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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From experimental and epidemiological evidence, radiation-induced cancers appear to arise as multistage, monoclonal growths, which are elicited through various mechanisms, depending on the neoplasm in question and the conditions of exposure. At the molecular level, the process of carcinogenesis may involve the activation of oncogenes and/or the inactivation or loss of anti-oncogenes, through chromosomal rearrangements, point mutations, and other effects of radiation on DNA. In contrast to these mechanisms of carcinogenesis, which result from the absorption of radiation by the tumor-forming cells themselves, abscopal effects resulting from irradiation of other cells may contribute to carcinogenesis under certain conditions, e.g. in the induction of tumors of endocrine target cells through radiation-induced disturbances of hormonal balance. Effects of the latter type, which require the killing of substantial numbers of cells, are not elicited at low doses, thus contrasting with effects of the former type, which may be presumed to have no thresholds. Because radiation carcinogenesis may be mediated through a diversity of effects, the relationship between incidence and dose can vary accordingly. The relationship between the incidence of radiation-induced tumors and the time elapsing after irradiation also varies, depending on the type of tumor in question, species, age at irradiation, exposure conditions, and other factors. Although the variations with dose and time are consistent with multistage models of tumor initiation, tumor promotion, and tumor progression, the precise nature of the successive steps that are involved remains to be determined. The tendency for the tumors to resemble their spontaneous counterparts in age-distribution points to interactions between radiation and other carcinogenic risk factors which are as yet poorly understood. Also poorly understood are species- and organ-differences in susceptibility to radiation carcinogenesis, which bear no consistent relationship to corresponding 'spontaneous' cancer rates.
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PMID:Evolving perspectives on the biology and mechanisms of carcinogenesis. 373 8

Interaction between cell and extracellular matrix (ECM) plays a crucial role in tumor invasiveness and metastasis. Using an immortalized human bronchial epithelial (BEP2D) cell model, we showed previously that expression of a list of genes including Betaig-h3 (induced by transforming growth factor-beta), DCC (deleted in colorectal cancer), p21(cipl), c-fos, Heat shock protein (HSP27) and cytokeratin 14 were differentially expressed in several independently generated, radiation-induced tumor cell lines (TL1-TL5) relative to parental BEP2D cells. Our previous data further demonstrated that loss of tumor suppressor gene(s) as a likely mechanism of radiation carcinogenesis. In the present study, we chose Betaig-h3 and DCC that were downregulated in tumorigenic cells for further study. Restored expression of Betaig-h3 gene, not DCC gene, by transfecting cDNA into tumor cells resulted in a significant reduction in tumor growth. While integrin receptor alpha 5 beta 1 was overexpressed in tumor cells, its expression was corrected to the level found in control BEP2D cells after Betaig-h3 transfection. These data suggest that Betaig-h3 gene is involved in tumor progression by regulating integrin alpha 5 beta 1 receptor. Furthermore, exogenous TGF- beta 1 induced expression of Betaig-h3 gene and inhibited the growth of both control and tumorigenic BEP2D cells. Therefore, downregulation of Betaig-h3 gene may results from the decreased expression of upstream mediators such as TGF-beta. The findings provide strong evidence that the Betaig-h3 gene has tumor suppressor function in radiation-induced tumorigenic human bronchial epithelial cells and suggest a potential target for interventional therapy.
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PMID:Tumor suppressor function of Betaig-h3 gene in radiation carcinogenesis. 1297 13

Ionizing radiation is a well-known carcinogen for various human tissues and a complete carcinogen that is able to initiate and promote neoplastic progression. Studies of radiation-induced mouse thymic lymphomas, one of the classic models in radiation carcinogenesis, demonstrated that even the unirradiated thymus is capable of developing into full malignancy when transplanted into the kidney capsule or subcutaneous tissue of irradiated mice. This suggests that radiation targets tissues other than thymocytes to allow expansion of cells with tumorigenic potential in the thymus. The idea is regarded as the 'indirect mechanism' for tumor development. This paper reviews the indirect mechanism and genes affecting the development of thymic lymphomas that we have analyzed. One is the Bcl11b/Rit1 tumor suppressor gene and the other is Mtf-1 gene affecting tumor susceptibility.
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PMID:Radiation carcinogenesis in mouse thymic lymphomas. 1682 96