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notes to flashcards year 2 - MCD > Cancer extra notes > Flashcards

Cancer extra notes Flashcards

1
Q

what do proto-oncogenes code for?

A

essential proteins involved in maintenance of cell/ division/ differentiation

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2
Q

How can proto-oncogenes become carcinogenic?

A
  • mutation
  • gene amplification
  • chromosomal translocation
  • insertional mutagenesis
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3
Q

what is the SRC gene and what cancers is it involved in?

A
  • tyrosine kinase

- overexpression = breast/colon/lung

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4
Q

what is the MYC gene?

A
  • TF

- translocation = Burkitt’s lymphoma

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5
Q

what is the JUN gene?

A
  • TF

- overexpression/deletion = lung

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6
Q

what is the Ha-RAS gene?

A
  • G protein

- point mutation = bladder

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7
Q

What is the Ki-RAS gene?

A
  • G protein

- point mutation = colon, lung

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8
Q

what is p53 and what cancers is it involved in?

A
  • cell cycle regulator

- colon, breast, bladder

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9
Q

what is BRCA1 and what cancers it it involved in?

A
  • cell cycle regulator

- breast, ovarian, prostate

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10
Q

what is PTEN?

A
  • tyrosine and lipid phosphatase

- prostrate, glioblastoma

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11
Q

what is APC?

A
  • cell signalling

- colon

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12
Q

what happens in the caspase cascade?

A
  • once apoptosis is initiated, initiator caspases cleave and activate effector caspases
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13
Q

where are death receptors found? when are they activated?

A
  • found on all cells on surface

- only activated when they encounter death ligands

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14
Q

describe the death receptor signalling process

A
  1. death ligand binds to death receptor
  2. death receptor undergoes trimerisation (brings 3 cytoplasmic DD domains together)
  3. trimersised death domains recruit positive adaptive protein FADD
  4. this binding causes recruitment and oligomerisation of procaspase 8
  5. binding of caspase 8 to FADD –> formation of DISC
  6. DISC formation results in cross activation of procaspase 8
  7. caspase 8 released, cleaves effector caspases
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15
Q

what are the 2 categories in the Bcl-2 family?

A
  • anti-apoptotic proteins (Bcl-2, Bcl-XL): mitochondrial membrane
  • pro-apoptotic proteins (Bid, Bad, Bax): cytosol or mitochondrial membrane
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16
Q

explain how growth factors go about having an anti-apoptotic effect

A
  • GF binding = dimerization = phosphorylation of tyrosine kinase receptors
  • initiates signal transduction pathways and creates docking sites for adaptor proteins
  • Grb2 binds and mediates Ras pathways = cell growth
  • another phosphorylation site triggers PI3-kinase pathway
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17
Q

what is PI3-K? describe its structure?

A

lipid kinase
involved in growth control and cell survival
- has targeting, adaptor and catalytic subunits

18
Q

describe the MoA of PI3-K?

A
  • phosphorylates PIP2 to PIP3
  • recognised by adaptor subunit of PKB
  • PKB recruited to cell membrane
  • is activated w/ anti-apoptotic effects
  • PKB phosphorylates Bad
19
Q

what happens when GFs are absent?

A
  • PkB fails to come to cell membrane
  • Bad phosphorylated and released from its heterodimer
  • Bad goes to mitochondrial membrane
  • Binds to BH3 domain on anti-apoptotic Bcl-2, displace pro-apoptotic Bcl-2
  • once pro-apoptotic are released, form a pore
  • this allows cytochrome C to escape into cytosol and induces apoptosis
20
Q

what are the roles of PKB?

A
  • phosphorylates and inactivates Bad
  • phosphorylated and inactivates capsape 9
  • inactivated FOXO transcription genes
  • stimulation of protein synthesis (MAPK/ERK)
21
Q

state the 2 extrinsic regulators of apoptosis

A
  • PTEN

- IAPs

22
Q

what is PTEN?

A
  • lipid phosphatase
  • counteracts production of PKB
  • reduces regulation of cell survival and promotes apoptosis
23
Q

what is IAPs?

A
  • regulate programmed cell death by binding to procaspases
  • prevent their activation
  • binds to active caspases and inhibits their activity
24
Q

what do replicated chromosomes consist of?

A
  • 2 pairs of sister chromatids

- each w/ kinetochore and central centromere

25
Q

what is a centrosome made up of?

A
  • 2 centrioles (made up of microtubules)
26
Q

what is ampehlic attachment of spindle to kinetochores?

A
  • normal

- kinetochores do not produce checkpoint signal

27
Q

what is merotelic attachment?

A
  • spindle attachment from same centrosome to both kinetochores
  • bad because kinetochores still don’t produce checkpoint signal
  • don’t know its abnormal
28
Q

what is monotelic attachment?

A
  • movement of both pairs of chromatids to same pole through attachment of 1 centrosome to 1 kinetochore
  • no attachment to other
  • will produce checkpoint signal
29
Q

what is syntelic attachment?

A
  • movement of both pairs of chromatids to same pole
  • attached to different spindles
  • both sister chromatid pairs are at same pole
  • one daughter cell has no chromosomes after cytokinesis
30
Q

what is the activity of Cdks regulated by?

A

their interaction with cyclins and their phosphorylation

31
Q

which cdk/cyclin is found in M phase?

A

cdk1-cyclin B

32
Q

which cdk/cyclin is found in S phase?

A

cdk2-cyclin A

33
Q

which cdk-cyclin is found in G1 phase?

A

cdk2-cyclin E

34
Q

which cdk-cyclin is found in transition from G0 to G1?

A

cdk4/6-cyclin D

35
Q

describe the model of sprouting angiogenesis

A
  1. need for new blood vessels
  2. GFs released that activate endothelial cells in pre-existing capillaries
  3. endothelial cells undergo conformational change
  4. go from being organised monolayer to sending out filopodia
  5. migrate towards GFs
  6. cytoskeleton of tip cell must be modified
  7. tip cells keep on moving until they find another tip cell
  8. they fuse and stabilise
36
Q

what does angiopoietin 1 do?

A

when it binds to Tie2, promotes quiescence in vasculature

37
Q

what does angiopoietin 2 do?

A

gets released when you need to form new blood vessels or need to respond to inflammation

38
Q

what are the 5 types of malignant melanoma?

A
  • superficial spreading
  • nodular
  • lentigo maligna melanoma
  • acral lentiginous
  • amelanotic
39
Q

what does listeria express at one pole of the bacterium? what does it mean?

A
  • ActA
  • can bind actin in host cytoplasm
  • only sufficient to allow limited motility
40
Q

how does listeria get full motility?

A
  • needs VASP binding to proline-rich region of protein
  • VASP recruits Arp complexes (inc. rate of comet tail formation)
  • also binds proffilin to this part of cell (ensures good supply of ATP-containing G-actin)
41
Q

what happens when the bacterium is in the acidic environment of phagolysosome?

A
  • produces lysin protein
  • protein breaks down organelle membrane
  • listeria enters cytoplasm

notes to flashcards year 2 - MCD (24 decks)

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