11 Molecular Basis of Cancer 2 Flashcards

1
Q

Apoptosis typically looks like?

A
  • nuclear condensation
  • cell shrinkage
  • scattered
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2
Q

necrosis typically looks like?

A

karryorhexis, karryolysis, pyknosis, inflammation, group

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3
Q

T/F apoptotic cells cut their DNA into specific chunks?

A

T (unlike necrosis)

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4
Q

T/F p53 activates apoptosis?

A

T

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5
Q

What is the mechanism of p53 action?

A

working p53 catches DNA damage-> transcribe p21 to arrest cell cycle, bax to apoptosis, or GADD45 for DNA repair

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6
Q

What creates hair loss, GI crypt death, bone marrow death in radiation treatment?

A

p53

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7
Q

T/F BOTH p53 and Rb must be lost to allow tumor development?

A

T

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8
Q

2 genes at the same Ink4 locus encode what?

A
  • p16 activates Rb (p16 inhibits cyclin D which inhibits Rb)
  • p14 activates p53 (p14 inhibits MDM2 which inhibits p53)
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9
Q

knocking out Ink4 would lead to?

A

cancer! (Rb inactivation)

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10
Q

activation of Rb leads to?

A

cell cycle shutdown at G1/S

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11
Q

T/F p53 is usually found in high levels in tumors?

A

T. (p53 in mutated form which can’t feedback to MDM2 to say “degrade me!”)

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12
Q

bcl2 does what?

A

stops apoptosis (present in follicular B cell lymphomas!)

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13
Q

t14:18 translocation should ring a bell for?

A

-Ig heavy chain enhancer stuck next to Bcl-2 (b-cell lymphomas)

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14
Q

how many doublings in a normal cell till senescence?

A

~60

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15
Q

T/F telomere shortening creates genetic instability when p53 is dead?

A

T

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16
Q

Telomerase dose?

A

lengthen telomeres

17
Q

PML-retinoic acid receptor gene product sounds like what disease?

A

acute promyelocytic leukemia

18
Q

acute promyelocytic leukemia: treatment?

A

all-trans-retinoic acid (induces terminal differentiation of leukemia cells) thus also reducing DIC (disseminated intravascular coagulation)

19
Q

limit of tumor growth distance from blood vessel?

A

1 mm

20
Q

angiogenesis is acquired early in tumor development?

A

F, late

21
Q

What factors promote angiogenesis?

A

VEGF

22
Q

What inhibits angiogenesis?

A

angiostatin, avastatin (anti-VEGF-Ab)

23
Q

What is thalidomide good for?

A

treating multiple myeloma (anti-angiogenic) and creating birth defects

24
Q

VERY important. Review don’t memorize: metastasis process? (11)

A
  • metastatic subclone
  • loosen intercellular junctions
  • adhere to basement membrane (fibronectin receptor, laminin receptor)
  • Invade basement membrane (type 4 collagenase)
  • pass thru ECM
  • intravasation
  • interact w/ lymphoid cells-> embolus
  • adhere to basement membrane
  • extravasate
  • deposit
  • angiogenesis
  • grow
25
Q

E-cadherin does what in tumors?

A

decreases, loosening intercellular junctions (esp gastric cancer!)

26
Q

What is a rule for metastasis end location? 3 classic examples?

A

often to first tissue encountered

  • sarcoma to lung
  • lung carcinoma to brain
  • colorectal cancer to liver
27
Q

Tumor tropism classic examples?

A
  • breast cancer to ovary

- clear cell carcinoma of kidney to thyroid

28
Q

Which HPV has greatest cervical cancer risk?

A

HPV 16

29
Q

Which HPV makes condylomas? (worts)

A

HPV 11

30
Q

How will you remember what E6 and E7 do?

A

-E6 inactivates p53
-E7 inactivates Rb
[6 before 7, p before r. NEITHER affects the actual gene.]

31
Q

4 steps of cervical cancer?

A
  • Rb, p53 loss (live longer)
  • HGSIL/CIS changes and angiogenesis
  • invasion
  • mets
32
Q

length of cervical cancer premalignant phase?

A

13 yrs

33
Q

Gardasil blocks what HPV types?

A
  • 16
  • 18
  • 6 (warts)
  • 11 (warts)