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Neoplasia. 6:603-10. Yoeli-Lerner, M., G.K. Yiu, I. Rabinovitz, P. Erhardt, S. Jauliac, and A. Toker. 2005. Akt blocks breast cancer cell motility and invasion through the transcription factor NFAT.
cancer.gov/cancertopics/factsheet/detection/Pap-HPV-testing World Health Organization. (2013). Human papillomavirus (HPV) and cervical cancer. Retrieved fromhttp://www.who.int/mediacentre/factsheets/fs380/en/
We imply that putative CSC subset for HCT116 cell line is CD44+/CD24-/CD133- (4,1% of all cells) and for HT29 cells – CD24+/CD44-/CD133- (4,9% of all cells). Keywords: tumor heterogeneity, colon cancer, cancer stem cells, HCT116, HT29 Introduction The concept of tumor heterogeneity being related to the course of the disease and clinical outcome in cancer patients draws additional attention in the era of personalized medicine (1). Current cancer treatment strategies are based on the site of origin of the primary tumor. However, it was shown that tumors developed from distinct cell types differ in their prognosis and response to cytotoxic therapies (2... ... middle of paper ... ...ozzi E, Biffoni M, Todaro M, Peschle C, et al. Identification and expansion of human colon-cancer-initiating cells.
One of the recent developments in the research behind oncogenesis and its relationship to cancer is the theory of “oncogenic addiction”. This theory explains the phenomena of “a tumor cell seemingly exhibiting dependence on a single oncogenic pathway or protein for its sustained proliferation and/or survival” (Sharma & Settleman 2007). These findings suggest that there may be a way to “switch off the crucial pathway of dependence”, which in theory should negatively affect or inhibit the cancer, “while sparing normal cells that are not similarly addicted” (Sharma & Settleman 2007). This has been established with the ability to inactivate “counterparts of oncogenic proteins in normal tissues” and see that there is toleration without “obvious consequences” (Sharma & Settleman 2007). This is the concept of “addiction” in cancer, and the dependence on particular genes to activate prolifer... ... middle of paper ... ...need to be developed to begin this study, we can infer from past research the steps in which determination of these relationships could be done.
6. Maelandsmo GM, Flørenes VA, Hovig E, Oyjord T, Engebraaten O, Holm R, Børresen AL, Fodstad O. (1996). Involvement of the pRb/p16/cdk4/cyclin D1 pathway in the tumorigenesis of sporadic malignant melanomas. Br J Cancer.
Reference(s): Hopkins, J. (2014, March 03). Leukemia. Retrieved from http://www.hopkinsmedicine.org/kimmel_cancer_center/types_cancer/leukemias.html Clinic, M. (2013, October 03). Treatments and drugs.
Leukemia may be acute or chronic, depending on the rate of progression of the disease. The exact cause is unknown, but some risk factors include exposure to toxic chemicals, radiation, chemotherapy and smoking. The goals of treatment in leukemia are to kill the cancer cells, to increase the supply of normal blood cells, and to boost one's immunity to cancer. Chemotherapy and high dose radiation therapy are often done to destroy cancer cells. A stem cell transplant may be done to increase the number of new cells, which will develop into normal blood cells.