The Hallmarks of Cancer
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1 The Hallmarks of Cancer Theresa L. Hodin, Ph.D. Clinical Research Services
2
3 Hippocrates
4 Cancer surgery, circa 1689
5 Cancer Surgery Today
6 1971: Nixon declares War on Cancer 2001: Andrew von Eschenbach eliminate suffering and death by : Why We're Losing The War On Cancer Fortune Magazine.. Age-adjusted Death rates
7
8 Cancer is the Result of a Multistep Process Colon Adenoma to Carcinoma Ductal Carcinoma in situ to Invasive Breast Cancer Prostatic intraepithelial neoplasia to Prostate Cancer normal --> ---> early ---> mid ----> late ---> carcinoma --> mets adenoma adenoma adenoma
9 What are the underlying events and how do they come about????? normal --> ---> early ---> mid ----> late ---> carcinoma --> mets adenoma adenoma adenoma
10 Review The Hallmarks of Cancer Douglas Hanahan* and Robert A. Weinberg Cell, Vol. 100, 57 70, January 7, 2000
11 Review Hallmarks of Cancer: The Next Generation Douglas Hanahan* and Robert A. Weinberg Cell, Vol. 144, , March 4, 2011
12 Acquired Capabilities of a Cancer Cell Cell 100, 57 70
13 Hanahan &Weinberg Cell 100:
14
15 In Vitro Studies
16
17 Oncogenes mutated forms of normal cellular genes generally involved in promoting cell proliferation. These mutations result in dominant gain of function. Tumor Suppressor genes genes whose normal function in regulating proliferation is to stop it. Mutation results in recessive loss of function.
18 Carcinogenesis: The accumulation of multiple genetic alterations that drives a normal cell to malignancy. Hypothesis: Mutation in one gene associated with each step in progression.
19
20 Early Molecular Model of Tumor Progression - Vogelstein
21 Karyotype Chaos
22 Tumor Heterogeneity Breastcancer.org
23 Acquired Capabilities of a Cancer Cell Cell 100, 57 70
24 Normal Mitogenic Growth Stimulation Transmembrane Receptor Signal Transduction Proteins Growth Factor Nucleus Cytoplasm
25 Strategies of Tumor Cell Self- Sufficiency
26 Insensitivity to Anti-Growth Signals Anti-Growth Signal such as TGFβ Smads Mad Max Myc Max TGFβR prb Cell Proliferation
27 Regulation of Apoptosis Sensor Molecules Mitochondrion Fas ligand Antiapoptosis signal Proapoptosis signal Fas p53? Bcl2 Bax Effector Molecules Cell Death
28 Limitless Replicative Potential Telomeres (TTAGG)nTTAGGTTAGGTTAGGTTAGGTTAGG (TTAGG)nTTAGGTTAGGTTAGGTTAGG (TTAGG)nTTAGGTTAGGTTAGG (TTAGG)nTTAGGTTAGG
29 Angiogenesis Angiogenic Factors Antiangiogenic Factors Region of insufficent blood supply
30 Invasion and Metastasis I Integrins Cell Adhesion Molecules (Adherens)
31 Invasion and Metastasis II Extracellular Proteases
32 Invasion and Metastasis III A. Epithelial-Mesenchymal Transition Normally during embryonic morphogenesis Epithelial cells acquire Mesenchymal traits Loss of adherens junctions Change in cellular morphology Expression of proteases Increased motility B. Collective Invasion C. Amoeboid Invasion Partial EMT?
33 Reductionist View of a Tumor
34 Realistic View of a Tumor
35
36 Immune Evasion Some data supports: Selective killing of highly immunogenic tumors, leaving weakly immunogenic ones Tumors disable parts of the immune system by secreting or recruiting cells that secrete immunosuppressive factors (ex. TGF B) Tumor cells down-regulate expression of MHC genes
37 Tumor-Promoting Inflammation Tumor- infiltrating immune cells provide factors which: Stimulate growth Inhibit cell death Promote angiogenesis Degrade extracellular matrices Induce epithelial-mesenchymal transition Damage DNA (reactive oxygen species)
38 Deregulating Cellular Energetics
39 PET SCAN
40 Cancer - evolution at a vastly accelerated rate favoring the growing tumor mass over the organism. Genomic Instability introduces genomic alterations and Natural Selection chooses the fittest tumor to survive.
41
42
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