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Metastatic Growth (metastatic + growth)
Selected AbstractsBiology of colorectal liver metastases: A reviewJOURNAL OF SURGICAL ONCOLOGY, Issue 1 2006Nigel C. Bird Abstract Metastatic growth is a selective, non-random process, which in the case of colorectal cancer, frequently occurs in the liver and is the major cause of cancer related death in these patients. This review summarises attempts to find biological and molecular markers of metastasis and their role in establishment of secondary tumours. Recent evidence suggests that liver metastases are phenotypically different to the primary from which they were derived and thus represent a separate disease entity. J. Surg. Oncol. 2006;94:68,80. © 2006 Wiley-Liss, Inc. [source] Prognostic and predictive factors in endocrine tumoursHISTOPATHOLOGY, Issue 6 2006T J Stephenson This review encompasses the diagnostic features of malignancy, the routinely observable prognostic features and the prognostic and predictive features emerging from research techniques in the principal endocrine neoplasms: pancreatic and extrapancreatic endocrine cell tumours, thyroid and parathyroid neoplasia, adrenal cortical neoplasms and adrenal and extra-adrenal paragangliomas. While each endocrine tissue has its own set of diagnostic features for malignancy, and prognostic features once a diagnosis of malignancy has been established, there are a few common themes. For several endocrine neoplasms, definite recognition of malignancy can be difficult and may depend upon frank invasive or metastatic growth at presentation. Endocrine tissues are dynamic, with hyperplastic and regressive phenomena, some of which may mimic malignancy. Even when unequivocal features of malignancy are available for observation, their distribution in tissue may be very focal, necessitating thorough sampling. The accurate documentation of routinely observable histological features interpreted in the light of current literature has not been superseded by special techniques in the statement of diagnosis or prognosis in the vast majority of endocrine neoplasms. [source] Osteopontin promotes gastric cancer metastasis by augmenting cell survival and invasion through Akt-mediated HIF-1, up-regulation and MMP9 activationJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 8b 2009Gang Song Abstract Osteopontin (OPN) is a secreted, integrin-binding matrix phosphorylated glycoprotein. OPN has been shown to facilitate the progression and metastasis of malignancies and has prognostic value in several types of cancer, including gastric cancer. However, the functional mechanism of OPN mediated metastatic growth in gastric cancer remains unclear. Here, using multiple in vitro and in vivo models, we report that OPN strongly promoted the progression and metastasis of gastric cancer. Immunohistochemical staining revealed that OPN, matrix metalloproteinase (MMP)9 and hypoxia-inducible factor (HIF)-1, have statistically significant different expression patterns between well- and poorly differentiated tissue samples (P < 0.05). Correlations existed between OPN and MMP9, and between OPN and HIF-1, (r1= 0.872, p1 < 0.01 and r2= 0.878, p2 < 0.01). Furthermore, OPN dramatically increased colony formation and invasion of gastric cancer cells in vitro and promoted tumour growth and metastasis in vivo. In addition, OPN potently protected gastric cancer cells from serum depletion-induced apoptosis. Further study shows that OPN activated phosphoinositide 3-kinase/Akt survival pathway and up-regulated HIF-1,via binding to ,v,3 integrins in gastric cancer cells. Moreover, we found that OPN could activate MMP9 and up-regulate MMP2. Taken together, our results suggest that the survival-promoting function is crucial for OPN to promote the development of gastric cancer, and HIF-1, and MMP9 may play key roles during this process. Thus, targeting OPN and its related signalling network may develop an effective therapeutic approach for the management of gastric cancer. [source] Eyeing tumorigenesis: Notch signaling and epigenetic silencing of Rb in DrosophilaBIOESSAYS, Issue 7 2006Håkan Axelson Notch signaling plays an essential role in the processes of embryogenesis and cellular differentiation, and it is believed that the oncogenic effects of dysregulated Notch signaling are an anomalous reflection of the normal functions of this cascade. Nonetheless, the cellular events associated with oncogenic Notch signaling have thus far remained elusive. In a recent report, Ferres-Marco et al.1 described how they used the Drosphila eye as a model system and found that elevated Notch signaling in combination with activation of components of the Polycomb complex of transcriptional repressors led to metastatic growth of tumors through epigenetic silencing of the Rbf gene. Rbf is the Drosophila homologue of the retinoblastoma tumor-suppressor gene (Rb), thus it represents a novel link between Notch signaling, tumor growth and metastasis. BioEssays 28: 692,695, 2006. © 2006 Wiley Periodicals, Inc. [source] |