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Immunology 3 > #5 Oncogenesis > Flashcards

#5 Oncogenesis Flashcards

1
Q

Oncoviruses are necessary but NOT _____for cancer devo.

A

sufficient

Many/most people infected with a given virus do not devo the cancer that the virus can cause

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2
Q

Viral cancers appear in context of ________infections. Occur many years to decades after acute infection

A

persitant/chronic

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3
Q

Immune system can play a _____ or a prote______ctive role in virally induced oncogenesis

A

deleterious

protective

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4
Q

see human visus associated cancers in association with

A

immunosuppresion/chronic inflammation

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5
Q

How viruses causes indirect cancer

A

Chronic infection causes cirrhosis, inflammation, tissue damage, high levels of cell division to increase chance of mutation to derail growth control

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6
Q

How do viruses directly cause cancer

A

stimulate cells to enter S phase and make viral proteins to contineu to direct cell to ovvride normal controls on growth

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7
Q

How can we tell if a cancer we’re seeing epidemiologically is viral related

A

we’ll see it in an immunosuppresed population

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8
Q

aggressive skin cancer in elderly/immunocompormised

A

Merkel Cell carcinoma

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9
Q

Mech of merkel cell carcinoma

A

common deletion renders virus unable to complete replication cycle; persistnat infecction

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10
Q

common deletion renders virus unable to complete replication cycle; persistnat infecction

A

Merkel cell carcinoma

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11
Q

Papillomaviurs is member of:
genome:
infectects:

A

papovavirus
dsDNA
mucosal/epithelial~ hands/feet/genital

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12
Q

this has ~100 sub types with 1/3 infecting genital strand

A

papillomavirus

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13
Q

E1 and E2 of HPV mediate:

A

E1 and E2 mediate replication and transcription of viral DNA

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14
Q

E4 of HPV will:

A

E4 distrupts cytokeratins to facilitate virus egress~ helps virus out of the tissue

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15
Q

L1 and L2 of HPV

A

compose the capid

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16
Q

distrupts cytokeratins to facilitate virus egress~ helps virus out of the tissue

A

E4

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17
Q

mediate replication and transcription of viral DNA

A

E1 and E2

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18
Q

E5, 6, and 7 of HPV

A

intersect with key elements of cellular growth control, are associated with oncogenesis

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19
Q

E5 in HPV

A

stimulates constituitive GF replicating signal thus the cell no longer needs the GF receptor to signal replication

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20
Q

stimulates constituitive GF replicating signal thus the cell no longer needs the GF receptor to signal replication

A

E5

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21
Q

E6 and E7 in HPV

A

neutralize major ‘brakes’ that regulate cell cyle—p53 and Rb—thus uncouple cell division from key regulatory controls

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22
Q

neutralize major ‘brakes’ that regulate cell cyle—p53 and Rb—thus uncouple cell division from key regulatory controls

A

E6 and E7

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23
Q

Cousre of HPV

A

Inocculation of epitherlium→ hand/foot/throat or cervix→ Local multiplication→ wart
–resulotion(latency) OR –cell transformation

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24
Q

Life cycle of papillomavirus is tied to the differenation state of

A

keratinocytes

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25
Q

Stage of HPV virions fucking you up

A

a. Early gene expression in the basal layer of E1, E2, E6 and E7
b. Late gene expression and viral genome amplication: in the spinous layer
c. Virion assembly and release in the cornified layer

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26
Q

a. Early gene expression in the_____ layer of E1, E2, E6 and E7

A

basal

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27
Q

Late gene expression and viral genome amplication: in the ____ layer

A

spinous

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28
Q

Virion assembly and release in the _____layer

A

cornified

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29
Q

HPV stimulation of cell cycle causes cell in _______ to replicate

A

stratum spinosum

the spinosum is spitting out hpv

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30
Q

Where are cells supposed to regulate?

A

the stratum basal

BASICALLy, the basal layer

31
Q

is the engine of the cell cycle: move the clel cycle ahead by phosphorylating key substrates

A

CDKs

32
Q

CDK regulation

A

by enZ synthsis, degredation of cyclins, phosphorylation events, inhibtiors

33
Q

key brake that blocks progression to S phase

A

Rb

34
Q

Rb-P is in its’

A

inactive state… lets cell go G1–> S

35
Q

how do we P Rb?

A

accumulate Cdk/cylcins and phosphorylate it

36
Q

____ protein of papillomavirus binds to Rb—targets it for proteosomal degradation

A

E7

—E7 like syltherin… sneaky snake bastard

37
Q

guaduain of genome to prevent proguression to S phase by making cyclins or inducing apoptosis

A

p53

38
Q

the killer of p53 by targeting upiquitin to it!

A

E6

666 like the devil and now the cell is immoral! aghh!

39
Q

two naughty function of E6

A

blocks p53 and increase telomerae

40
Q

More then 99% of cervical cancers specimens show evidence of infection with ‘high risk’ strains of HPV strains

A

HPV 16 (50-60%)
HPV 18 (10-20%),
HPV6
HPV 11

41
Q

See correlation btwn high risk strains and activity of_______proteins in vitro assays of cell transformation

A

E6 and E7

42
Q

a. high risk; E6 + E7 can immortalize

A

keratinocytes

43
Q

Early stage of acute and persistent HPV infection, viral DNA is maintained as

A

episome

-stays as a little extra chromo on its own then gets integrated into host DNA

44
Q

Devo of carcinoma associated with integration of DNA into the host as what is retained?

A

E6 and E7 (always retained in cancer cells)

45
Q

Integration disrupts expression of ________, which is transcriptional repressor, allow increased levles of E6 and E7

A

E2 gene

*Replication of integrated DNA triggers DNA amplications and chromosomal abnormalities

46
Q

Our transcriptional repressor that is disrupted during integration of HPV into genome

A

E2

47
Q

______ _______ key step towards oncogeneis in HPV

A

Genome integration

48
Q

LSIL is

A

low grade squamous intraepitheilal lesion

49
Q

HSIL

A

HIgh grade squamous intraepithelilal lesion

50
Q

CIN

A

cervical intraepithelial neoplasia

51
Q

productive infection we see ______

with low E7 and low viral DNA

A

LSIL; productive infection

52
Q

Cellular Gene Deregulation:

we see increased:

A

E7 and viral DNA

53
Q

Cervical cancer: DNA integration we see a break in ______

with high levels of

A

basal membrane

E7

54
Q

Normal cervix→ to HPV invected cervix: seen in 370 million and often

A

cleared

55
Q

HPV infected cervix→ to Low grade SIL: in about 70 million and can______ or move to ______

A

regress

HG-SIL

56
Q

causes that precipitate moving from LSIL to HG-SIL

A

(especially if they smoke, OC use, viralload, coinfections)

57
Q

HG-SIL (in 10 million) can regress or move on to

A

cervicle cancer:

in .5 million cases and can’t go back

58
Q

How do we progress from HG-SIL to cervical cancer

A

occurs in viral integration methylation

59
Q
  • **E6/E7 mRNA is present as we______

* **___ will disappear as we move to cancer

A

progress

L1

60
Q

cytological evidence of displasia or neoplasia; detect koilocytotic cells (vacuolated cytoplasm) which are rounded and appear in clumps

A

Pap smear

61
Q

Pap smear that show evidence of displasia or neoplasia looks like:

A

detect koilocytotic cells~~~ round and clumpy

62
Q

Step 1: Release nucleic acid: clincial specimes are combined with a base solution which release target

A

DNA

63
Q

Step 2. Hybridize RNA probe with Target DNA: target DNA combines with specific RNA probes creating

A

RNA:DNA hybrids

64
Q
  1. Capture Hybrids: multiple RNA:DNA hybrids captured onto solid phase coated with universal capsure _____ specific for RNA:DNA hybrids
A

antiBs

65
Q
  1. Label for detection: captured hybrids dectected with multiple antiBs conjugated to ______. Signal then amplified 3000 fold
A

alkaline phosphatase

66
Q
  1. Detect, read and interpret results: bound alkaline phosphates detected with ________ substrate. Upon cleavage by alkaline phosphatase, substartes produce light measure on luminometer in ______
A

chemiluminsent

Relative Light Units (RLUs)

67
Q

Vaccine issues

A

a. need mucosal infection d/t route of infection
b. need to recognize multiple high risk strains
c. admin of vaccine that includes oncogenes not possible
d. societal issues: is this a vaccine to prevent cancer or STD

68
Q

Capsid protein L1 will induce:

A

humoral innuminty

69
Q

recombinant L1 can be made in culture

b.L1 self-assembles into_____ that resemble virions and induce appropriate immunological response

A

“VLPs”

70
Q

Vaccine contains purifed VLPs

induces protective, humoral immunity

A

antiBs present at mucosal surfacee prevent incoming HPV from establishing infection

71
Q

Guardasil

1. prevents precancerous lesion and warts: HPV

A

6, 11, 16, and 18

72
Q

Gardasil admin age

A
  1. can be administerd as young as 9 and as old as 26
73
Q

Type of vaccine Gardasil is?

when and why do you use it?

A

HPV is leading cause of cervicle cancer
should be given before onset of sexual activity but either way get vaccinated
this is a tetravelant vaccine

74
Q

Cervical cancer stats FYI

A
  1. 15,000/year in US infected with cervcle cancer and 4,100 die per year d/t this
  2. 500,000 new cases /yr worldwide and see 250,000 deaths
  3. second or thrid most common cancer among women
  4. Vaccines for pre-adolescent girls with VPL vaccine and vaccine for men to deplete high risk HPV from popuation
  5. HPV is associated with penile cancers, vulvar cancers and anal cancer~ %25 of oroparnyeal cancers

Immunology 3 (20 decks)

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