Transcript Slide 1
Exam Review: March 9, 2010 50110Xm1Review.PPt Updated: March 8, 2010 Intro501: Introduction to Cancer Biology and to the Course (501Intro.ppt) Banding pattern of normal metaphase human chromosomes Figure 1.11a The Biology of Cancer (© Garland Science 2007) Fluorescent in situ hybridization (FISH) of normal metaphase human chromosomes using chromosome specific DNA probes with different fluorescent dyes Figure 1.11b The Biology of Cancer (© Garland Science 2007) Aneuploid karyotype of human breast cancer cell. Note “scrambling” of colors demonstrating chromosomal reciprocal translocations Figure 1.11c The Biology of Cancer (© Garland Science 2007) Intrachromosonal inversion by M-band fluorescent in situ hybridization( mFISH) Figure 1.11d The Biology of Cancer (© Garland Science 2007) Cytoskeleton: Actin microfilaments Microtubules Intermediate filaments Figure 1.14a The Biology of Cancer (© Garland Science 2007) Intermediate Filaments of epithelial cell (keratin) in green Plasma membrane in blue Figure 1.14b The Biology of Cancer (© Garland Science 2007) 3T3 Mouse Fibroblast attached to fibronectin extracellular matrix by integrin receptors Figure 1.14d The Biology of Cancer (© Garland Science 2007) Clinical Presentation of Cancers (Clinical.ppt) Please be sure to send in your name under “Send User Data” as Usual: Then respond: I am here for this Exam Review. 1. 2. 3. Yes No Not Sure Figure 16.1b The Biology of Cancer (© Garland Science 2007) Figure 16.1a The Biology of Cancer (© Garland Science 2007) Figure 16.45a The Biology of Cancer (© Garland Science 2007) Incidence of Various Kinds of Cancers in Men and Women as a Function of Age See Figure 11.1, Cancer incidence at various ages for men and women. p. 400. Weinberg. Note maximum incidence per 100,000 population at about age 70, then drop off after that age. Serious incidence begins around age 35 except for breast cancer which can have an earlier onset depending on genetics. Figure 16.45c The Biology of Cancer (© Garland Science 2007) Figure 11.8b The Biology of Cancer (© Garland Science 2007) Figure 14.50a The Biology of Cancer (© Garland Science 2007) Figure 14.50b The Biology of Cancer (© Garland Science 2007) Epidemiology of Cancers (Epidemio.ppt) Incidence of Burkitt’s Lymphoma in Relation to Infectious Disease Etiology: Aedes simpsoni mosquito transmission vector for malaria and Epstein Barr Virus co-infection Figure 4.12 The Biology of Cancer (© Garland Science 2007) Cancer Incidence Following Migration Figure 2.20 The Biology of Cancer (© Garland Science 2007) p. 45 CigBooze Definitions of Classifications of Cancer (DefClass.ppt) Normal Secretory & Ciliated Epithelial Cells Figure 16-19, ECB, 1998, p. 528 Ciliated Epithelium of Human Respiratory Tract RespCilia Prpgression in Neoplastic Development: Weinberg, Chapter 11 on Multistep Tumorigenesis. Figure 11.7 Figure 11.7 The Biology of Cancer (© Garland Science 2007) Cancer Incidence 2002: 1,285,000. Cancer Deaths 555,000. 43% Death Rate Cancer Incidence 2009: 1,479,000. Cancer Deaths 562,000. 38% Death Rate Table 2.3 The Biology of Cancer (© Garland Science 2007) p. 33 Hematopoiesis (formation of blood cells) Fig 2-1, Kuby 4th Ed. p. 28 HematoAll Pluripotent Stem Cell and Lymphoid and Myeloid Lineages (Fig 2-1, Kuby 4th Ed. p. 28 StemCell Myeloid Stem Cell Lymphoid Lineage Fig 2-1 Kuby 4th Ed p. 28 Myeloid Lineage (Kuby, Fig 2-1, 4th Ed., p. 28) Myeloid Disease Progression in Chronic Myelogenous Leukemia p. 293 Figure 8.32 The Biology of Cancer (© Garland Science 2007) Model Systems in the Study of Cancers (Models.ppt) Comparisons of Two Primary Cancers vs the Cancers Propagated as Model Systems Primary excised surgical tumor pieces Cancer Comparisons Surgical specimens after 3 to 6 months growth sub-cutaneously in SCID Mice Prostate and colon cancer cell lines propagated in vitro and implanted Figure 13.8 The Biology of Cancer (© Garland Science 2007) p. 539 Cancer Model Systems In Vitro (in Cell, Tissue, or Organ Culture) Normal Cells in Culture • Transformed Cells Chemically Virally By Irradiation • Neoplastic Cells from Animal Tumors • Neoplastic Cells Cultured from Human Cancers CxVitro Animal Tumor Models in Vivo Source of the Tumor Challenge Cells • Implanted Cultured Neoplastic Cells • Transplanted from Donor Animals Early vs Later Transplant Generations • Induced in the Tumor-bearing Host Animals Spontaneous (by Genetic Selection) Chemical, Viral, Radiation Induction • Excised fromVeterinaryAnimals AnimlCx1 Clinical Human Cancers as "Model" Systems Advantages: • The Closest "Model" to the Ultimate Goals ...The Best Model for Human Cancer • Patient Feed-back and Cooperation Limitations • Unmatched, genetically unique subjects • Powerful ethical limitations • Patient Independence and Failure to Comply • Prior or Concomitant Treatment Video on Clinical Trials in Patients A note on Experimental Cancer Therapy and National Health-Care Policy – Keith Olbermann, MSNBC Countdown, February 9, 2010 Properties of Cancer Cells and Tissues (CellProp.ppt) Senescence of Human Fibroblasts Passaged Beyond 60 Cell Doublings In Cell Culture Figure 10.2 The Biology of Cancer (© Garland Science 2007) p. 359 Protective Effect of Telomeres on Chromosome Integrity Telomeres* on normal cells protect chromosome ends * Telomeres labelled green by Fluorescence in situ hybridization with DNA probe that recognizes repeated nucleotide base sequence in telomeric DNA p. 369 Cells with blocked telomere formation show extensive chromosme fusion leading to cell death Figure 10.11 The Biology of Cancer (© Garland Science 2007) Note integrin signaling 12 Different Cellsignaling pathways potentially containing aberrant protein components in 24 different patients with pancreatic cancers. From Science, Sept. 26, 2008 Jones et al. pp 1801-1806 Cancer Cell Heterogeneity (Hetero.ppt) Pleural effusion, non-small cell lung carcinoma in a patient. Heterogeneit y in chromosome number and in nuclear size Figure 11.19 The Biology of Cancer (© Garland Science 2007) p. 422 Chromosome 11 is Blue-Green. Chromosome 17 is pink by FISH with DNA Probes Progression in Cancer Initiation and Development (Progress. Ppt) Progressive Steps in Neoplastic Cell Development: Hyperplasia and Dysplasia Progressive Steps in Neoplastic Cell Development: Cancer In situ and Invasive Cancer Situ&Invade Loss of Tumor Suppressor Genes (TSG) in Progression in Colon Carcinoma “DCC” Gene = Deleted in Colon Carcinoma “APC” = Adenomatous polyposis coli gene (Cancer suppressor gene) “K-ras” = Oncogene activated, transduced, or mutated, first identified in virally-induced rat sarcoma p. 409 Figure 11.10 The Biology of Cancer (© Garland Science 2007) Ras Pathway Growth Factors PMA GAP GTP GRB2 Ras SOS P Ras GEF GDP P P CD-GEGII PLC-ε p120GAP PI3K RalGDS P Raf Rac Rap1A Ral GTP P p190-B MEKs PAKs PLD RalBP1 Rho MEKK1 PLD Pathway ERKs CDC42 P Stress Fibers and Focal Adhesions JNKK ERKs JNK JNK Elk1 c-Jun ATF2 c-Fos Gene Expression C 2009 ProteinLounge.com Figure 11.43 The Biology of Cancer (© Garland Science 2007) hTert = Telomerase catalytic subunit p. 459 A Note About Completing Matching Questions 1. Each response in column B can be used only once. 2. Strike off a response from Column B when you use it in column A. 3. You have to match the best response from column B to the item in column A, not just one that might fit. 4. If you use a less-than-optimal response from Column B, you won’t have that response when you need it. 5. Answer the matching items that you are completely sure about. 6. That reduces the number of options you have to deal with. 7. The more you actually know for sure, the easier this kind of question is because it reduces your uncertainties to a very low number of options. This slide will be set to anonymous so it should say “Not accepting user data”. Your response is important so please provide your opinion. Please respond to the following: This review for the mid-term exam was 33% 33% 33% 0 of 95 . s .. ou Y id ea . od ly A re al ly go ab ea so n R N ot ve ry us ef u la us ef u nd no l. O ve tw ra . ... . 1. Not very useful and not worth doing. 2. Reasonably useful. Overall worth doing. 3. A really good idea. You should do it for other exams.