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14 Onco > Molecular Onco 1 > Flashcards

Molecular Onco 1 Flashcards

1
Q

cancer growth strategies

A
  • signal activation
  • deactivation of growth signal controls
  • process promotion
  • escaping death
  • immortalization
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2
Q

genes that have a main role to initiate cellular growth in response to certain scenarios

A

oncogenes

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3
Q

important characteristics of oncogenes

A
  • dominant expression (need to activate only one gene)
  • highly conservative (always off = protooncogene)
  • two types: viral and cellular
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4
Q

classification of oncogenes

A

*secreted growth factors
*cell surface receptors
*intracellular transducers
*dna-binding nuclear proteins
regulators of the cell cycle

  • = components of signal transduction pathways
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5
Q

mutations where there is a change in one single dna nucleotide

A

point mutations

ex. bladder ca hrasa gene point mutation changes glycine to valine

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6
Q

types of point mutations

A
  • transition
  • transversion
  • nonsense
  • silent
  • missense: conservative or non conservative
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7
Q

mutation where there is a loss or gain of nucleotide in a given gene

A

frameshift mutation

- loss or insertion

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8
Q

mutations that occur during the process of extracting the coding portion of genetic code

A

splice site mutation

  • intron not excised
  • exon that is removed
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9
Q

mutations that occur as chromosomes start to deteriorate with age

A

breakage-fusion-bridge cycle

- fraying of the ends of chromosomes = exposure of nucleotides to the environment

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10
Q

attempts of chromosomes to cover breakage-fusion-bridge cycle mutations

A
  • homologous fusion: both chromosomes of a distinct pair

- nonhomologous fusion: occur between chromosomes that are part of a different pair (translocations)

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11
Q

effects of fusion in b-f-b c mutations

A
  • fused chromosomes are under pressure
  • bridge will break
  • unequal distribution of genetic material
  • –> one chromosome will have multiple copies = amplification
  • –> lose important genetic material = deletion
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12
Q

t/f in gene amplification, a chromosome acquires multiple copes of a particular gene

A

true, results in multiple copies of the protein

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13
Q

example of gene amplification

A

her2 oncogene = increased egfr2 on breast ca

  • increased egfr2 = increased proliferation even in physiologic levels of growth factors
  • more aggressive disease, poorer prognosis
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14
Q

mutation caused by fusion between nonhomologous pairs of chromosomes

A

translocation, results in coupling of genes that are normally far apart
- can result to activation of oncogenes

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15
Q

example of translocations

A

bcr-abl fusion gene

  • chromosome 9 and 22 fusion
  • coupling generates a proliferative signal = malignancy
  • philadelphia chromosome
  • hallmark of chronic myelogenous leukemia
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16
Q

what happens in viral activated oncogenes

A
  • virus incorporates genetic profile into nucleus of cell
  • viral genome is an oncogene that stimulates proliferation
  • oncogene remains incorporated in genome
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17
Q

control signals (genes) that prevent the onset of uncontrolled proliferation, preventing growth of tumors

A

tumor suppressor genes

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18
Q

characteristics of tumor suppressor gene

A
  • inhibit growth and multiplication of mutated cells
  • prevent neoplastic transformation
  • recessive and highly conserved (always on)

ex. rb1 and tp53

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19
Q

t/f only one tumor suppressor gene needs to lose activity to initiate malignancy

A

false! two hit hypothesis

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20
Q

knudson’s two hit hypothesis: two wild type tumor suppressor genes

A

first hit: mutation in one pair, but the other is still functioning
second hit: mutation in second pair, FUNCTION HAS BEEN LOST

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21
Q

knudson’s two hit hypothesis: one wild type, one inherited mutated gene

A

first hit: inherited mutated gene, other still intact
second hit: mutation in second gene, FUNCTION HAS BEEN LOST

will acquire disease younger

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22
Q

individuals who have inherited a mutated tumor suppressor gene from their parents are termed ___

A

heterozygous

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23
Q

when does loss of heterozygosity happen

A
  • when they lose the function of the remaining wild type

- they become homozygous

24
Q

what is contact inhibition

A
  • body’s way of ensuring that its microscopic architecture remains intact
  • normal: cells are side by side, no cell invades neighbors
25
Q

genes that maintain contact inhibition

A

nf2 gene -> merlin
- adhesive molecule keeping tight cell junctions intact

lkb1 gene -> epithelial polarity protein
- organizes cells into functioning epithelial structures by maintaining the integrity of entire tissue

26
Q

what are anti-proliferative cytokines

A

substances produced in the cell microenvironment that keep proliferation activities subdued

27
Q

example of anti proliferative cytokines

A

tgf-b

- can be used by cancer to help develop malignant phenotype

28
Q

what are dna repair genes

A
  • ensures fidelity of replication
  • checks and correct nucleotide pairing
  • deactivated = mismatches are unnoticed
29
Q

areas of nucleotide mismatches are also known as ___

A

microsatellite instabilities or min+

30
Q

two types of dna repair gene function processes

A

mismatch: detected by msh2 and msh6, replaced by mlh1 and pms2

insertion or deletion: detected by msh2 and msh3, excised or reinserted by mlh1 and ml3

31
Q

in order for an individual to develop malignancy, there must be ___

A
  • gain of function of protooncogene
  • loss of function of tumor suppressor gene
  • loss of function of mutator gene
32
Q

acquisition of growth signaling

A
  • production of growth factor ligands
  • autocrine stimulation
  • paracrine stimulation of normal cells (to produce substances)
  • altered receptor expression
33
Q

example of cell suicide

A

p53 in embryonic development

- webbed fingers and tails are removed through programmed cell death

34
Q

cyclin regulators

A

effector gene p21 (inhibits cell cycle progression and permits dna repair) and tumor suppression gene p53

35
Q

what is p53

A
  • detects presence of dna damage before s phase
  • damage -> halts cell cycle progression through p21 and recruits repair genes
  • after repair, p53 deactivates p21
  • severe damage -> p53 activates apoptotic pathway
36
Q

extrinsic component of bcl2

A

proteins: bh3 components
receptors: nbk/bik, bmf, bid, bim, puma, noxa, bad
(detect signals from environment)

signals are strongly pro-apoptotic

37
Q

signals from environment that trigger extrinsic component of bcl2

A 
genetic stress
p53 activation
loss of nutrients
protein synthesis damage
cytotoxic agents' effects
38
Q

intrinsic component of bcl2

A

proteins: bcl2, bclxl, bclw, mcl1, e1b19k

anti-apoptotic function

39
Q

how is apoptosis avoided by intrinsic component

A
  • prevent fusion of bax-bak
  • bax from cytoplasm, bak from mitochondria

fusion = apoptosis

40
Q

component of the mitochrondria released in response to apoptotic signal which activates a set of proteases

A

cytochrome c

41
Q

cysteine containing aspartate specific proteases activated by cytochrome c

A

caspases

  • initiator: activated in response to cell death signal
  • executioner or effector: activates cascade resulting in dna fragmentation and cell death
42
Q

ways to evade death signal

A
  • mutate p53 (ts gene)

- mutate intrinsic component = always antiapoptotic even if bh3 is signaling

43
Q

what is autophagy

A
  • triggered when there is nutrient deficiency
  • exhibits cross signaling with apoptotic pathway
  • protective for cancer cells
44
Q

how does necrosis cause cancer

A
  • release proinflammatory antigens to recruit more cells to become cancer cells
  • stimulates neighbors to become neoplastic
45
Q

hayflick limit or cellular senesence

A

there are only finite number of replications available

46
Q

functions of telomeres

A
  • cap that protects dna strands
  • prevents recombination and shortening of lagging strand
  • biological clock
47
Q

what is telomerase

A

mediates ability to add additional dna (6 nucleotide repeats to 3’-oh end)

48
Q

how does telomerase promote cancer

A
  • maintains telomere length, overcoming senesence
  • low levels in premalignancy, but promotes mutations leading to telomerase expression
  • overt carcinomas have high telomerase
49
Q

most active receptor in angiogenesis

A

vegfr2

50
Q

events that induce angiogenesis

A
  • hypoxia in tumor bed!!!
  • sex hormones
  • growth factors
  • genetic events (p53 mutations, vhl gene expression, pten mutation, oncogene activation)
51
Q

clinical implications of angiogenesis

A
  • more blood vessels = more risk for metastasis

- grow faster and more aggressive

52
Q

characteristics of new blood vessels

A
  • dilated
  • tortuous with multiple branches
  • bms with varied thickness = leakage = icn oncotic pressure = barrier to cytotoxic drugs
  • chaotic blood flow
53
Q

drivers of angiogenesis

A

pericytes and bone marrow derevied cells

54
Q

other mechanisms of vascularization

A
  • vascular co-option
  • intussusceptive vascular growth (splitting angiogenesis)
  • vasculogenic mimicry (stem cell like)
55
Q

metabolic adjustments to angiogenesis

A

warburg cells

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14 Onco (27 decks)

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