Bld 204 Exam 3 Hallmarks Of Cancer1

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Most Growth Factor action on normal cells is

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paracrine

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Cancer cells make their own _______
OR they...

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-growth factors

-or they tell the stroma to make them some

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Cancer cells over-express _____ _____ _____
OR they...

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-growth factor receptors
-or they always have mutated receptors that are "always on" sending signals continuously even without growth factor

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What do you see when there's an
Overexpression of EGF

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-80% squamous cell carcinomas of lung
-50% glioblastomas
-80-100% epithelial tumors of head/neck

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What do we see when there's an
Overexpression of ERBB2

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25-30% of breast cancers

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In Signal Tranducing Proteins:
Inside the cell, mutations occur...

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further downstream, on the signally proteins
(inside the cell)

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In Signaling Tranducing Proteins:
There is a direct signal to _______ without...

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-nucleus
-without growth receptor signal

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In Signaling Tranducing Proteins:
Two most common mutations are in
______ and ______

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-RAS
-ABL

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In Signaling Transducing Proteins:
RAS -

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-most commonly mutated gene in human tumors
-small protein that binds GTP, GDP

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In Signaling Transducing Proteins:
ABL -

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-tyrosine kinase
-translocation in chronic myelogenous leukemia from chromosome 9 to 22
-fuses with BCR there and make fusion protein that has constitutive activity

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In Nuclear Transcription Factors:
Transcription Factors -

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regulate expression of proteins by controlling transcription of DNA

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Cancer-related mutations in transcription factors can result

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result in expression of more growth promoting genes like growth factor genes

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In Nuclear Transcription Factors:
MYC -

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-activates or repress:
-activates genes that encourage progression thru cell cycle like cyclins
-repress genes that stops it

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In Nuclear Transcription Factors:
MYC encourages ____ _____ and ____ _____

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-aerobic glycolysis
-glutamine utilization

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In Nuclear Transcription Factors:
MYC is an example of

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Burkitt's lymphoma

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Cyclins

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regulate progression through the cell cycle

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Cyclin-Dependent Kinases:

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-maintain orderly progression
-activated by binding to cyclins

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Cyclin-Dependent Kinase Inhibitors:

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broad and selective inhibitors of CDKs

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All cancers seem to have mutations that disable

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the G1-S checkpoint

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All cancers seem to have ↑ _____ ___ and ____ ____

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-cyclin D
-CDK4 expression

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All cancers, what is disabled by mutation or silenced?

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CDKIs

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Self-sufficiency of proliferation is opposed by 2 cellular pathways:

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-Apoptosis
-Senescence

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How many hallmarks is there?

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6

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In Insensitivity to Growth Inhibition Signals:
Tumor suppressor genes "brakes" for

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proliferation

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In Insensitivity to Growth Inhibition Signals:
4 major targets:

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-RB (governor)
-TP53 (guardian)
-TGF-Beta Pathway
-Contact Inhibition pathways

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In Insensitivity to Growth Inhibition Signals:
List characteristics of RB (6)

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-DNA-binding
-regulates G1-S checkpoint
-is cell cycle clock (important in development)
-common mutation
-many viruses that are oncogenic bind RB
-this gene involve in retinoblastoma
(rare childhood cancer)

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In Insensitivity to Growth Inhibition Signals:
List characteristics of TP53 (5)

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-Anoxia (absense of oxygen), DNA damage,
inappropriate signaling
-encourage transcription of CDKI which stops cell cycle
-Blocks G1 to S during repair
-if no repair → induces senescence/apoptosis
-Viruses can subvert (overthrow it) like RB

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In Insensitivity to Growth Inhibition Signals:
TGF-Beta Pathway has normal proliferation
inhibitor in which cells (3)

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-epithelial
-endothelial
-hematopoetic

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In Insensitivity to Growth Inhibition Signals:
TGF-Beta Pathways has mutations in -
_____% of ______ ______
_____% of ______ ______

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-100% of pancreatic cancers
-83% of colon cancers

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In Insensitivity to Growth Inhibition Signals:
Transformed cells in Contact Inhibition does what?

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They don't show contact inhibition in cell culture

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In Insensitivity to Growth Inhibition Signals:
Contact Inhibition, _______ mediate cell-cell contact

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Cadherins

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In Insensitivity to Growth Inhibition Signals:
What faciliates E cadherin contact inhibition?

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NF2 gene product merlin

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In Insensitivity to Growth Inhibition Signals:
_____ gene product loss can be involved in loss of contact inhibition by...

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-APC (patients lots of polyps)
-destroying beta-catenin which can be a growth promoting transcription factor

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APC -

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condition where patients get lots of polyps

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In Apoptosis:
-2 pathways are ______ & _____
-Both results in activation of _____ _______

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-intrinsic (mitochondrial pathway), extrinsic
-caspase cascade

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In Apoptosis:
The intrinsic or Mitochondrial Pathway, what happens?

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-cell injured (DNA damage, proteins misfolding)
-sensors in BCL-2 family activate Bax and Bak = make holes in mito's membrane
-mito proteins like cytochrome c escape and activate caspase cascade

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In Apoptosis evasion:
BAX-BAK pro-apoptotic action is regulated by

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BCL2 which is anti-apoptotic

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In Apoptosis evasion:
Mutations that activate BCL2 are common in

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B cell lymphomas

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How do cancer cells avoid autopagy?

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by mutation or taking over it to get "parts" to grow