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Cancer Related Death (cancer + relate_death)
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] Evidence for downregulation of calcium signaling proteins in advanced mouse adenocarcinomaTHE PROSTATE, Issue 2 2005Viola C. Ruddat Abstract BACKGROUND Prostate cancer (PCa) is the leading cancer related death in America. Gleason grading is currently the predominant method for prediction, with only few biomarkers available. More biomarkers, especially as they relate to cancer progression are desirable. METHODS The abundance of several important proteins in prostate tissue was compared between wild-type mouse dorsal prostate and well-differentiated transgenic adenocarcinoma mouse prostate (TRAMP) mouse dorsal prostates, and between wild-type mouse dorsal prostate and poorly-differentiated TRAMP mouse tumor tissue. 2DIGE method in conjunction with MALDI-ToF and Western blots was used to determine differential expression. RESULTS In TRAMP dorsal prostates with well-differentiated adenocarcinoma, there were few significant changes in the protein abundances compared to wild-type dorsal prostates, with the exception of increases in proliferating cell nuclear antigen (PCNA) and beta tubulin, two proteins implicated in cell proliferation, and a more than 2-fold increase in Hsp60, a protein involved in the suppression of apoptosis. In the poorly-differentiated tumors, the changes in protein abundance were substantial. While some of those changes could be related to the disappearance of stromal tissue or the appearance of epithelial tissue, other changes in protein abundance were more significant to the cancer development itself. Most notable was the overall decrease in calcium homeostasis proteins with a 10-fold decrease in calreticulin and Hsp70 and a 40-fold decrease in creatine kinase bb in the cancerous tissue. CONCLUSIONS Proteomics of TRAMP mice provide an excellent method to observe changes in protein abundance, revealing changes in pathways during cancer progression. © 2005 Wiley-Liss, Inc. [source] Regulation of signaling pathways involved in lupeol induced inhibition of proliferation and induction of apoptosis in human prostate cancer cellsMOLECULAR CARCINOGENESIS, Issue 12 2008Sahdeo Prasad Abstract Prostate cancer (PCa) is the most frequently diagnosed noncutaneous cancer and the leading cause of cancer related deaths in men in the United States and many other Asian countries. Dietary factors are considered as a strategic agent to control the risk of PCa. Lupeol, a triterpene, present in fruits and medicinal plants, has been shown to possess many pharmacological properties including anticancer effects. Here, effect of lupeol on cell proliferation and cell death was evaluated using human PCa cells, PC-3. In MTT assay, lupeol inhibited the cell proliferation (12,71%) in dose (50,800 µM) and time dependent manner. Flow-cytometric analysis of cell-cycle revealed that an antiproliferative effect of lupeol (400,600 µM) is associated with an increase in G2/M-phase arrest (34,58%). RT-PCR analysis showed that lupeol-induced G2/M-phase arrest was mediated through the inhibition of cyclin regulated signaling pathway. Lupeol inhibited the expression of cyclin B, cdc25C, and plk1 but induced the expression of 14-3-3, genes. However no changes were observed in the expression of gadd45, p21waf1/cip1 and cdc2 genes. Results of western blot showed that lupeol regulates the phosphorylation of cdc2 (Tyr15) and cdc25C (Ser198). Further, on increase of lupeol exposure to PC-3 cells an induction of apoptosis was recorded, which was associated with upregulation of bax, caspase-3, -9, and apaf1 genes and down regulation of antiapoptotic bcl-2 gene. The role of caspase-induced apoptosis was confirmed by increase in reactive oxygen species, loss of mitochondrial membrane potential followed by DNA fragmentation. Thus, our study suggests that lupeol possess novel antiproliferative and apoptotic potential against PCa. © 2008 Wiley-Liss, Inc. [source] Survival in surgically treated, nodal positive prostate cancer patients is predicted by histopathological characteristics of the primary tumor and its lymph node metastases ,THE PROSTATE, Issue 4 2009Achim Fleischmann Abstract BACKGROUND Histopathological risk factors for survival stratification of surgically treated nodal positive prostate cancer patients are poorly defined as reflected by only one category for nodal metastases. METHODS We evaluated biochemical recurrence-free survival (RFS), disease-specific survival (DSS), and overall survival (OS) in 102 nodal positive, hormone treatment-naïve prostate cancer patients (median age: 65 years, range: 45,75 years; median follow-up 7.7 years, range: 1.0,15.9 years) who underwent radical prostatectomy and standardized extended lymphadenectomy. RESULTS A significant stratification was possible, with the Gleason score of the primary and virtually all nodal parameters favoring patients with better differentiated primaries and metastases, lower nodal tumor burden, and without extranodal extension of metastases. In multivariate analyses, diameter of the largest metastasis (,10 mm vs. >10 mm) was the strongest independent predictor for RFS (P,<,0.001), DSS (P,<,0.001), and OS (P,<,0.001) with a more than quadrupled relative risk of cancer related deaths for patients with larger metastases (Hazard ratio: 4.2, Confidence interval: 2.0,8.9; 5-year RFS/DSS/OS: 18%/57%/54%). The highest 5-year survival rates were seen in patients with micrometastases only (RFS/DSS/OS: 47%/94%/94%). CONCLUSION The TNM classification's current allocation of only one category for nodal metastases in prostate cancers is unsatisfactory since subgroups with significantly different prognoses can be identified. The diameter of the patient's largest metastasis (,10 mm vs. >10 mm) should be used for substaging because of its independent prognostic value. The substage "micrometastasis only" is also useful in nodal positive prostate cancer since it designates the subgroup with the most favorable outcome. Prostate 69:352,362, 2009. © 2008 Wiley-Liss, Inc. [source] | ||||||||||