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FOM 3 wks 7-9 > cellular homeostasis & cancer > Flashcards

cellular homeostasis & cancer Flashcards

(57 cards)

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1
Q

6 DNA repair pathways

A

-direct reversal pathway
-mismatch repair pathway
-base excision repair
-nucleotide excision repair
-homologous recombination pathway
-non-homologous end joining (NHEJ) pathway

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2
Q

where does endogenous DNA damage occur

A

in active DNA participating in cellular activity like cell division (intracellular causes)

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3
Q

causes of exogenous DNA damage & 3 examples

A

environmental, physical, chemical agents

ex.
UV & ionizing radiation
alkylating agents
crosslinking agents

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4
Q

the two categories of DNA mismatch repair enzymes

A

MutS enzymes
MutL enzymes

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5
Q

MutS enzymes are associated with which DNA mismatch repair genes

A

MSH2
MSH3
MSH6

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6
Q

MutL enzymes are associated with which DNA mismatch repair genes

A

MLH1
MLH3
PMS1
PMS2

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7
Q

4 causes of cell cycle arrest

A

damaged DNA
unrepaired DNA
partially repaired DNA
cell size too small

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8
Q

(CDKs) stands for

A

cyclin dependent kinases

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9
Q

4 things that CDKs control in the cell cycle

A

DNA replication
transcription
chromatin remodeling
mRNA processing

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10
Q

CDK activation mechanism

A

CDKs inactive at baseline
->
activated when cyclins bind
->
cyclin/CDK complex modifies target proteins via phosphorylation during cell cycle

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11
Q

cyclin/CDK complexes are activated by _____

A

mitogens

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12
Q

cyclin/CDK complexes are inhibited by _____

A

the activation of cell cycle checkpoints (control points) in response to DNA damage

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13
Q

cyclin D

-active in what phase
-function & mechanism of action

A

G1 phase

promotes cell growth & entry into S phase by activating CDK4, CDK6

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14
Q

cyclin E

-active in what phase
-function

A

transition from G1 to S phase

activates CDK2 to initiate DNA replication

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15
Q

cyclin A

-active in what phase
-function

A

late S phase & G2 phase

regulates DNA replication & prepares cell for mitosis

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16
Q

cyclin B

-active in what phase
-function & mechanism of action

A

M phase

drives events of mitosis (spindle formation & chromosome alignment) by activating CDK1

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17
Q

growth factors are needed _____, and are NOT needed _____

A

needed during early G1 phase

NOT needed after the restriction point (late G1 phase)

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18
Q

each growth factor binds to _____

A

a specific cell-surface receptor with receptor tyrosine kinase (RTK) activity

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19
Q

how do growth factors drive the cell cycle

A

activate RTKS & downstream signaling pathways
->
which regulates cyclin/CDK complexes

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20
Q

what is a senescent cell

A

a cell that can no longer divide

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21
Q

main benefit of cell death

A

maintains tissue homeostasis

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22
Q

3 common types of cell death

A

apoptosis
necrosis
autophagy

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23
Q

apoptosis

-definition
-mechanism
-benefit of mechanism

Study These Flashcards
A

“programmed cell death”

membrane blebbing -> cell shrinkage -> condensation of chromatin -> fragmentation of DNA -> apoptotic bodies -> dead cell rapidly engulfed by neighbors

absence of inflammation during cell death

24
Q

necrosis

-definition
-mechanism
-consequence of mechanism

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A

“non-programmed cell death”

cell swells -> plasma membrane ruptures -> lysis of cell -> damages surrounding tissue

presence of inflammation during cell death

25
aggressive tumors _____ via necrosis
die from the inside out
26
necrosis is associated with _____
increased dissemination of cancer cells
27
autophagy -definition -benefit for cell
"break down & reuse old cell parts" autophagic vacuoles -> membrane blebbing -> increased lysosomal activity helps cell survival & maintenance
28
in a late phase tumor, autophagy supports & enhances _____
tumor growth
29
in early stages of cancer, autophagy has _____, which _____
anti-metastatic / protective role limits cancer necrosis & inflammation
30
ferroptosis -definition -mechanism -2 features -triggered by
iron-dependent cell death via genetic changes in iron homeostasis & lipid peroxidation metabolism increased membrane density & small mitochondria triggered by accumulation of iron
31
ferroptosis plays a critical role in _____
tumor suppression (may also activate tumors but research unclear)
32
pyroptosis -definition -mechanism -causes release of -triggered by
caspase-dependent inflammatory cell death NLRP3 activated -> caspase-1 perforates cell membrane (by forming nonselective pores) -> water influx -> cell swelling, membrane rupture, lysis & cell death causes release of alarmins (DAMPs, S100 proteins) (proinflammatory signals) triggered by infection
33
pyroptosis is both _____ & _____
a tumor promotor & tumor suppressor
34
necroptosis -definition -protein & substrate needed
caspase-independent "cellular suicide" protein RIPK3 & substrate MLKL
35
necroptosis is a tumor _____
suppressor
36
which programmed necrosis cell death type has maintained mitochondrial integrity
pyroptosis
37
what are driver mutations
mutations that cause a selective growth advantage to somatic cells in their microenvironment
38
driver mutations drive the cell lineage to _____
cancer (promote cancer development)
39
driver mutations in the _____ gene, encoding the _____ protein, are found in a majority of cancers
TP53 gene p53 protein
40
what types of genes do driver mutations occur in
driver genes
41
an example of driver genes
oncogenes
42
mutation mechanisms that lead to proto-oncogene activation
-coding mutation -regulatory mutation -translocation -gene amplification
43
_____ or _____ contribute to oncogenesis
abnormal proteins excessive amount of protein
44
what are proto-oncogenes
genes that normally regulate cell growth & proliferation, or help cells stay alive
45
what activates a proto-oncogene
mutation or presence of multiple copies of the proto-oncogene
46
what is an activated proto-oncogene called
oncogene
47
what is the "molecular basis of cancer"
oncogenes inducing cell transformation
48
what is epigenetics
the study of how environmental factors can cause cells to modify gene expression (WITHOUT changing the actual DNA sequence)
49
examples of epigenetic changes
acetylation methylation hypermethylation phosphorylation ubiquitylation
50
acetylation _____ gene expression; methylation _____ gene expression
acetylation increases gene expression methylation decreases gene expression
51
epigenetic changes are _____; genetic changes are _____
epigenetic changes = reversible genetic changes = irreversible
52
5 mechanisms that may promote tumorigenesis
-impaired DNA repair -epigenetic modification -chromosomal shattering -impaired protein synthesis -cell transformation
53
_____ is the underlying cause of tumorigenesis
mutation
54
mutation in proto-oncogene results in _____ and promotes _____
GOF tumorigenesis
55
common oncogenes
MYC RET PDGFRA MET KIT FLT3 EGFR BRAF
56
common tumor suppressor genes
TP53 TGFRB2 RB1 PTEN CHEK2 CDKN2A BRCA1 BRCA2 APC
57
mutation in tumor suppressor gene results in _____ and promotes _____
LOF tumorigenesis

FOM 3 wks 7-9 (24 decks)

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