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CMCB Fall > #30 Cancer > Flashcards

#30 Cancer Flashcards

1
Q

What gets activated by bcr/abl in CML?

A

the c-able protooncogene encodes a prtoein tyrosine kinase that helps control cell proliferation

proto-oncogene is specially altered at the break point in both Burkitt’s and CML of these chormosomal translocation

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2
Q

what is sis oncogene?

A

Secreted Growth factor

in Platelet derived growth factor

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3
Q

what is erbB?

A

located in PM

epidermal growth factor recetptor (truncated)

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4
Q

Waht is erbA?

A

nuclear

thyroid hormone receptor

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5
Q

What is src oncogene?

A

rous avian sarcoma in cytoplasm

PROTEIN TYRSOINE KINASE that phosphoryaltes tyrosine residues

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6
Q

what is abl?

A

animal retrovirus (jbelson murine leukemia)

and nonviral tumor (CML)

cytoplasm and nucleus

protein kinase

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7
Q

what is Ha-ras>

A

animal retrovirus-harvey murine sarcoma

nonviral tumor- bladder, mammary, skin

plasma memebrane

Guanine nucleoide (GTP) bindign protein with GTPase activity

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8
Q

myc

A

animal retrovirus- avian myeloctamosus

nucleus

transcription factor

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9
Q

what is Rb?

A

nonviral tumor- retinobastoma and osteosarcome

nucleus

transcciption factor
tumore suppressor protein

(anti oncogenes

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10
Q

what is p53

A

nonviral tumor - most types of human cancer

nucleus

tumor suppressor proetins (anti-oncogenes)

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11
Q

what are teh two tumor suppressors we learned about?

A

p53

rb

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12
Q

what are four modes of intercellular signaling

A

1endocrine- hormone into blood

  1. paracrine- secretory ecll to adjacent target cell
  2. Autocrine- target sites on secreteory cell
  3. Juxtacrine- signaling cell to adjeance ttarget cell via cell surface proteins
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13
Q

What are two general classes of hormones and NTs?

A
  1. lipoholic with intracellular receptors (steroid, thryoxine, retinoids)
  2. soluble (H20) with PM receptors
    generate 2nd messnegers, GTP coupled epi, glucagon, serotonin< enzymeatic activity (try kinase)
    receptor interacts with enzme

reeptor is an ion channel

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14
Q

What are downstream effects of Hormones and NTs

A
  1. effect on enzyms in metabolic pathways
    cAMP–> PKA –> glycogen
  2. Effect on enzyme controlling cell scyle and cell division

EGFR–> Ras –> MAP kinase –> Rb, P53, Cdk, etc

effects on nuclear events, particualrly transcription
EGFR–> Ras –> Raf –> MAP kinase –> SRF –> SRE

effect

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15
Q

Growth factor singal transduction pathway

A

GF–> GFR –> P I3 Kinase (inosital) –> protein kinase activation –> active eIF4E or phopshoryted S6 kinase –> incerased mRNA translation –> sitmulation of cell growth

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16
Q

mitogen signal pathway

A

migoten –> mitogen cell rR –> act RAS –> MAP kinase –> myc gene transcribes Myc

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17
Q

What is p21 RAS

A

key regulator of intracellular signaling pathwya and contributing factor in many cancers

mutated in 30% of cancers

g protein or GTP-bidningprotein- active when GTP is bound0 inactive when GDP is bound

GTPase activity- slowly hyrolyzes bound GTP to GDP –> self inactivates

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18
Q

what are Ras and Myc

A

two oncogenes

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19
Q

mutation of two oncogens is more lethal than one

A

yep

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20
Q

What are the minimum requirements for teh transformation of human cells

A
  1. telomerase (prevent telomer shortenting) (hTERT telomerase catalytic subunit)
  2. large T-antigen (SV40) - hits Rb and p53
  3. Ras
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21
Q

what are th minimum requiremnts for transormation of rodent cells

A

Ras

T antigen (SV40) or myc

22
Q

What are the DIRECT gene/processes that functions under myc oncogene?

A
  1. cyclin D

2 SCF subunit

  1. E2F
23
Q

What are the indirect gene/processes that function under myc oncogene

A
  1. C1-Cdk
  2. Degradatin of p27 (inhitibor of porliferation)
  3. G1/S-CdK activation- via Rb phosphorylation
  4. increased E2F activity, via phosphorylation
  5. S-phase entry- via above mehcanism
24
Q

how does a normal cell respond to excess myc?

A

induceds cell cycle arrest or apoptosis

25
how does an abnormal cell respond to excess myc?
will further inactivate p53 leading to a tumor
26
What is the dosage hypotheses (ways proto oncogene can be converted into an oncogene)
celular ongene directs sytnehssis of an amt of a normal protein produt tha tis required for nomral growth and that transofmraiton to cancerous growht results form overproduciton of noamrl protein tumor retrovirus, overproduciton may be directed by viral oncgoene uner viral control
27
what is the mutationtal therory of goinf rom proto-oncogene to oncogen
gene product fro oncogene is differnt form gene product form proto oncogene differnec ein aa sequene is thought to lead to unregulated activity or othrwise abnromal actiity ras gene and src gene
28
what causes colorectal cancer?
K=ras mutations
29
how does cetuximab medicaion help with K-ras colorectal cancer mutations
cetuximab is anbitody directected toward EGF R patients with tumor beairn mutated K-ras DOES NOT benefit from cetuximab patiens with tumor bearing wilt type K-ras DID benegift form cetuximab
30
what is Her 2 Receptor --> Neu
conversion of native protein to hyperactive oncoprotein by mutatino (ligand dependent proto-oncogene receptor proteins) Val --> Gln in TM
31
difference between formation of tumor from proto-ocncogene vs tumor suppressor gene
Proto-oncogenen (accelerator) - only need ONE mutatuion to be overexpressed to cause cancer Tumor suppressor gene (brakes) - need mutaiton in BOTH copies to be inactivated
32
What are the six hot spot residues of p53
``` R249 R248 R273 R282 G245 R175 ```
33
which hot spots direclty ontact DNA (while the others are necessary for integrit of structurla elements?
R 248 | R 273
34
What does HPV cause? what causes HPV
warts and cervical cancer virus induced cancer, p53 and environtmentm
35
molecular biology of HPV induction of cancery
by inactivation of P53 and Rb through p53 inactivated thorugh E6 oncoprotein Rb inactivated by E7
36
what is Arg/Pro 72
common polymorphism in p53 R72 is more susceptible to E6 indueced degradation
37
do paitents with HPV ass. tumors have R72?
yes
38
how many more time susceptila is a patient with arg 72 to have HPV-associated tumorigenesis than heterozyge?
7x more susceptible to HPV
39
what are capsases?
protease invovled in the apoptotic process ultimately proteoglyze a large specific set of downstream proteins and enzymes, activating some and inactivating others
40
what inititatates P53 for directing apoptosies
1. killer cells in immune system 2. UV light 3. intrinsic inducement form damage to mitochondria by reactive ROS or canges in membrane ptoenttial that lead to relase of cytoscome dowstream events lead to activation of capase cased
41
what are caspases
aspartyl cysteinyl proteases that exist in a proform that can be proteolyzed to active caspase form activation of endonucleases lead to framentation of DNA into discrete sizes
42
apoptosis from outside (cell extrincic pathway)
killer T cells --> assembly of DISC --> activatino and cleavage of procaspase 8, 10 or both -> apoptotic target cells
43
apoptosis from inside (intrincisc pathway
relese of cyt c (apoptotic stimulatou --> act by aparf 1 --> CARD domain --> apoptosome --> recrutiment of act of procasase 9 --> caspase 9 cleaves and thereby activates executional procaspases
44
what stimulates extrinsic apoptosis 2
1. killer cell | 2. trohic support removal
45
what are players of extrinsic apoptosis 3
1. Fas lignad 2. Fas reeptor 3. DISC
46
What is initatior Caspase
caspase 8/10
47
what is executionaer caspase
caspase 3
48
what is intrinsic stimulus for apotposis
1. DNA Damage | 2. Mitochondrial damage (memrane potential loss , ROS)
49
what are players for intrinsic apptosis
Cyt c apaf 1, apoptsome Bcl12 (ant, bax, bad (pro
50
what is initiator caspase intrisncic
caspase 9
51
what is execulationar capsas
caspase 3
52
difference between apoptosis and Autophagy
autophagy lack chromatin condensation lack DNA ladders amssive cacualization of cytoplasm accumulation ofdouble membrane autophagic vacuoles little or no uptake by phagocytic cells, in vivo

CMCB Fall (17 decks)

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