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MDTI > Molecular Mechanisms of Cancer > Flashcards

Molecular Mechanisms of Cancer Flashcards

1
Q

how many cell divisions before cancer can be seen on X-ray?

A

10^8

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2
Q

how many cell divisions before cancer is palpable?

A

10^9

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3
Q

how many cell divisions before death?

A

10^12

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4
Q

definition of “hallmarks of cancer”

A

the homeostatic cellular processes most commonly disrupted in cancers, and which are dysregulated through mutation of critical regulatory genes

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5
Q

six hallmarks of cancer

A
  1. growth factor independence
  2. loss of response to antigrowth signals and differentiated state
  3. resistance to apoptosis
  4. limitless replicative potential
  5. recruitment of blood/lymph
  6. invasion and metastasis
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6
Q

what gives cancer its growth factor independence?

A

oncogenes

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7
Q

what gives cancer its loss of response to anti-growth and differentiated state?

A

tumor suppressors

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8
Q

what gives cancer its limitless replicative potential?

A

telomerase

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9
Q

proto-oncogene

A

normal genes with important roles in complex signaling pathways (regulating division, differentiation, survival, and movement)

any gene that can promote tumor formation or growth through mutation

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10
Q

oncogene

A

mutant counterparts of proto-oncogenes. characterized by unregulated activity.

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11
Q

what type of mutation creates oncogenes?

A

gain of function (over expression, amplification, constitutive activity)

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12
Q

what type of mutation creates tumor suppressors?

A

loss of function

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13
Q

relationship of oncogenes to growth factor

A

GF independent

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14
Q

PI3K (phosphatidylinositol 3-kinase)

A

lipid kinase that phosphorylates membrane (PIP2 to PIP3)

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15
Q

PIP2 (phosphatidylinositol biphosphate)

A

substrate for PI3K

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16
Q

activator of PI3K?

A

receptor tyrosine kinases (RTKs)

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17
Q

PIP3

A

organization hub for cytoplasmic signaling. docking site for important signaling proteins containing pleckstrin homology (PH) domains.

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18
Q

primary downstream effector of PI3K signaling?

A

AKT (aka PKB). can be oncogenic if over expressed!! promotes cellular metabolism, cell growth, survival, motility, etc

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19
Q

biomechanical consequence of activated AKT in cancer cells?

A

increased glucose transport and glycolysis

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20
Q

warburg effect

A

high glycolytic rate in many human cancer cells. allows for increased ATP and intermediates for cell growth.

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21
Q

positron emission tomograpgy (PET)

A

visualizes the uptake of 18-F labeled deoxyglucose to identify tumors. Can’t be metabolized and cancer cells with their high glucose transport light up like crazy

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22
Q

PET positive

A

cancers with elevated AKT levels

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23
Q

protein that negatively controls PI3K pathway?

A

PTEN (phosphatase and tensin homolog). de-phosphorylates PIP3

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24
Q

mutations in PTEN that lead to cancer?

A

loss of function mutations. leads to elevated AKT activity

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25
Q

tumor suppressor genes

A

genes in which loss of function mutations promote cancer

26
Q

more common mutation in PI3K/AKT pathway?

A

loss of PTEN function

27
Q

most common mutated tumor suppressor gene?

A

p53

28
Q

role of p53

A

activates cell cycle arrest or apoptosis in cells exposed to stress (DNA damage or oncogene activation)

29
Q

Li-Fraumeni syndrome

A

one germ-line mutant p53 inherited. more prone to cancers associated with loss of functional p53 allele (loss of heterozygosity)

30
Q

what type of TF is p53?

A

DNA binding TF.

31
Q

what types of mutations render p53 nonfunctional?

A

loss of function and missense mutations decrease p53’s ability to bind DNA

32
Q

what activates the p53 pathway?

A

stress

33
Q

consequences of p53 activation?

A

cell cycle arrest & apoptosis (but also DNA repair and block of angiogenesis)

34
Q

p21

A

cyclin/CDK inhibitor that leads to cell cycle arrest. regulated by p53.

35
Q

GADD45

A

DNA repair. regulated by p53

36
Q

proapoptotic proteins turned on by p53?

A

Bak, Bax, Puma, Noxa

37
Q

MDM2

A

ubiquitylates p53, targeting it for proteasomal degradation. negative feedback since it is activated by p53

38
Q

at what level is p53 regulated?

A

post translational stabilization. phosphorylated on different residues by different tumor suppressors in times of stress, which stabilizes it.

39
Q

auto regulation of p53

A

MDM2

40
Q

level of p53 in tumors?

A

high accumulation. nonfunctional p53 can’t bind DNA to activate genes and therefore MDM2 can’t target it for degradation.

41
Q

caspases

A

proteases that use conserved cysteine residue in active site to cleave proteins after aspartate residue. initiators and executioners. effect cellular destruction.

42
Q

intrinsic apoptotic pathway

A

cytochrome c released from mitochondria and binds to Apaf-1, forming apoptosome and activating procaspase 9 to caspase 9, which activates executioner caspases.

43
Q

components of apoptosome

A

cytochrome c, Apaf-1, procaspase 9

44
Q

which protein family regulates the mitochondrial membrane permeability to cytochrome c?

A

Bcl-2 family

45
Q

Bcl-2

A

anti-apoptotic

46
Q

pro-apoptotic proteins in mitochondrial membrane?

A

BH3, Bak, Bax, Puma, Noxa

47
Q

extrinsic (death receptor) apoptotic pathway

A

Fas/FasL binding and executioner caspase activation. Not a stress response like intrinsic pathway**

48
Q

how can cancer cells bypass apoptosis?

A

over expression of Bcl2, down regulation of Bax/Bak, loss of p53, down regulating Fas/FasL

49
Q

telomerase

A

enzyme that adds telomere sequence to chromosome ends, but is not typically expressed in adult somatic cells. cancers acquire it somehow.

50
Q

where is telomerase activated?

A

Expressed embryonically, in stem cells, and lymphocytes

51
Q

hayflick limit

A

the number of times cells divide before losing enough telomeric sequences to reach replicative senescence (permanent cell cycle arrest)

52
Q

consequence of telomere loss?

A

breakage fusion bridge during anaphase (inappropriate fusion) that leads to ds strand breaks –> amplifications and deletions.

53
Q

angiogenic switch

A

the ability to recruit functional blood vessels from surrounding tissue. occurs after solid tissues grow beyond 2mm

54
Q

problem of angiogenesis in tumors?

A

vessels serve as conduit for metastatic cells

55
Q

problem of telomerase in tumors?

A

if telomeres are stabilized after a fusion event, stabilized chromosomes are aberrant

56
Q

when does tumor growth really kickstart?

A

after the angiogenic switch

57
Q

gross morphology of tumor vasculature

A

disorganized and dysregulated. highly chaotic.

58
Q

VEGF (vascular endothelial growth factor)

A

stimulates EC division, survival, differentiation, etc. master regulator of angiogenesis. increased in tumors

59
Q

what does VEGF activate?

A

receptor tyrosine kinases on endothelial cells

60
Q

avastin

A

human monoclonal antibody against VGEF. works better in mice

61
Q

how do cancer cells metastasize

A

through the blood and lymph

MDTI (42 decks)

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