Relevant bibliographies by topics / Dimethylbenzanthracene

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  1. Journal articles

Academic literature on the topic 'Dimethylbenzanthracene'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Dimethylbenzanthracene"

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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Abstract:
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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