exam review: march 9, 2010 50110xm1review.ppt updated: march 8, 2010
TRANSCRIPT
Exam Review: March 9, 2010
50110Xm1Review.PPt
Updated: March 8, 2010
Intro501: Introduction to Cancer Biology and to the Course
(501Intro.ppt)
Figure 1.11a The Biology of Cancer (© Garland Science 2007)
Banding pattern of normal metaphase human chromosomes
Figure 1.11b 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 1.11c The Biology of Cancer (© Garland Science 2007)
Aneuploid karyotype of human breast cancer cell.
Note “scrambling” of colors demonstrating chromosomal reciprocal translocations
Figure 1.11d The Biology of Cancer (© Garland Science 2007)
Intra-chromosonal inversion by M-band fluorescent in situ hybridization(mFISH)
Figure 1.14a The Biology of Cancer (© Garland Science 2007)
Cytoskeleton:
Actin microfilaments
Microtubules
Intermediate filaments
Figure 1.14b The Biology of Cancer (© Garland Science 2007)
Intermediate Filaments of epithelial cell (keratin) in green
Plasma membrane in blue
Figure 1.14d The Biology of Cancer (© Garland Science 2007)
3T3 Mouse Fibroblast attached to fibronectin extra-cellular matrix by integrin receptors
Clinical Presentation of Cancers
(Clinical.ppt)
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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)
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.
Incidence of Various Kinds of Cancers in Men and Women as a Function of Age
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)
Figure 4.12 The Biology of Cancer (© Garland Science 2007)
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 2.20 The Biology of Cancer (© Garland Science 2007)
Cancer Incidence Following Migration
p. 45
CigBooze
Definitions of Classifications of Cancer
(DefClass.ppt)
Normal Secretory & Ciliated Epithelial Cells
Figure 16-19, ECB, 1998, p. 528RespCilia
Ciliated Epithelium ofHuman Respiratory Tract
Figure 11.7 The Biology of Cancer (© Garland Science 2007)
Prpgression in Neoplastic Development: Weinberg, Chapter 11 on Multistep Tumorigenesis. Figure 11.7
Cancer Incidence 2002: 1,285,000. Cancer Deaths 555,000. 43% Death RateCancer 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 Celland Lymphoid andMyeloid Lineages
(Fig 2-1, Kuby 4th Ed. p. 28
Myeloid Stem Cell
StemCell
Lymphoid Lineage
Fig 2-1 Kuby 4th Ed
p. 28
MyeloidLineage(Kuby, Fig 2-1,4th Ed., p. 28)
Myeloid
Figure 8.32 The Biology of Cancer (© Garland Science 2007)
Disease Progression in Chronic Myelogenous Leukemia
p. 293
Model Systems in the Study of Cancers
(Models.ppt)
Figure 13.8 The Biology of Cancer (© Garland Science 2007) p. 539
Primary excised surgical tumor pieces
Surgical specimens after 3 to 6 months growth sub-cutaneously in SCID Mice
Prostate and colon cancer cell lines propagated in vitro and implanted
Comparisons of Two Primary Cancers vs the Cancers Propagated as Model Systems
Cancer Comparisons
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 VivoSource 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 fromVeterinaryAnimalsAnimlCx1
Clinical Human Cancers as "Model" Systems
Advantages:• The Closest "Model" to the Ultimate Goals ...The Best Model for Human Cancer• Patient Feed-back and CooperationLimitations• Unmatched, genetically unique subjects• Powerful ethical limitations• Patient Independence and Failure to Comply• Prior or Concomitant TreatmentVideo 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)
Figure 10.2 The Biology of Cancer (© Garland Science 2007) p. 359
Senescence of Human Fibroblasts Passaged Beyond 60 Cell Doublings
In Cell Culture
Figure 10.11 The Biology of Cancer (© Garland Science 2007)p. 369
Telomeres* on normal cells protect chromosome ends
Cells with blocked telomere formation show extensive chromosme fusion leading to cell death* Telomeres labelled green by Fluorescence in situ
hybridization with DNA probe that recognizes repeated nucleotide base sequence in telomeric DNA
Protective Effect of Telomeres on Chromosome Integrity
12 Different Cell-signaling pathways
potentially containing aberrant protein
components in 24 different patients with
pancreatic cancers.
From Science, Sept. 26, 2008
Jones et al.pp 1801-1806
Note integrin signaling
Cancer Cell Heterogeneity
(Hetero.ppt)
Figure 11.19 The Biology of Cancer (© Garland Science 2007)
p. 422Chromosome 11 is Blue-Green. Chromosome 17 is pink by FISH with DNA Probes
Pleural effusion,
non-small cell lung
carcinoma in a patient.
Heterogeneity in
chromosome number and
in nuclear size
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
Figure 11.10 The Biology of Cancer (© Garland Science 2007)
p. 409
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
R
T
K
R
T
K
Ras Pathway
SHC
GDP
GTP CD-GEGIIGAP
GTP
Elk1
c-FosATF2
c-Jun
Actin
Cytosk
eleton
PP P
P
P
P
Stress Fibers and Focal AdhesionsStress Fibers and Focal Adhesions
GeneExpression
GeneExpression
PLDPathway
PLDPathway
PMAPMA
Growth FactorsGrowth FactorsIncreased T Cell
AdhesionIncreased T Cell
Adhesion
IntegrinsIntegrins
β1β1β2β2 β2β2
β1β1β1β1SOS
p120-GAP
p190-B
Rho
PI3KPLC-ε
Rap1A
PLD RalBP1
PAKs
ERKs
ERKs
JNKK
JNKJNK
MEKK1
CDC42
Rac
MEKs
RafRalGDS
Ral
GRB2
TC
R
TC
R
AntigenAntigen
LckGEF
Ras Ras
2009ProteinLounge.com 2009ProteinLounge.com
C
Figure 11.43 The Biology of Cancer (© Garland Science 2007)p. 459
hTert = Telomerase catalytic subunit
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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.
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