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BIOL 202 > Lecture 31 > Flashcards

Lecture 31 Flashcards

1
Q

6 important hallmarks of cancer

A
  1. sustaining proliferative signaling
  2. evading growth suppressors
  3. activating invasion and metastasis
  4. replicative immortality
  5. angiogenesis
  6. resisting cell death
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2
Q

describe normal vs transformed 3T3 cells

A

normally stop growing when confluent bc of contact inhibition

with Src oncogene, no contact inhibition so will keep growing

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3
Q

what 2 hallmarks of cancer are involved in transformed 3T3 cells?

A
  1. sustaining proliferative signals
  2. evading growth inhibition
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4
Q

example of cancer that is genetic disease

A

Li-Fraumeni syndrome

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5
Q

genes involved in breast and ovarian cancer

A

BRCA1, BRCA2

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6
Q

gene involved in Li-Fraumeni syndrome

A

p53

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7
Q

gene involved in familial adenomatous polyposis (colorectal cancer)

A

APC

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8
Q

gene involved in retinoblastoma

A

RB1

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9
Q

what are oncogenes?

A

activated to drive tumorigenesis (positive regulators)

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10
Q

what are tumour suppressors?

A

inactivated to drive tumorigenesis (negative regulators)

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11
Q

describe involvement of DNA repair genes in cancer

A

prevent mutations to maintain DNA integrity

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12
Q

describe discovery of RSV

A
  1. crush up sarcoma from chicken
  2. pass filtrate thru fine-pore filter that does not block viruses
  3. inject filtrate into chicken
  4. chicken develops sarcoma

therefore, RSV carrying cancer-causing gene

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13
Q

what is the cancer-causing gene in RSV?

A

v-Src

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14
Q

what kind of gene is v-Src?

A

oncogene

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15
Q

what is c-Src?

A

the proto-oncogene

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16
Q

what is a proto-oncogene?

A

required for normal cell function but when mutated become oncogene

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17
Q

how do retroviruses make oncogenes? (5 steps)

A
  1. virus infects and creates provirus next to proto-oncogene
  2. cell transcribes provirus and proto-oncogene
  3. when virus reproduces, proto-oncogene is incorporated into virus
  4. with repeated rounds of viral infection and replication, proto-oncogene becomes rearranged/mutation (this is when it becomes a problem!)
  5. now oncogene is inserted back in host chromosome and promotes cancer
18
Q

alternative way how retroviruses make oncogenes

A
  1. virus infects and creates provirus next to proto-oncogene
  2. strong viral promoter stimulates overexpression of proto-oncogene
19
Q

are all proto-oncogenes activated from viruses?

A

no

20
Q

2 ways (other than viruses) that proto-oncogenes are activated?

A
  1. mutations in coding sequences
  2. chromosome abnormalities
21
Q

2 chromosome abnormalities that lead to proto-oncogene activations?

A
  1. increased expression
  2. fusion protein
22
Q

what is RTK?

A

cell surface protein that binds extracellular signaling molecules, leading to phosphorylation of tyrosine residues

23
Q

describe how RTK activates Ras

A
  1. growth factor binds RTK
  2. adaptor molecules bind the receptor, linking RTK to Ras
  3. Ras binds GTP and is activated
  4. GTP-Ras binds Raf to cause phosphorylation cascade
  5. activates TFs that promote cellular growth
24
Q

what kind of protein is Ras?

A

GTPase

25
Q

what kind of protein is Raf?

A

kinase

26
Q

describe normal regulation of Ras

A

normally has intrinsic GTPase activity so GTP-Ras automatically turns into GDP-Ras

27
Q

why is it important that GTP-Ras can automatically become GDP-Ras?

A

so it’s not constitutively on and activating genes for cell growth

28
Q

what causes Ras to become dysregulated and drive tumorigenesis?

A

1 point mutation in AA 12 turns Ras from proto-oncogene to oncogene

29
Q

describe oncogene form of Ras

A

stuck in GTP-Ras state so it is constitutively on

30
Q

are oncogene mutations haplosufficient or haploinsufficient? why?

A

haploinsufficient because oncogene mutations are DOMINANT

31
Q

describe oncogene mutants as dominant

A

mutants creating oncogenes are DOMINANT –> 1 copy of mutant allele is enough to induce excessive cell proliferation

32
Q

difference btwn cancer mutation and mendelian genetic diseases

A

cancer involves mutation in single cell to make disease

other genetic diseases inherited by mendelian genetics affect every cell in an organism

33
Q

what causes Burkitt lymphoma?

A

reciprocal translocation btwn Chr 8 and Chr 14 in B cells

34
Q

what gene is involved in Burkitt lymphoma?

A

c-Myc

35
Q

what is c-Myc?

A

TF whose normal function promotes cellular growth/proliferation (proto-oncogene)

36
Q

what chromosome is Myc on?

A

chromosome 8

37
Q

describe how translocation leads to activation of c-Myc into oncogene

A

regulatory element of chromosome 14 is for immunoglobulin

when translocation, this regulatory element is upstream of Myc and leads to overexpression of Myc –> Myc loses tight regulation

38
Q

what causes chronic myelogenous leukemia?

A

translocation btwn chromosome 9 and 22

39
Q

what is c-Abl?

A

protein kinase involved in cell survival

40
Q

what is produced in the CML translocation?

A

Bcr1-Abl chimeric protein is made and is a HYPERACTIVATED KINASE

41
Q

why is it easy to target Bcr-Abl?

A

bc not found in normal cells

BIOL 202 (29 decks)

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