ジメチルベンズアントラセン
- 関
- [[7,12-dimethylbenz[a]anthracene]]、9,10-dimethyl-1,2-benzanthracene、dimethyl benzanthracene
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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2015/09/20 18:08:39」(JST)
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DMBA may refer to:
- 2,4-Dimethoxybenzaldehyde, a reagent used to specifically quantify phlorotannins
- para-Dimethylaminobenzaldehyde, a reagent used in Ehrlich's reagent for determination of hydrazine and Kovac's reagent for microbiology's indole test
- 7,12-Dimethylbenz(a)anthracene, an immunosuppressor and a powerful organ-specific laboratory carcinogen
- 1,3-Dimethylbutylamine, an unapproved stimulant used as an adulterant in some dietary supplements
English Journal
- Loss of PPARγ expression in mammary secretory epithelial cells creates a pro-breast tumorigenic environment.
- Apostoli AJ, Skelhorne-Gross GE, Rubino RE, Peterson NT, Di Lena MA, Schneider MM, Sengupta SK, Nicol CJ.Author information Department of Pathology and Molecular Medicine, Queen's University, Kingston, ON, Canada.AbstractBreast cancer is the leading cause of new cancer diagnoses among women. Using peroxisome proliferator-activated receptor (PPAR)γ((+/-)) mice, we showed normal expression of PPARγ was critical to stop 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast tumorigenesis. PPARγ is expressed in many breast cell types including mammary secretory epithelial (MSE) cells. MSEs proliferate as required during pregnancy, and undergo apoptosis or reversible transdifferentiation during involution once lactation is complete. Thus, MSE-specific loss of PPARγ was hypothesized to enhance DMBA-mediated breast tumorigenesis. To test this, MSE cell-specific PPARγ knockout (PPARγ-MSE KO) and control (PPARγ-WT) mice were generated, mated and allowed to nurse for three days. One week after involution, dams were treated with DMBA to initiate breast tumors, and randomized on week 7 to continue receiving a normal chow diet (DMBA Only: PPARγ-WT, n = 15; PPARγ-MSE KO, n = 25) or one supplemented with a PPARγ activating drug (DMBA + ROSI: PPARγ-WT, n = 17; PPARγ-MSE KO, n = 24), and monitored for changes in breast tumor outcomes. PPARγ-MSE KOs had significantly lower overall survival and decreased mammary tumor latency as compared to PPARγ-WT controls. PPARγ activation significantly reduced DMBA-mediated malignant mammary tumor volumes irrespective of genotype. MSE-specific PPARγ loss resulted in decreased mammary gland expression of PTEN and Bax, increased superoxide anion production, and elevated serum eotaxin and RANTES, creating a protumorigenic environment. Moreover, PPARγ activation in MSEs delayed mammary tumor growth in part by down-regulating Cox-1, Cox-2 and cyclin D1. Collectively, these studies highlight a protective role of MSE-specific PPARγ during breast tumorigenesis, and support a novel chemotherapeutic role of PPARγ activation in breast cancer.
- International journal of cancer. Journal international du cancer.Int J Cancer.2014 Mar 1;134(5):1055-66. doi: 10.1002/ijc.28432. Epub 2013 Sep 19.
- Breast cancer is the leading cause of new cancer diagnoses among women. Using peroxisome proliferator-activated receptor (PPAR)γ((+/-)) mice, we showed normal expression of PPARγ was critical to stop 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast tumorigenesis. PPARγ is expressed in many br
- PMID 23934545
- The many faces of calmodulin in cell proliferation, programmed cell death, autophagy, and cancer.
- Berchtold MW1, Villalobo A2.Author information 1Department of Biology, University of Copenhagen, Copenhagen Biocenter 4-2-09 Ole Maaløes Vej 5, DK-2200 Copenhagen N, Denmark. Electronic address: mabe@my.molbio.ku.dk.2Instituto de Investigaciones Biomédicas, Department of Cancer Biology, Consejo Superior de Investigaciones Científicas and Universidad Autónoma de Madrid, c/Arturo Duperier 4, E-28029 Madrid, Spain. Electronic address: antonio.villalobo@iib.uam.es.AbstractCalmodulin (CaM) is a ubiquitous Ca(2+) receptor protein mediating a large number of signaling processes in all eukaryotic cells. CaM plays a central role in regulating a myriad of cellular functions via interaction with multiple target proteins. This review focuses on the action of CaM and CaM-dependent signaling systems in the control of vertebrate cell proliferation, programmed cell death and autophagy. The significance of CaM and interconnected CaM-regulated systems for the physiology of cancer cells including tumor stem cells, and processes required for tumor progression such as growth, tumor-associated angiogenesis and metastasis are highlighted. Furthermore, the potential targeting of CaM-dependent signaling processes for therapeutic use is discussed.
- Biochimica et biophysica acta.Biochim Biophys Acta.2014 Feb;1843(2):398-435. doi: 10.1016/j.bbamcr.2013.10.021. Epub 2013 Nov 2.
- Calmodulin (CaM) is a ubiquitous Ca(2+) receptor protein mediating a large number of signaling processes in all eukaryotic cells. CaM plays a central role in regulating a myriad of cellular functions via interaction with multiple target proteins. This review focuses on the action of CaM and CaM-depe
- PMID 24188867
- Evaluation of the effects of ellagic acid (EA) on 7,12-dimethylbenz(α) anthracene (DMBA) induced micronuclei in mammalian cells in vitro and in vivo.
- Grossi MR, Berni A, Pepe G, Filippi S, Meschini R, Papeschi C, Natarajan AT, Palitti F.Author information Department of Ecological and Biological Sciences, Università degli Studi della Tuscia, Largo dell'Università, snc, I-01100 Viterbo, Italy.AbstractWe evaluated the protective effects of EA, a promising dietary constituent against degenerative diseases, on the clastogenic action of the model carcinogen DMBA in vitro on human hepatoma cells (HepG2) and in vivo on bone marrow of mice, using the frequencies of induced micronuclei as the end point. Pre-, post- and simultaneous treatments with EA and the carcinogen were carried out in vitro. Simultaneous treatment with EA caused a statistically significant increase of DMBA induced MN, suggesting a direct interaction between the two agents. No significant reduction in DMBA induced MN was found by pre- or post treatment with EA. Similar effects were observed in the toxicity assay. In in vivo experiments, EA pre-treatment did not affect the frequencies of MN in PCEs of bone marrow induced by DMBA. A good correlation was found between in vitro and in vivo experiments. Our results did not reveal any clear indication on the efficacy of EA on the induction of micronuclei by DMBA. EA by itself did not show any harmful effects.
- Toxicology letters.Toxicol Lett.2014 Jan 13;224(2):240-5. doi: 10.1016/j.toxlet.2013.10.012. Epub 2013 Nov 1.
- We evaluated the protective effects of EA, a promising dietary constituent against degenerative diseases, on the clastogenic action of the model carcinogen DMBA in vitro on human hepatoma cells (HepG2) and in vivo on bone marrow of mice, using the frequencies of induced micronuclei as the end point.
- PMID 24188931
Japanese Journal
- Identification of Stmm3 locus Conferring Resistance to Late-stage Chemically Induced Skin Papillomas on Mouse Chromosome 4 by Congenic Mapping and Allele-specific Alteration Analysis
- SAITO Megumi,OKUMURA Kazuhiro,MIURA Ikuo [他]
- Experimental animals 63(3), 339-348, 2014-07
- NAID 40020130193
- Isoflavone intake inhibits the development of 7,12-dimethylbenz(a)anthracene(DMBA)-induced mammary tumors in normal and ovariectomized rats
- Ma Defu,Zhang Yumei,Yang Titi,Xue Yong,Wang Peiyu
- Journal of Clinical Biochemistry and Nutrition 54(1), 31-38, 2014
- To determine the associations between isoflavone (49.72% genistin, 5.32% daidzin, 34.54% glycitin) and breast cancer risk, 150 rats were given 5 mg 7,12-dimethylbenz(a)anthracene and half of them were …
- NAID 130004466735
- The correlations between BRCA1 defect and environmental factors in the risk of breast cancer
- Kang Hyo Jin,Hong Young Bin,Yi Yong Weon,Cho Chi-Heum,Wang Antai,Bae Insoo
- The Journal of Toxicological Sciences 38(3), 355-361, 2013
- … In addition, TCDD, DMBA, 3MC, and BPA enhanced the BaP-induced ROS production. … In this setting, the addition of paraquat, TCDD, DMBA, 2OHE2 or 4OHE2 significantly augmented ROS generation in BRCA1-KD MCF10A cells. … In addition, TCDD and DMBA significantly increased BaP-DNA adduct formation in the absence of BRCA1. …
- NAID 130004447052
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- 英
- dimethyl benzanthracene、[[7,12-dimethylbenz[a]anthracene]]、DMBA
- 関
- 7,12-ジメチルベンズアントラセン、9,10-ジメチル-1,2-ベンズアントラセン
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ジメチルベンズアントラセン
- 関
- [[7,12-dimethylbenz[a]anthracene]]、DMBA
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- 同
- 5, 6-dimethylbenzimidazole
- 同
- 5, 6-dimethylbenzimidazole