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Journal articles on the topic 'Dimethylbenzanthracene'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Dandekar, S., S. Sukumar, H. Zarbl, L. J. Young, and R. D. Cardiff. "Specific activation of the cellular Harvey-ras oncogene in dimethylbenzanthracene-induced mouse mammary tumors." Molecular and Cellular Biology 6, no. 11 (1986): 4104–8. http://dx.doi.org/10.1128/mcb.6.11.4104.

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Genomic DNAs from dimethylbenzanthracene-induced BALB/c mouse mammary tumors arising from the transplantable hyperplastic outgrowth (HPO) line designated DI/UCD transformed NIH 3T3 cells upon transfection. Transforming activity was attributed to the presence of activated Harvey ras-1 oncogenes containing an A----T transversion at the middle adenosine nucleotide in codon 61. DNAs from untreated DI/UCD HPO cells and radiation-induced and spontaneous mammary tumors from the DI/UCD HPO line failed to transform NIH 3T3 cells. The results indicated that the mutation activation of Harvey ras-1 oncogenes was specific to dimethylbenzanthracene treatment in the mouse mammary tumor system.

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2

Dandekar, S., S. Sukumar, H. Zarbl, L. J. Young, and R. D. Cardiff. "Specific activation of the cellular Harvey-ras oncogene in dimethylbenzanthracene-induced mouse mammary tumors." Molecular and Cellular Biology 6, no. 11 (1986): 4104–8. http://dx.doi.org/10.1128/mcb.6.11.4104-4108.1986.

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Genomic DNAs from dimethylbenzanthracene-induced BALB/c mouse mammary tumors arising from the transplantable hyperplastic outgrowth (HPO) line designated DI/UCD transformed NIH 3T3 cells upon transfection. Transforming activity was attributed to the presence of activated Harvey ras-1 oncogenes containing an A----T transversion at the middle adenosine nucleotide in codon 61. DNAs from untreated DI/UCD HPO cells and radiation-induced and spontaneous mammary tumors from the DI/UCD HPO line failed to transform NIH 3T3 cells. The results indicated that the mutation activation of Harvey ras-1 oncogenes was specific to dimethylbenzanthracene treatment in the mouse mammary tumor system.

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3

FLOERSHEIM, George L. "Radiosensitization by dimethylbenzanthracene, diphenylcyclopropenone and aminoanthraquinones." Journal of Toxicological Sciences 20, no. 2 (1995): 149–54. http://dx.doi.org/10.2131/jts.20.149.

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4

Chipman, J. K., and J. E. Davies. "Inhibition of dimethylbenzanthracene mutagenicity by butylated hydroxytoluene." Food and Chemical Toxicology 24, no. 6-7 (1986): 704. http://dx.doi.org/10.1016/0278-6915(86)90165-1.

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5

Eğimezer, G., ÜV Üstündağ, PS Ateş, et al. "Methylnitrosourea, dimethylbenzanthracene and benzoapyrene differentially affect redox pathways, apoptosis and immunity in zebrafish." Human & Experimental Toxicology 39, no. 7 (2020): 920–29. http://dx.doi.org/10.1177/0960327120905961.

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Cancer continues to be a major cause of mortality globally. Zebrafish present suitable models for studying the mechanisms of genotoxic carcinogens. The aim of this study was to investigate the interaction between oxidant–antioxidant status, apoptosis and immunity in zebrafish that were exposed to three different genotoxic carcinogens methylnitrosourea, dimethylbenzanthracene, benzoapyrene and methylnitrosourea + dimethylbenzanthracene starting from early embryogenesis for 30 days. Lipid peroxidation, nitric oxide levels, superoxide dismutase and glutathione- S-transferase activities and mRNA levels of apoptosis genes p53, bax, casp3a, casp2 and immunity genes fas, tnfα and ifnγ1 were evaluated. The disruption of the oxidant–antioxidant balance accompanied by altered expressions of apoptotic and immunity related genes were observed in different levels according to the carcinogen applied. Noteworthy, ifnγ expressions decreased in all carcinogen-exposed groups. Our results will provide basic data for further carcinogenesis research in zebrafish models.

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6

Rogers, Adrianne E., and Barbara H. Conner. "Dimethylbenzanthracene-induced mammary tumorigenesis in ethanol-fed rats." Nutrition Research 10, no. 8 (1990): 915–28. http://dx.doi.org/10.1016/s0271-5317(05)80055-7.

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7

LÓPEZ-FONTANA, CONSTANZA MATILDE, CORINA VERÓNICA SASSO, MARÍA EUGENIA MASELLI, et al. "Experimental hypothyroidism increases apoptosis in dimethylbenzanthracene-induced mammary tumors." Oncology Reports 30, no. 4 (2013): 1651–60. http://dx.doi.org/10.3892/or.2013.2648.

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8

Perrin, C., C. Astre, E. Broquerie, B. Saint Aubert, and H. Joyeux. "Lingual fibrosarcoma induced by 7,12-dimethylbenzanthracene in the rat." Journal of Oral Pathology and Medicine 19, no. 1 (1990): 13–15. http://dx.doi.org/10.1111/j.1600-0714.1990.tb00775.x.

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9

Tsambaos, D., F. Sampalis, and H. Berger. "Generalized Cutaneous Hyperpigmentation in Hairless Mice Induced by Topical Dimethylbenzanthracene." Pathobiology 57, no. 6 (1989): 292–99. http://dx.doi.org/10.1159/000163541.

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10

Melhem, MF, HF Gabriel, ED Eskander, and KN Rao. "Cholestyramine promotes 7,12-dimethylbenzanthracene induced mammary cancer in Wistar rats." British Journal of Cancer 56, no. 1 (1987): 45–48. http://dx.doi.org/10.1038/bjc.1987.150.

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11

Jimenez, Ramon E., Kaspar Z'graggen, Werner Hartwig, Fiona Graeme-Cook, Andrew L. Warshaw, and Carlos Fernandez-del Castillo. "Immunohistochemical Characterization of Pancreatic Tumors Induced by Dimethylbenzanthracene in Rats." American Journal of Pathology 154, no. 4 (1999): 1223–29. http://dx.doi.org/10.1016/s0002-9440(10)65374-6.

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12

McMillan, M. D., and A. C. Smillie. "Scanning electron microscopy of dimethylbenzanthracene (DMBA)-treated hamster cheek pouch." Journal of Oral Pathology and Medicine 25, no. 1 (1996): 14–19. http://dx.doi.org/10.1111/j.1600-0714.1996.tb01217.x.

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13

McCabe, Daniel. "Polar Solvents in the Chemoprevention of Dimethylbenzanthracene-Induced Rat Mammary Cancer." Archives of Surgery 121, no. 12 (1986): 1455. http://dx.doi.org/10.1001/archsurg.1986.01400120105017.

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14

Roomi, M. W., N. W. Roomi, T. Kalinovsky, V. Ivanov, M. Rath, and A. Niedzwiecki. "Inhibition of 7,12-dimethylbenzanthracene-induced skin tumors by a nutrient mixture." Medical Oncology 25, no. 3 (2008): 333–40. http://dx.doi.org/10.1007/s12032-008-9041-7.

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15

Hidayati, Titiek, Akrom Akrom, Indrayanti Indrayanti, and Suny Sun. "Thymoquinone Increased Expression of CD4CD25Treg in Sprague-Dawley Rats Induced Dimethylbenzanthracene." Open Access Macedonian Journal of Medical Sciences 9, T4 (2021): 87–91. http://dx.doi.org/10.3889/oamjms.2021.5855.

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BACKGROUND: The carcinogen dimethylbenzanthracene (DMBA) is immunotoxic. Thymoquinone, meanwhile, is known to have antioxidant and anti-inflammatory effects. AIM: This study aims to determine the effect of thymoquinone and tamoxifen on the CD4CD25Treg count in Sprague-Dawley (SD) rats induced by DMBA. METHODS: The 50 SD rats were divided into five groups. Group I (normal control) was given standard drinking and food. Group II was given thymoquinone, Group III was given tamoxifen, Group IV was given DMBA, and Group V was given solvent control. Thymoquinone, tamoxifen, and solvent control administration started 2 weeks before DMBA administration and continued during DMBA induction. In the 3rd week, except for the normal group, all groups were created to be induced with 10 × 20 mg/kg body weight of DMBA for 5 weeks. In the 21st week, surgery and data collection were performed. The hematology profile and CD4CD25Treg number were carried out employing a flow cytometer. The difference in the average number of CD4CD25Treg and blood cells between groups was analyzed with one-way analysis of variance RESULTS: The results revealed that DMBA induction reduced the number of erythrocytes, HB levels, platelet counts, and leukocyte counts (p < 0.05). The administration of thymoquinone and tamoxifen reduced the hematopoiesis effect of DMBA. The thymoquinone and tamoxifen group had a higher number of CD4CD25Treg and leukocytes than the DMBA group (p < 0.05). CONCLUSION: There was no difference in the average CD4CD25Treg, leukocyte count, lymphocyte count, and monocyte count between the thymoquinone and the tamoxifen groups (p > 0.05).

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16

M, Bolandpayeh, Hassanpour-Ezzati M, and Mousavi Z. "Effects of Enoxaparin Emulsion on Dimethylbenzanthracene-induced Breast Cancer in Female Rats." Research in Molecular Medicine 5, no. 4 (2018): 23. http://dx.doi.org/10.18502/rmm.v5i4.3062.

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Introduction: Enoxaparin is an anticoagulant medication. Anticoagulation inhibits tumor cell-mediated release of angiogenic proteins and diminishes angiogenic response. Angiogenesis is an important event in various cancers such as breast cancer. Angiogenesis provide oxygen and nutrients to tumor cells and causes tumor progression. The aim of the present study was to evaluate the anti-angiogenesis effect of an enoxaparin cream on breast cancer induced by dimethylbenzanthracene in rats. Methods: In this experimental in vivo study, 50 Wistar female rats were divided into negative control (vehicle), positive control (cream base), and 3 groups with enoxaparin treatment (40, 60, and 80 mg/ml). After one month of treatment along with breast cancer induction by dimethylbenzanthracene, breast tissue samples were isolated and stained with hematoxylin-eosin, and tumor growth suppression rate was calculated. Tumor size (length and width) was measured using a clipper, and the tumor volume was calculated using the following formula: V = (L × W × W)/2, where V is tumor volume, W is tumor width, L is tumor length. The data were analyzed using one-way ANOVA and Tukey’s post hoc test. Results: Tumor suppression was significantly increased in enoxaparin treatment groups compared to the positive control group (40 mg/ml of enoxaparin treated versus positive control group; P = 0.017, 60 mg/ml of enoxaparin treated versus positive control; P = 0.015, 40 mg/ml of enoxaparin treated versus positive control; P = 0.009, 60 mg/ml of enoxaparin treated versus 40 mg/ml of enoxaparin treated; P = 0.019, and 80 mg/ml of enoxaparin treated versus 40 mg/ml of enoxaparin treated; P = 0.011 in a dose-dependent manner. Conclusion: Enoxaparin inhibits breast cancer in a dose-dependent manner. The application of enoxaparin cream in patients with breast cancer may considerably reduce tumor growth.

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17

Wurz, Gregory T., Karla C. Read, Cristina Marchisano-Karpman, et al. "Ospemifene inhibits the growth of dimethylbenzanthracene-induced mammary tumors in Sencar mice." Journal of Steroid Biochemistry and Molecular Biology 97, no. 3 (2005): 230–40. http://dx.doi.org/10.1016/j.jsbmb.2005.06.027.

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18

Shuler, C. F., R. Mostofi, L. M. Lin, and S. A. Schwartz. "Keratin protein identification in dimethylbenzanthracene-induced hamster cheek-pouch squamous cell carcinomas." Journal of Oral Pathology & Medicine 16, no. 4 (2007): 159–63. http://dx.doi.org/10.1111/j.1600-0714.1987.tb02059.x.

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19

Jenkins, Sarah, Nandini Raghuraman, Isam Eltoum, Mark Carpenter, Jose Russo, and Coral A. Lamartiniere. "Oral Exposure to Bisphenol A Increases Dimethylbenzanthracene-Induced Mammary Cancer in Rats." Environmental Health Perspectives 117, no. 6 (2009): 910–15. http://dx.doi.org/10.1289/ehp.11751.

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20

Akrom, A., Mustofa, and L. H. Nurani. "Ethanolic Extract of Black Cumin Seed Reduced Radical Reactive from Dimethylbenzanthracene Compounds." IOP Conference Series: Earth and Environmental Science 810, no. 1 (2021): 012037. http://dx.doi.org/10.1088/1755-1315/810/1/012037.

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21

FUJII, Taro, and Tadashi INOUE. "Modulating effect of dimethylbenzanthracene on gamma-ray mutagenesis in the soybean test system." Japanese journal of genetics 62, no. 5 (1987): 425–30. http://dx.doi.org/10.1266/jjg.62.425.

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22

Sakai, Toshiharu, Naomi Hosaka, Katsuhiko Ishida, et al. "Effects of Tamsulosin Hydrochloride on 7,12-Dimethylbenzanthracene(DMBA)-induced Mammary Tumor in Rats." Journal of Toxicologic Pathology 10, no. 1 (1997): 39–44. http://dx.doi.org/10.1293/tox.10.39.

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23

Kumar, Sushil, Yogeshwer Shukla, Arun Kumar Prasad, et al. "Protection against 7,12-dimethylbenzanthracene-induced tumour initiation by protein A in mouse skin." Cancer Letters 61, no. 2 (1992): 105–10. http://dx.doi.org/10.1016/0304-3835(92)90167-t.

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24

Oliveira, Krishna Duro de, Gabriela Uliana Avanzo, Marcello Vannucci Tedardi, et al. "Chemical carcinogenesis by DMBA (7,12-dimethylbenzanthracene) in female BALB/c mice: new facts." Brazilian Journal of Veterinary Research and Animal Science 52, no. 2 (2015): 125. http://dx.doi.org/10.11606/issn.1678-4456.v52i2p125-133.

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<p>Hidrocarbonetos policíclicos e aromáticos são carcinógenos usados em modelos experimentais em roedores. Neste estudo, o carcinógeno DMBA (7,12-dimetilbenzantraceno) foi administrado por gavagem, diluído em óleo de milho, para camundongos BALB/c em doses hebdomadárias de 1 mg por animal por 1, 3, 6 ou 9 semanas. Os animais foram pesados e monitorados semanalmente até a morte. Os animais remanescentes foram eutanasiados com a idade de 53 semanas. Na necroscopia, fragmentos representativos das neoplasias foram colhidos e rotineiramente processados para exame histopatológico. De todos os animais que receberam DMBA, 68,57% desenvolveram algum tipo de tumor. Entre os 70 camundongos tratados com diferentes doses de DMBA, 22 (31,43%) desenvolveram neoplasias mamárias. O adenoacantoma foi o tumor mamário mais comumente diagnosticado (18,75%). Pulmões (15,71%), tecido linfoide (11,43%), estômago (7,14%) e pele (2,86%) foram também locais primários de desenvolvimento de neoplasias. Um terço (33,33%) dos camundongos que receberam 1 mg de DMBA desenvolveram neoplasias pulmonares. Portanto, a administração de DMBA foi considerada um modelo eficiente de carcinogênese em camundongos, especialmente para o estudo de neoplasias mamárias, quando a maior dose é utilizada, e de neoplasias pulmonares, quando utilizada a menor dose. Os modelos de carcinogênese química têm sido usados para diversos estudos na pesquisa em câncer, os resultados aqui apresentados mostram novos fatos para um modelo clássico de carcinogênese.</p>

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25

Raza, H., and W. Montague. "Metabolism of benzo(a)pyrene, dimethylbenzanthracene and aflatoxin B1 by camel liver microsomes." Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology 107, no. 3 (1994): 379–86. http://dx.doi.org/10.1016/1367-8280(94)90065-5.

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26

Halliday, Gary M., Lois L. Cavanagh, and H. Konrad Muller. "Immunophenotypic and cell cycle analysis of lymph node cells from dimethylbenzanthracene-treated mice." Virchows Archiv B Cell Pathology Including Molecular Pathology 58, no. 1 (1989): 389–95. http://dx.doi.org/10.1007/bf02890097.

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27

Spinola, P. G., B. Marchetti, and F. Labrie. "64 Adrenal steroids stimulate the growth of dimethylbenzanthracene (DMBA)- induced rat mammary tumors." Journal of Steroid Biochemistry 23 (January 1985): 46. http://dx.doi.org/10.1016/0022-4731(85)90387-5.

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28

Lanzafame, Raymond J., David W. Rogers, John O. Naim, H. Raul Herrera, and J. Raymond Hinshaw. "Effect of hematoporphyrin derivative on estrogen receptors in the dimethylbenzanthracene-mammary tumor model." Lasers in Surgery and Medicine 6, no. 6 (1987): 543–45. http://dx.doi.org/10.1002/lsm.1900060613.

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29

Şengün, Dilara Nur, Gülşah Demirci, and İnci Rana Karaca. "Antioxidant Efficacy of Hypericum Perforatum L. on 7,12-Dimethylbenzanthracene-Applied Rat Tongue Tissues." Current Medical Research 2, no. 1 (2021): 33–37. http://dx.doi.org/10.47482/acmr.2021.12.

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30

Amin, Amr. "Protective Effect of Green Alage Against 7,12-Dimethylbenzanthracene (DMBA)-Induced Breast Cancer in Rats." International Journal of Cancer Research 5, no. 1 (2008): 12–24. http://dx.doi.org/10.3923/ijcr.2009.12.24.

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31

Wurz, Gregory T., Cristina Marchisano-Karpman, and Michael W. DeGregorio. "Ineffectiveness of American Ginseng in the Prevention of Dimethylbenzanthracene-Induced Mammary Tumors in Mice." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 16, no. 6 (2006): 251–60. http://dx.doi.org/10.3727/000000006783981017.

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32

Blankenstein, Marinus A., Jan-Henk Voskuil, J. Fred Verzeijlbergen, Geert J. Ensing, and Jacobus D. M. Herscheid. "Biodistribution of 123I-Labeled 4-hydroxytamoxifen derivatives in rats with dimethylbenzanthracene-induced mammary carcinomas." Nuclear Medicine and Biology 24, no. 8 (1997): 719–22. http://dx.doi.org/10.1016/s0969-8051(97)00111-x.

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33

Holcomb, M., and S. Safe. "Inhibition of 7,12-dimethylbenzanthracene-induced rat mammary tumor growth by 2,3,7,8-tetrachlorodibenzo-p-dioxin." Cancer Letters 82, no. 1 (1994): 43–47. http://dx.doi.org/10.1016/0304-3835(94)90144-9.

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34

Robinson, Simon P., Delinda A. Mauel, and V. Craig Jordan. "Antitumor actions of toremifene in the 7,12-dimethylbenzanthracene (DMBA)-induced rat mammary tumor model." European Journal of Cancer and Clinical Oncology 24, no. 12 (1988): 1817–21. http://dx.doi.org/10.1016/0277-5379(88)90091-0.

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35

Shearer, B. H., M. D. McMillan, and H. F. Jenkinson. "Differential expression of type I cytokeratins in hamster cheek pouch epithelium following treatment with dimethylbenzanthracene." Journal of Oral Pathology and Medicine 26, no. 10 (1997): 470–76. http://dx.doi.org/10.1111/j.1600-0714.1997.tb00018.x.

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36

Kimura, Kenji, Kennichi Satoh, Atsushi Kanno, et al. "Activation of Notch signaling in tumorigenesis of experimental pancreatic cancer induced by dimethylbenzanthracene in mice." Cancer Science 98, no. 2 (2007): 155–62. http://dx.doi.org/10.1111/j.1349-7006.2006.00369.x.

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37

Laher, J. M., and J. A. Barrowman. "Role of the lymphatic system in the transport of absorbed 7,12-dimethylbenzanthracene in the rat." Lipids 22, no. 3 (1987): 152–55. http://dx.doi.org/10.1007/bf02537294.

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38

Hidayati, Titiek, Akrom Akrom, Indrayanti Indrayanti, and Sagiran Sagiran. "Black cumin seed oil increase leucocyte and CD4Thelper number in sprague-dawley rats induced with dimethylbenzanthracene." International Journal of Public Health Science (IJPHS) 8, no. 2 (2019): 238. http://dx.doi.org/10.11591/ijphs.v8i2.17930.

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<p>Cigarette smoke contains 7, 12 dimethylbenzanthracene (DMBA). Metabolic of DMBA is immunosuppressive. Black cumin seed oil (BCSO) is an immunomodulation. The aim of this study was to determine the effect of BCSO on leukocyte, CD4Th and CD4CD25Treg in Sprague-Dawley (SD) mice induced with DMBA. The 96 SD rats were divided into 8 groups of 12. Group I received aquabidest and standard feeding. Groups II, III and IV received BCSO (an equivalent of 6.8, 68 and 136 mg/kg BW / day thymoquinone, respectively). Group V received thymoquinone (50 mg / kg BW / day) and group VI received tamoxifen (60 mg / kg BW). Group VII (DMBA) was induced with DMBA (10x20mg / kg BW for 5 weeks). Group VIII received standard feeding and corn oil treatment. In the third week, all groups began to be induced with DMBA (20 mg/kg BW twice per week for five weeks). Data collection of leukocytes, CD4Th and CD4CD25Treg was performed at week 27th. The mean difference of CD4Th and CD4CD25Treg counts between groups was calculated with one way ANOVA. Results: The administration of BCSO, thymoquinone, and tamoxifen had increased leukocytes and CD4 Th cell count. The CD4Th cell count of the treatment groups was higher than that of the DMBA group (p <0.05). BCSO equivalent doses of 6.8 and 68 mg/kg BW / day thymoquinone showed immunoprotective effects. Conclusion: It can be concluded that the BCSO administration at doses of 6.8 and 68 mg/kg BW / day shows immunoprotective effects due to DMBA induction.</p>

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39

Di Salle, E., T. Zaccheo, R. Rossi, and E. Pesenti. "Chemopreventive effect of the aromatase inactivator exemestane in the dimethylbenzanthracene (DMBA)-induced mammary tumors in rats." Journal of Clinical Oncology 22, no. 14_suppl (2004): 3108. http://dx.doi.org/10.1200/jco.2004.22.14_suppl.3108.

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40

Aldaz, C. Marcelo, Qiao Yin Liao, Michael LaBate, and Dennis A. Johnston. "Medroxyprogesterone acetate accelerates the development and increases the incidence of mouse mammary tumors induced by dimethylbenzanthracene." Carcinogenesis 17, no. 9 (1996): 2069–72. http://dx.doi.org/10.1093/carcin/17.9.2069.

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41

Doyle, C. E., J. M. Mackay, and J. Ashby. "Failure of N-acetylcysteine to protect the mouse bone marrow against the clastogenicity of 7,12-dimethylbenzanthracene." Mutagenesis 8, no. 6 (1993): 583–84. http://dx.doi.org/10.1093/mutage/8.6.583.

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42

Di Salle, E., T. Zaccheo, R. Rossi, and E. Pesenti. "Chemopreventive effect of the aromatase inactivator exemestane in the dimethylbenzanthracene (DMBA)-induced mammary tumors in rats." Journal of Clinical Oncology 22, no. 14_suppl (2004): 3108. http://dx.doi.org/10.1200/jco.2004.22.90140.3108.

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43

Marchetti, Antonio, Juraj Svec, Elena Hlavay, Zuzanna Veselovska, Maura Castagna, and Francesco Squartini. "Morphologic and Antigenic Properties of Mouse Mammary Tumor Virus Produced in a Hormone-Responsive Fashion by C57B1/10 Mammary Tumors of Non-Viral Origin." Tumori Journal 74, no. 3 (1988): 261–67. http://dx.doi.org/10.1177/030089168807400304.

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Bl-MaTU/A1 mouse mammary tumor cells, derived from a C57B1/10 mammary adenocarcinoma induced by dimethylbenzanthracene and mammotropic hormones, express virus particles and proteins related to mouse mammary tumor virus (MMTV). Immunocytochemical analysis by means of monospecific and monoclonal anti-gp52 sera revealed a different localization of the main structural proteins of MMTV in Bl-MaTU/A1 and GR cells (the latter used as a positive virus-producing control). Immunoelectron microscopy of B-type particles budding from the microvilli of dexamethasone-stimulated Bl-MaTU/A1 cells showed remarkably weak reactivity of the viral envelope with anti-gp52-protein A-gold complexes as compared with that of dexamethasone-stimulated GR cells. Since Bl-MaTU/A1-associated MMTV originates from the amplified unit II of endogenous MMTV, which is altered probably within the env gene, the observed antigenic difference in the Bl-MaTU/A1-associated MMTV may be due to altered synthesis of gp52 glycoprotein in these cells.

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44

Giuliani, Michele, Daniela Antuzzi, Carlo Lajolo, Lucia Vitaioli, Daniele Tommasoni, and Roberta Ricci. "Lysosomal glycosidases and their natural substrates in major salivary glands of hamsters treated with 7,12-dimethylbenzanthracene (DMBA)." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 133, no. 1 (2002): 135–42. http://dx.doi.org/10.1016/s1096-4959(02)00120-3.

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45

Murdoch, William J., Edward A. Van Kirk, and Youqing Shen. "Pathogenic Reactions of the Ovarian Surface Epithelium to Ovulation, Dimethylbenzanthracene, and Estrogen Are Negated by Vitamin E." Biology of Reproduction 78, Suppl_1 (2008): 178. http://dx.doi.org/10.1093/biolreprod/78.s1.178a.

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46

Murdoch, William J., Edward A. Van Kirk, and Youqing Shen. "Pathogenic Reactions of the Ovarian Surface Epithelium to Ovulation, Dimethylbenzanthracene, and Estrogen are Negated by Vitamin E." Reproductive Sciences 15, no. 8 (2008): 839–45. http://dx.doi.org/10.1177/1933719108322435.

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47

Halliday, Gary M., Lois L. Cavanagh, and H. Konrad Muller. "Antigen presented in the local lymph node by cells from dimethylbenzanthracene-treated murine epidermis activates suppressor cells." Cellular Immunology 117, no. 2 (1988): 289–302. http://dx.doi.org/10.1016/0008-8749(88)90119-0.

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Singh, Harmeet. "Hepatoprotective Activity of Turmeric and Garlic against 7-12, Dimethylbenzanthracene Induced Liver Damage in Wistar Albino Rats." European Journal of Medicinal Plants 1, no. 4 (2011): 162–70. http://dx.doi.org/10.9734/ejmp/2011/587.

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Duro de Oliveira, Krishna, Marcello Vannucci Tedardi, Bruno Cogliati, and Maria Lúcia Zaidan Dagli. "Higher Incidence of Lung Adenocarcinomas Induced by DMBA in Connexin 43 Heterozygous Knockout Mice." BioMed Research International 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/618475.

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Abstract:

Gap junctions are communicating junctions which are important for tissue homeostasis, and their disruption is involved in carcinogenic processes. This study aimed to verify the influence of deletion of one allele of the Connexin 43 gene on cancer incidence in different organs. The 7, 12-dimethylbenzanthracene (DMBA) carcinogenic model, using hebdomadary doses by gavage of 9 mg per animal, was used to induce tumors in Connexin 43 heterozygous or wild-type mice. The experiment began in the eighth week of the mice life, and all of them were euthanized when reaching inadequate physical condition, or at the end of 53 weeks. No statistical differences occurred for weight gain and cancer survival time (P=0.9853) between heterozygous and wild-type mice. Cx43+/−mice presented significantly higher susceptibility to lung cancer (P=0.0200) which was not evidenced for benign neoplasms (P=0.3449). In addition, incidence of ovarian neoplasms was 2.5-fold higher in Cx43+/−mice, although not statistically significant. Other organs showed a very similar cancer occurrence between Cx43 groups. The experiment strengthens the evidence of the relationship between Connexin 43 deficiency and carcinogenesis.

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Kim, Ji Young, Seung Gee Lee, Jin-Yong Chung, et al. "7,12-Dimethylbenzanthracene induces apoptosis in RL95-2 human endometrial cancer cells: Ligand-selective activation of cytochrome P450 1B1." Toxicology and Applied Pharmacology 260, no. 2 (2012): 124–34. http://dx.doi.org/10.1016/j.taap.2012.01.027.

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