@article {204,
	title = {Hematein, a casein kinase II inhibitor, inhibits lung cancer tumor growth in a murine xenograft model.},
	journal = {Int J Oncol},
	volume = {43},
	year = {2013},
	month = {2013 Nov},
	pages = {1517-22},
	abstract = {<p>Casein kinase II (CK2) inhibitors suppress cancer cell growth. In this study, we examined the inhibitory effects of a novel CK2 inhibitor, hematein, on tumor growth in a murine xenograft model. We found that in lung cancer cells, hematein inhibited cancer cell growth, Akt/PKB Ser129 phosphorylation, the Wnt/TCF pathway and increased apoptosis. In a murine xenograft model of lung cancer, hematein inhibited tumor growth without significant toxicity to the mice tested. Molecular docking showed that hematein binds to CK2α in durable binding sites. Collectively, our results suggest that hematein is an allosteric inhibitor of protein kinase CK2 and has antitumor activity to lung cancer.</p>},
	keywords = {Animals, Apoptosis, Blotting, Casein Kinase II, Cultured, Enzyme Inhibitors, Female, Hematoxylin, Humans, Immunoenzyme Techniques, Inbred BALB C, Lung Neoplasms, Mice, Phosphorylation, Proto-Oncogene Proteins c-akt, T Cell Transcription Factor 1, Tumor Cells, Western, Wnt Proteins, Xenograft Model Antitumor Assays},
	issn = {1791-2423},
	doi = {10.3892/ijo.2013.2087},
	author = {Hung, Ming-Szu and Xu, Zhidong and Chen, Yu and Smith, Emmanuel and Jiang-Hua Mao and Hsieh, David and Lin, Yu-Ching and Yang, Cheng-Ta and Jablons, David M and You, Liang}
}
@article {177,
	title = {Radiation acts on the microenvironment to affect breast carcinogenesis by distinct mechanisms that decrease cancer latency and affect tumor type.},
	journal = {Cancer Cell},
	volume = {19},
	year = {2011},
	month = {2011 May 17},
	pages = {640-51},
	abstract = {<p>Tissue microenvironment is an important determinant of carcinogenesis. We demonstrate that ionizing radiation, a known carcinogen, affects cancer frequency and characteristics by acting on the microenvironment. Using a mammary chimera model in which an irradiated host is transplanted with oncogenic Trp53 null epithelium, we show accelerated development of aggressive tumors whose molecular signatures were distinct from tumors arising in nonirradiated hosts. Molecular and genetic approaches show that TGFβ mediated tumor acceleration. Tumor molecular signatures implicated TGFβ, and genetically reducing TGFβ abrogated the effect on latency. Surprisingly, tumors from irradiated hosts were predominantly estrogen receptor negative. This effect was TGFβ independent and linked to mammary stem cell activity. Thus, the irradiated microenvironment affects latency and clinically relevant features of cancer through distinct and unexpected mechanisms.</p>},
	keywords = {Animal, Animals, Breast Neoplasms, Cell Transformation, Dose-Response Relationship, Epithelial Cells, Estrogen, Female, Gene Expression Profiling, Gene Expression Regulation, Gene Regulatory Networks, Inbred BALB C, Knockout, Mammary Glands, Mice, Neoplasms, Neoplastic, Radiation, Radiation Chimera, Radiation-Induced, Reaction Time, Receptors, Time Factors, Transforming Growth Factor beta1, Tumor Burden, Tumor Microenvironment, Tumor Suppressor Protein p53, Whole-Body Irradiation},
	issn = {1878-3686},
	doi = {10.1016/j.ccr.2011.03.011},
	author = {Nguyen, David H and Oketch-Rabah, Hellen A and Illa-Bochaca, Irineu and Geyer, Felipe C and Reis-Filho, Jorge S and Jiang-Hua Mao and Ravani, Shraddha A and Zavadil, Jiri and Borowsky, Alexander D and Jerry, D Joseph and Dunphy, Karen A and Seo, Jae Hong and Haslam, Sandra and Medina, Daniel and Barcellos-Hoff, Mary Helen}
}
