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Summary of all lectures, workgroups and small teaching activities + literature for themes 1a and 1b of the mechanisms of disease 2 block
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Test Item File- Practice Test Bank - Robbins and Cotran Pathologic Basis of Disease,9e
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THEME IA MECHANISMS OF DISEASE II, THEME IA: CANCER BIOLOGY AND GENETICS
HALLMARKS OF CANCER
sustaining proliferative signaling
I - Over-expression of growth factors (EGF, VEGF)
II - Over-expression of cell surface receptors or activating
mutations (EGFR, HER-II)
*Activating mutations in EGFR are common in cancers like
lung cancer
*Amplification of ERBBII (HER-II) are common in cancers like
breast cancer
III - Overexpression of intracellular signaling molecules or
activating mutations (KRAS, BRAF)
*Goal to make cells independent of extracellular signals
IV - Overexpression of transcription factors (MYC, beta-catenin)
*MYC is proto-oncogen (= gene that can stimulate cancer
development)
V - Take away inhibiting component of pathway (PTEN, GAP)
evading growth suppressors
In healthy cells, growth suppressors are in abundance, while in cancers cells there are more
growth promotors than growth suprressors
- Suppressors make sure nothing in cell cycle goes wrong
Start checkpoint control: E2F under extreme control of retinoblastoma protein
- Loss of control: mutations of growth inhibitors
- Gain of control-function: mutations of growth factors
TP53 = the major tumor suppressor Mutated in more than fifty percent of all
resisting cell death human tumors (guardian of the genome)
P53 related pathways affected in more
than ninety percent of all tumors
Loss of this enzyme means loss of cell
cycle checkpoints and proliferation of
- cells with DNA damage
- Hereditary mutation in TP53 gene =
Li Fraumeni syndrome - develop
multiple primary tumors of various
kinds at young age - dominant
WNT signalling: other pathway that is often compromised in tumors
- Related to homeostasis in colorectum evade immune destruction
- Beta catenin maintains cell-cell contact I - HLA/MHC class I is lost
- is oncogen II - Signals which express inflammation
- E-cadherin does the attachment
- APC is destruction complex of beta-catenin activation of invasion and metastasis
- Loosening up of tumor cell to tumor cell interactions
(inactivation of E-cadherin)
- Degradation of ECM (expression of proteolytic enzymes
- Epithelial tumors: lose epithelial differentiation
enabling replicative immortality - Metastasis is inefficient process, few cells are able to
Normal cells have limited proliferative capacity metastasize
Enter state of replicative senescence - lost inducing angiogenesis
ability to re-enter cell cycle: telomeres become shorter and shorter - if Like normal tissues, tumors require nutrients and oxygen
gone, no more multiplication as well as an ability to evacuate waste products
Number of doublings dependent on species, tissue and age of organisms Tumor size is limited by the capacity of cancer cells to
Telomerase: increases/maintains size of telomeres induce angiogenesis
- Not in somatic cells
, THEME IA: CANCER BIOLOGY AND GENETICS
HALLMARKS OF CANCER
resisting cell death deregulating cellular energetics
- Less molecules for oxidative phosphorylation
Is shut down
- Cell goes into glycolysis
= Warburg effect
tumor promoting inflammation
Cancer-enabling effects of inflammatory cells and resident stromal cells:
• Release of factors that promote proliferation.
• Removal of growth suppressors.
• Enhanced resistance to cell death.
• Inducing angiogenesis.
• Activating invasion and metastasis.
• Evading immune destruction.
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