DTD.CancerLect.LodishChapt25

DTD.CancerLect.LodishChapt25 - Harvey Lodish Arnold Berk...

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1 Molecular Cell Biology Sixth Edition Harvey Lodish • Arnold Berk •Chris A. Kaiser • Monty Krieger • Matthew P. Scott • Anthony Bretscher • Hidde Ploegh • Paul Matsudaira Chapter 25: Cancer Sections 25.1 - 25.5, Osteopontin D.T. Denhardt Dec. 10, 2009 Section 25.1: Tumor Cells and the Onset of Cancer Cancer causes about 20% of deaths in the US each year. Cancers arise as the result of an interplay between your genetic heritage, the environment, luck, and your choice of lifestyle and occupation. Older therapies included radiation and chemotherapy; newer therapies entail targeting specific tumors with appropriate drugs, including monoclonal antibodies. Inhibitors (angiostatin, endostatin) of factors (VEGF, FGF, TGF α ) inducing angiogenesis hold great promise. Benign tumors do not spread – warts for example. Malignant tumors (cancers) invade and spread throughout the body (metastasis). Carcinomas – arise from endoderm (gut) or ectoderm (skin, neural epithelium). Sarcomas – arise from mesodermal tissues (muscle, blood, connective tissue). Cancers arise more readily in tissues that contain proliferating (stem) cells. Fig. 25-1: Blood supply necessary for the tumor to grow and spread. It t i d Necessary for continued proliferation. Necessary for continued proliferation. Six characteristics of metastatic (malignant) tumor cells Benign tumor cells are not metastatic. Intravasation and extravasation. Requires protease activity to penetrate basement membranes and the extracellular matrix. Otherwise the tumor cells will die, Otherwise the tumor will not grow. Inhibition of one or more of these characteristics can inhibit cancer progression. Initial steps in metastasis: Proliferation of the primary tumor; invasion of the blood or lymphatic circulation (intravasation).
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2 25-4: Possible origins of cancer stem cells. The extent to which pre-existing normal stem cells are the source of cancer cells remains unclear. Much evidence indicates that multiple mutations are usually required to produce a malignant cell. Some of these mutations may mimic what is found in a normal stem cells. Bottom line: A diverse population of cells make up a tumor. “Niche” refers to the microenvironment in which the stem cell resides. It is crucial to maintaining the stem cell phenotype. Fig. 25-6: Experimental evidence for the presence of oncogenes in tumor cells. Oncogenes are by definition cancer-promoting genes that arise as the result of a mutation in, or abnormal expression of, a normal gene (“proto-oncogene”). 3T3 cells are an immortal mouse fibroblast line. “Transformed” tumor cells are able to continue proliferating; the immortal cells stop proliferating (enter Go) as the result of contact inhibition. Transfection of cells with DNA is a very inefficient
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This note was uploaded on 09/02/2010 for the course BME 314 taught by Professor Frey during the Spring '08 term at University of Texas at Austin.

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DTD.CancerLect.LodishChapt25 - Harvey Lodish Arnold Berk...

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