α-Mangostin inhibits DMBA/TPA-induced skin cancer through inhibiting inflammation and promoting autophagy and apoptosis by regulating PI3K/Akt/mTOR signaling pathway in mice." Biomedicine & Pharmacotherapy 92 (August 2017): 672–80. http://dx.doi.org/10.1016/j.biopha.2017.05.129.

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Costa, Alexandra C., Joana M. O. Santos, Beatriz Medeiros-Fonseca, Paula A. Oliveira, Margarida M. S. M. Bastos, Haissa O. Brito, Rui M. Gil da Costa, and Rui Medeiros. "Characterizing the Inflammatory Microenvironment in K14-HPV16 Transgenic Mice: Mast Cell Infiltration and MicroRNA Expression." Cancers 14, no. 9 (April 28, 2022): 2216. http://dx.doi.org/10.3390/cancers14092216.

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High-risk human papillomavirus (HPV) is the etiologic agent of several types of cancer. Mast cells’ role as either a driving or opposing force for cancer progression remains controversial. MicroRNAs are dysregulated in several HPV-induced cancers, and can influence mast cell biology. The aim of this study was to evaluate mast cell infiltration and to identify microRNAs potentially regulating this process. Transgenic male mice (K14-HPV16; HPV+) and matched wild-type mice (HPV−) received 7,12-Dimethylbenz[a]anthracene (DMBA) (or vehicle) over 17 weeks. Following euthanasia, chest skin and ear tissue samples were collected. Mast cell infiltration was evaluated by immunohistochemistry. MicroRNAs associated with mast cell infiltration were identified using bioinformatic tools. MicroRNA and mRNA relative expression was evaluated by RT-qPCR. Immunohistochemistry showed increased mast cell infiltration in HPV+ mice (p < 0.001). DMBA did not have any statistically significant influence on this distribution. Ear tissue of HPV+ mice showed increased mast cell infiltration (p < 0.01) when compared with chest skin samples. Additionally, reduced relative expression of miR-125b-5p (p = 0.008, 2−ΔΔCt = 2.09) and miR-223-3p (p = 0.013, 2−ΔΔCt = 4.42) seems to be associated with mast cell infiltration and increased expression of target gene Cxcl10. These results indicate that HPV16 may increase mast cell infiltration by down-regulating miR-223-3p and miR-125b-5p.

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Arora, Annu, and Yogeshwer Shukla. "Induction of Apoptosis by Diallyl Sulfide in DMBA-Induced Mouse Skin Tumors." Nutrition and Cancer 44, no. 1 (September 2002): 89–94. http://dx.doi.org/10.1207/s15327914nc441_12.

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Natarajamurthy, Sindhuja H., and Shylaja M. Dharmesh. "REMOVED: Protective effect of Daucus carota against UV–DMBA induced skin cancer in mice." Chemico-Biological Interactions 219 (August 2014): 48–56. http://dx.doi.org/10.1016/j.cbi.2014.04.013.

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Manna, Debashri, Shabnam Akhtar, Pragati Maiti, Samiran Mondal, Tapan Kumar Mandal, and Rita Ghosh. "Anticancer activity of a 1,4-dihydropyridine in DMBA-induced mouse skin tumor model." Anti-Cancer Drugs 31, no. 4 (April 2020): 394–402. http://dx.doi.org/10.1097/cad.0000000000000887.

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

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