2012 Bio 314 Chapter 11

2012 Bio 314 Chapter 11 - Robert A. Weinberg The Biology of...

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The Biology of Cancer First Edition Chapter 11: Multi-Step Tumorigenesis Copyright © Garland Science 2007 Robert A. Weinberg
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11.1 Most human cancers develop over many decades of  time Progression from  normal to  malignant  requires a  succession of  genetic/epigeneti c changes, most  human cancers  develop over  decades of time Cancer deaths as a function of age
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Figure 11.2   The Biology of Cancer  (© Garland Science 2007) Dramatic increase in lung cancer deaths lags ~35 years  after dramatic increase in smoking. Now, 1.1 million lung cancer deaths annually, peak is still to come. Peak = 1990 Peak = 2020
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Figure 11.4   The Biology of Cancer  (© Garland Science 2007) Cancer incidence and carcinogen exposure: duration of exposure  determines onset, regardless of age. Exposure raises rate of tumor  progression orders of magnitude above spontaneous rate. asbestos/mesothelioma    mouse animal model
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Figure 20-3 Molecular Biology of the Cell (© Garland Science 2008) 11.2 Histopathology provides evidence of multi-step tumor formation
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Figure 20-9 Molecular Biology of the Cell (© Garland Science 2008)
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Figure 11.7   The Biology of Cancer  (© Garland Science 2007) Multi-step tumorigenesis {hyperplastic, dysplastic, adenoma (polyps), carcinoma,  metastasi s} is seen  in a variety of organ sites, suggests similar biological mechanisms  for all epithelial-derived cancers.  (“IN” = intraepithelial neoplasia; “CIS” = carcinoma in situ)
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Figure 20-2 Essential Cell Biology (© Garland Science 2010) Direct evidence of  progression  (precusor-product);  a carcinoma  growing directly out  of a benign polyp  (adenoma )
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Figure 11.8b   The Biology of Cancer  (© Garland Science 2007) More direct evidence of progression. Removal of benign polyps (adenomas)  markedly reduces incidence of cancer (by ~ 80%)
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Figure 11.9   The Biology of Cancer  (© Garland Science 2007) LOH 5q (later shown to be APC gene) then, mutant (activated)  K-ras, then, LOH on 18q  (unknown TSG a/k/a DCC) and 17p (p53) 3 tumor suppressors, 1 oncogene Genetic changes accompany progression in the colon 11.3 Colonic growths accumulate genetic alterations as tumor progression proceeds
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Figure 20-52 Essential Cell Biology (© Garland Science 2010) Hypomethylation appears to  contribute to genomic  instability, which facilitates LOH.  APC loss  90% K-ras activation 40-50% p53 loss 50-70% Usually, # lost TSGs > # activated oncogenes Sequence analyses suggest alternate pathways, such  as mutant Raf or mutant PI3K  instead of  mutant Ras - 15% of all colon cancers have a mutation in a kinase!
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Figure 11.10   The Biology of Cancer  (© Garland Science 2007) Familial polyposis (FAP) results from an inherited mutant APC allele, analogous to
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2012 Bio 314 Chapter 11 - Robert A. Weinberg The Biology of...

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