Path Lecture: Neoplasia Targeted Review: Hallmarks of Cancer: self sufficient growth and insensitive to inhibition

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1

at what levels could a tumor self-sufficiently provide its own growth signals

growth factor
growth factor receptor
signal transductin pathway
nuclear regulatory gene
progression of cell cycle inappropriately

2

what type of cancer is assocaited with a self sufficient growth factor

glioblastoma

3

what factor and receptor does glioblastoma use to provide its own impetus for replication

PDGF and PDGFR

4

what type of cancer has a mutation/overexpression of its growth factor receptors and uses it for replication

breast carcinoma

5

what is the growth factor receptor that breast cancer uses to proliferate

hER2/NEU amplification

6

what is the special anti-her2/neu antibody that breast cancer is fought with

herceptin

7

what normally activates Ras protein (quiescent GDP Ras)

EGF or PDGF activates it to GTP Ras

8

what does GTP Ras stimualte downstream regulators of proliferation through (pathways)

Raf or PI3K pathways

9

what hydrolyzes GTP ras back to a quiescent form

GTPase

10

what proteins activate GTPase acritiy

GTPase activating proteins (GAPs)

11

what can Ras point mutations lead to

decreased GTP hydrolysis

12

what cancer is implicated in Ras pont mutations

Colon and pancreatic adenocarcinomas

13

what ca RAF or pi3k mutations lead to

increased proliferation

14

what cancers are implicated in raf or pi3k mtuations

melanomas

15

what can GTPase actiating protein mutations lead to

increased proliferation

16

what cancers are implicated in GAP protein mutations

NF1 in neurofibromatosis

17

what type of protein is ABL

non-receptor tyrosine kinase signal transduction molecule

18

what is the activity of BCR-ABL hybrid protein

constitutive tyrosine kinas acritiy

19

what cancer is ABL BCR protein implicated in

CML

20

what is the bcr-abl treatment

gleevec

21

can CML exist just with bcr-abl proliferation

no it needs oncogene too

22

what is the normal role of myc with the CDK and CDKIs

activates CDKs, inhibits CDKis

23

what does myc do to energy use of the cell

warburg effect: aerobic glycolysis

24

what cancer shows myc translocation

burkitt's lymphoma 8:14

25

what are two OTHER myc trsncritpin factor error laden cancers

nmyc: nueroblastoma
lmyc: lung small cell caarcinomas

26

what cancer shows cyclin D overexpression

mantle cell lymphoma

27

what cancer shows cyclin CDK4 amplification

melanoma

28

what cancer shows CDKI disabling

pancreatic carcinoma

29

how is the cell cycle regulated by Rb with regard to cyclin E

G1 to S requires cyclin E/CDK2, and cyclin E production requries E2F transcritipon factors

active hypophosphorylated Rb binds E2F, prohibiting transcritpion of cyclin E

30

how is the cell cylce regulated by Rb with regard to cyclin D

mitogenic signals produce cyclin D and activate cyclin D/CDK4/6 complexes

cyclin D-CDK4/6 complexes phosphorylate Rb, releasing E2F, allowing transcritpino of cyclin E

31

what is the two hit hypothesis

both normal alleles of tumor suprpesor are inactivated

32

what is usually the case in familial cases of the Rb defective gene

one inherited defective gene and one somatic mutation are present

33

what is usually the case in the sporadic cases of the Rb defective gene

two somatic mutations

34

what will happen in a situation where you have mutational activation of CDK4

"not enough inhibtion" promotes growth with a constituitively active CDK4

35

what virus acts by binding hypophosphoyrlated Rb

HPV

36

what are some common examples of how mutations can cause the bypassing of cell cycle checkpoints not counting Rb

mutational (constitiutive) activation of CDK4

overexpresison of cyclin D

mutational inactivation of CDKIs

oncogenic DNA binds Rb

37

what is the most commonly mutated gene in human cancers

p53

38

what is the halflife of p53

20 minutes

39

what destroys p53

mdm2 protein

40

in what sitations will p53 avoid mdm2

cellular stress: anoxia, loss of DNA integrity, presence of oncogpotein

41

what will cellular stress do to keep p53 around

post-translational modification

42

does p53 activate just a few genes or not many

yes lots

43

how does p53 arrest the cell cycle

by p21 (CDKN1A) transritpion

44

what does CDKN1A (p21) transcritpion do

inhibits cyclin-CDK complexes and prevents Rb phosphorylation

45

what does p53 do for DNA repair genes

induces expression

46

what is a main DNA repair gene

GADD45

47

what are two paths that the cell can head down after p53 stops the cell

sensecence

apoptosis

48

what protein does p53 activate for apoptosi

Bax

49

does p53 participate in any microRNA prudction

yes

50

what DNA viruese tend to act on p53 instead of Rb

HBV and EBV

51

does TGF beta inhibit or promote proliferation

inhibtor

52

what does TGF beta use to combat cell proliferation

transcriptional activation of CDKIs

repression of growth promoting genes (myc, CDK2

53

how many of pancreatic cancers have a mutation in TGF beta signialing pathway

all

54

what cancers involve a defect in contact inhibition

NF2 and APC

55

what mediates cell-cell contact inhibition in NF2

cadherins

56

what mediates cell-cell contact inhibition in APC

cadherins

57

how does APC product work in most cells with relation to beta-catenin

binds it and destroys it

58

the APC protein regulates the stability and function of what molecule

beta catenin

59

what pathway do APC and beta catenin both belong to

Wnt

60

what will abnormal APC lead to in the cell molecularly

beta catenin mediated transcription of cell cycle proliferative genes

61

what will abnormmal APC lead to in the cell grossly

thousands of adenomatous colon polyps