exam review: march 9, 2010 50110xm1review.ppt updated: march 8, 2010

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

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:

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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.

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