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Oral Cancer > Aetiology - viruses > Flashcards

Aetiology - viruses Flashcards

1
Q

what are causes of oral cancer?

A

tobacco, alcohol, HPV, poor nutrition, UV light, immunocompromise, genetic, potentially malignant conditions

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2
Q

describe the structure of HPV

A

double stranded DNA
circular
small
non-enveloped
capsid
72 capsomeres

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3
Q

what does HPV target?

A

mucosa

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4
Q

what are the types of HPV?

A

Alpha
beta
gamma
Mu
Nu

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5
Q

what are high risk HPV types associated with carncinogens?

A

16 and 18

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6
Q

what does HPV 16 target?

A

tumorous suppressor genes E6+7

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7
Q

what types of cells does HPV16 infect?

A

undifferentiated proliferative basal cells capable of dividing

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8
Q

what is an episome?

A

when DNA localises into the nucleus

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9
Q

with HPV16 infection, what viral proteins are transcribed from the early promotor?

A

E1,2,6,7

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10
Q

what do E6+7 do in HPV infection?

A

disturb the normal terminal differentiation by stimulating cellular proliferation and DNA synthesis

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11
Q

where do capsid proteins L1 and 2 accumulate during HPV infection?

A

mature epithelial cells

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12
Q

where does assembly of infectious virions take place?

A

terminally differentiated cells of upper epithelial layers

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13
Q

what is an epidermodysplasia verruciformis?

A

exuberant growth by HPV
rare autosomal recessive genetic condition that effects skin and increases the risk of carcinoma of the skin

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14
Q

what is a papilloma?

A

harmless/ benign
common on soft palate
small raised white lesion

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15
Q

how would you treat a papilloma?

A

X vision

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16
Q

what types of cancers may high risk HPV cause?

A

cervical, anal, oropharyngeal, vaginal, vulvar, penile

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17
Q

how are most oropharyngeal cancers spread?

A

sexual contact

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18
Q

who are most at risk of HPV cancers?

A

white, non-smoking males aged 35 to 55

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19
Q

where is HPV associated oropharyngeal cancer commonly seen?

A

base of tongue and tonsillar bed

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20
Q

how may HPV infection result in latency and malignant transformation?

A

interactions of E6 and E7 with p53 and PrB.

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21
Q

where is DNA kept during the normal HPV cycle?

A

episomally in the nucleus of affected cell

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22
Q

,what are low risk HPV types?

A

6 and 11

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23
Q

where does the HPV lifecyle start?

A

basement membrane

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24
Q

in the HPV lifecycle, where do mutagenic changes occur?

A

stratum spinosium

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25
Q

what is angiogenesis?

A

formation of new blood vessels

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26
Q

what are the differences between low risk and high risk HPV?

A

low risk doesn’t have:
E6 products that knock out tumour suppressor genes
no binding of PdX protein domains (doesn’t inhibit apoptosis)

after infection of low risk you don’t get bypass of growth arrest, i.e., weaker inhibition of interferon response.

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27
Q

what are the 2 types of benign oral HPV lesions?

A

papilloma
condylomata

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28
Q

describe an oral papilloma

A

layers of finger like projections

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29
Q

where would you find oral papillomas?

A

soft palate

30
Q

are oral papillomas high or low risk?

A

low

31
Q

transmission of oral papilloma?

A

sexual contact

32
Q

what are the types of malignant oral HPV lesions?

A

keratinised lesion on ventral tongue
SCC mucosa of gingivae surrounding teeth
keratotic attached gingivae
mixed red/white indurated alveolar surrounding teeth

33
Q

what makes the lingual gutter a high risk site?

A

saliva pools and if contained carcinogens from tobacco and alcohol it will be in direct contact with mucosa

34
Q

why may a SCC of gingivae be mistaken for perio disease?

A

mobile teeth

35
Q

what does indurated mean?

A

hard and rubbery

36
Q

what does exophytic mean?

A

growing out the way

37
Q

what does endophytic mean?

A

breaks down underlying structure

38
Q

what are HPV risk factors?

A

high number of sexual partners
weakened immune system

39
Q

what are the 2 HPV detection methods?

A

p16 staining
in-situ hybridisation

40
Q

how does p16 staining work?

A

looks for p16 protein down streaming of p53 and retinoblastoma gene (when these 2 genes are targeted by HPV, there is an increase in p16 expression)

41
Q

how does in-situ hybridisation work?

A

looks for HPV RNA/DNA in cells (dark brown staining within epithelial cells

42
Q

what are the 3 vaccines for HPV

A

Quadrivalent Gardasil
Bivalent Cervarix
Nonvalent Gardasil

43
Q

what types of HPV is quadrivalent gardasil for?

A

6 11 16 18

44
Q

what types of HPV is Bivalent cervarix for?

A

16 18

45
Q

what types of HPV is nonvalent gardasil for?

A

16 18 31 33 45 52 58

46
Q

what are low risk HPV types?

A

6 11
genital warts, papillomas

47
Q

what are high risk HPV types?

A

16 18
mouth cancer

48
Q

what is EPV?

A

a type of herpes

49
Q

what can EBV present as?

A
  • Mononucleosis
  • Lymphoma
  • Nose and throat cancers
50
Q

how is EBV transmitted?

A

saliva
sexual
blood transfusions
organ transplantation

51
Q

what are the 3 herpes subfamilies?

A

alpha
beta
gamma

52
Q

what is EBV categorised in to?

A

lymphocryptovirus
Rhadinovirus

53
Q

what does EBV infect?

A

B-lymphocytes

54
Q

features of EBV?

A
  • Toroid-shaped protein core, wrapped in DNA.
  • Nucleocapsid with 162 capsomeres.
  • Protein tegument between nucleocapsid and envelope.
  • Outer envelope with external glycoprotein spikes.
55
Q

What is the common impact of EBV in african countries?

A

direct impact on the nasopharynx causing a tumour called nasopharyngeal carcinoma

56
Q

what does EBV in mononucleic form cause?

A

glandular fever

57
Q

what are symptoms of glandular fever?

A
  • Lymphadenopathy (enlargement of tonsillar bed)
  • Sore throat
  • Hepatomegaly and splenomegaly
  • Rash
58
Q

what is Burkitt’s lymphoma?

A

cancer of nasopharynx associated with EBV

59
Q

what does HIV increase risk of?

A
  • Kaposi sarcoma
  • Lymphomas
  • Cancers of cervix, anus, lungs, liver, and throat
60
Q

how is HIV transmitted?

A

blood
sexual

61
Q

what are oral symptoms of HIV?

A
  • Candidiasis
  • Hairy leucoplakia (unusual white patch)
  • Accelerated periodontal disease.
  • Kaposis’s sarcoma
  • Salivary gland disease
  • Oral ulcers
62
Q

Who is at risk of HIV?

A
  • Men who have unprotected sex with other men.
  • People who share needles for drug injection
  • Heterosexual individuals who have unprotected sex with multiple partners
63
Q

how is HIV treated?

A

HAART

64
Q

what is human herpesvirus - 8?

A

kaposi sarcoma- associated herpesvirus

65
Q

what can KSHV cause?

A

Kaposi sarcoma, primary effusion lymphoma, multicentric Castleman disease

66
Q

how may people with HIV lower their risks of KSHV complications?

A

antiviral therapy

67
Q

what is kaposi sarcoma?

A

rare type of cancer that affects skin mouth and internal organs

68
Q

what causes kaposi sarcoma?

A

HHV-8 and HIV infection

69
Q

symptoms of kaposi sarcoma?

A
  • Red, purple, or brown patches.
  • Plaques, or nodules on skin.
70
Q

what gives lesions purplish blue colour?

A

Abnormal growth of small blood vessels just below skin

Oral Cancer (5 decks)

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