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The common biology of cancer and ageing: Nature, Vol. 448, No. 7155., pp. 767-774.Toren Finkel, Manuel Serrano, Maria Blasco

Source: Nature, Vol. 448, No. 7155., pp. 767-774.
Network analysis of oncogenic Ras activation in cancer.: Science, Vol. 318, No. 5849. (19 October 2007), pp. 463-467.To investigate the unregulated Ras activation associated with cancer, we developed and validated a mathematical model of Ras signaling. The model-based predictions and associated experiments help explain why only one of two classes of activating Ras point mutations with in vitro transformation potential is commonly found in cancers. Model-based analysis of these mutants uncovered a systems-level process that contributes to total Ras activation in cells. This predicted behavior was supported by experimental observations. We also used the model to identify a strategy in which a drug could cause stronger inhibition on the cancerous Ras network than on the wild-type network. This system-level analysis of the oncogenic Ras network provides new insights and potential therapeutic strategies.EC Stites, PC Trampont, Z Ma, KS Ravichandran

Source: Science, Vol. 318, No. 5849. (19 October 2007), pp. 463-467.
Network-based classification of breast cancer metastasis: Mol Syst Biol, Vol. 3 (16 October 2007)Han-Yu Chuang, Eunjung Lee, Yu-Tsueng Liu, Doheon Lee, Trey Ideker

Source: Mol Syst Biol, Vol. 3 (16 October 2007)
Changing pattern of expression of the epidermal growth factor receptor and transforming growth factor alpha in the progression of prostatic neoplasms: Clin Cancer Res, Vol. 1, No. 5. (1 May 1995), pp. 545-550.Hi Scher, A Sarkis, V Reuter, D Cohen, G Netto, D Petrylak, P Lianes, Z Fuks, J Mendelsohn, C Cordon-Cardo

Source: Clin Cancer Res, Vol. 1, No. 5. (1 May 1995), pp. 545-550.
The management of hormone refractory prostate cancer.: Eur Urol, Vol. 29 Suppl 2 (1996), pp. 69-74.Prostate cancer patients deemed unsuitable for curative therapy by means of radical prostatectomy or radiation are offered androgen ablation or suppression therapy, which normally results in an inhibition of prostate cellular growth for a period of 12-18 months. Death of patients from prostate cancer is directly related to the development of clones of cells capable of multiplying and metastasising without androgen stimulation, and to date efforts to suppress these cells have been singularly unsuccessful. There are a number of treatment options available, and these include secondary hormone therapy, growth factor inhibition, chemotherapy, combination therapies and interstitial radiotherapy. The merits and disadvantages of these management approaches are discussed.DW Newling

Source: Eur Urol, Vol. 29 Suppl 2 (1996), pp. 69-74.
Detection and clinical importance of micrometastati c disease.: J Natl Cancer Inst, Vol. 91, No. 13. (7 July 1999), pp. 1113-1124.Meta static relapse in patients with solid tumors is caused by systemic preoperative or perioperative dissemination of tumor cells. The presence of individual tumor cells in bone marrow and in peripheral blood can be detected by immunologic or molecular methods and is being regarded increasingly as a clinically relevant prognostic factor. Because the goal of adjuvant therapy is the eradication of occult micrometastati c tumor cells before metastatic disease becomes clinically evident, the early detection of micrometastase s could identify the patients who are most (and least) likely to benefit from adjuvant therapy. In addition, more sensitive methods for detecting such cells should increase knowledge about the biologic mechanisms of metastasis and improve the diagnosis and treatment of micrometastati c disease. In contrast to solid metastatic tumors, micrometastati c tumor cells are appropriate targets for intravenously applied agents because macromolecules and immunocompeten t effector cells should have access to the tumor cells. Because the majority of micrometastati c tumor cells may be nonproliferati ve (G0 phase), standard cytotoxic chemotherapies aimed at proliferating cells may be less effective, which might explain, in part, the failure of chemotherapy. Thus, adjuvant therapies that are aimed at dividing and quiescent cells, such as antibody-based therapies, are of considerable interest. From a literature search that used the databases MEDLINE(R), CANCERLIT(R), Biosis(R), Embase(R), and SciSearch(R), we discuss the current state of research on minimal residual cancer in patients with epithelial tumors and the diagnostic and clinical implications of these findings.K Pantel, RJ Cote, O Fodstad

Source: J Natl Cancer Inst, Vol. 91, No. 13. (7 July 1999), pp. 1113-1124.
Natural history of progression after PSA elevation following radical prostatectomy.: JAMA, Vol. 281, No. 17. (5 May 1999), pp. 1591-1597.CONT EXT: In men who develop an elevated serum prostate-speci fic antigen level (PSA) after having undergone a radical prostatectomy, the natural history of progression to distant metastases and death due to prostate cancer is unknown. OBJECTIVE: To characterize the time course of disease progression in men with biochemical recurrence after radical prostatectomy. DESIGN: A retrospective review of a large surgical series with median (SD) follow-up of 5.3 (3.7) years (range, 0.5-15 years) between April 1982 and April 1997. SETTING: An urban academic tertiary referral institution. PATIENTS: A total of 1997 men undergoing radical prostatectomy, by a single surgeon, for clinically localized prostate cancer. None received neoadjuvant therapy, and none had received adjuvant hormonal therapy prior to documented distant metastases. MAIN OUTCOME MEASURES: After surgery, men were followed up with PSA assays and digital rectal examinations every 3 months for the first year, semiannually for the second year, and annually thereafter. A detectable serum PSA level of at least 0.2 ng/mL was evidence of biochemical recurrence. Distant metastases were diagnosed by radionuclide bone scan, chest radiograph, or other body imaging, which was performed at the time of biochemical recurrence and annually thereafter. RESULTS: The actuarial metastasis-fre e survival for all 1997 men was 82% (95% confidence interval, 76%-88%) at 15 years after surgery. Of the 1997 men, 315 (15%) developed biochemical PSA level elevation. Eleven of these underwent early hormone therapy after the recurrence and are not included in the study. Of the remaining 304 men, 103 (34%) developed metastatic disease within the study period. The median actuarial time to metastases was 8 years from the time of PSA level elevation. In survival analysis, time to biochemical progression (P

Source: JAMA, Vol. 281, No. 17. (5 May 1999), pp. 1591-1597.
Novel expressed sequences identified in a model of androgen independent prostate cancer: BMC Genomics, Vol. 8 (26 January 2007), 32.Steven Quayle, Heidi Hare, Allen Delaney, Martin Hirst, Dorothy Hwang, Jacqueline Schein, Steven Jones, Marco Marra, Marianne Sadar

Source: BMC Genomics, Vol. 8 (26 January 2007), 32.
Differential expression of CD10 in prostate cancer and its clinical implication: BMC Urology, Vol. 7 (02 March 2007), 3.Marc Dall'era, Lawrence True, Andrew Siegel, Michael Porter, Tracy Sherertz, Alvin Liu

Source: BMC Urology, Vol. 7 (02 March 2007), 3.
Prostate cancer: therapeutic, diagnostic, and basic studies.: Lab Invest, Vol. 67, No. 5. (November 1992), pp. 540-552.ME Stearns, T McGarvey

Source: Lab Invest, Vol. 67, No. 5. (November 1992), pp. 540-552.

If you would like to find additional social bookmark based links on the topic of cancer we recommend the Open Tag Directory > Cancer. If you would like to find related tags we recommend Tag Patterns > Cancer.