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First Year med - dundee > 61. Neoplasia part 2 > Flashcards

61. Neoplasia part 2 Flashcards

1
Q

Describe carcinoma in situ

A

very severe dysplasia, potential to become malignant and invasive, has not yet breached basement membrane

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2
Q

what is an environmental factor that causes cancer

A

carcinogen

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3
Q

how is carcinogenesis identified

A

epidemiological studies, occupational risk, direct evidence (eg chornobyl), and experimental testing

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4
Q

Carcinogenic risk cannot be determined by …….. alone

A

structural formula

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5
Q

what is the difference between Direct and Indirect carcinogens

A

direct is a carcinogen entering your body as it is (e.g. smoking)
indirect is Procarcinogens undergoing metabolic conversion into active carcinogens (nitrate into nitrosamine)

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6
Q

name some carcinogen requirements

A

resisting cell death
insensitivity to growth inhibitors
sustained angiogenesis
metastasize
invasion

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7
Q

how are neoplastic cells immortal (3 reasons)

A

Autocrine growth simulation
reduced apoptosis
telomerase activity

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8
Q

describe Autocrine growth simulation

A

abnormal expression of oncogenes and inactivation of tumor suppressors

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9
Q

describe reduced apoptosis

A

abnormal gene expression leads to inhibition of apoptosis

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10
Q

describe telomerase activity

A

in normal cells the telomeres shorten with each division. this means a cell only divides a certain amount. Telomerase prevents this

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11
Q

which gene encodes a protein that regulating apoptosis so when its inhibited reduced apoptosis happens

A

BCL-2 is a gene that encodes a protein playing a crucial role in regulating apoptosis

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12
Q

what gene inhibits neoplastic growth

A

Tp53 that encodes for p53

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13
Q

p53 is known as what type of gene

A

tumor suppressor gene

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14
Q

what do caretaker genes do

A

repair dna

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15
Q

what do gatekeeper genes do

A

stop damaged cells dividing (inhibit proliferation or induce apoptosis)

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16
Q

describe p53

A

has gatekeeper and caretaker function
“guardian of the genome”
most frequent mutated gene in cancer

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17
Q

what mutations can p53 go through

A

missense and nonsense

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18
Q

what does p53 binding to oncoproteins (encoded by DNA viruses) lead to

A

HPV

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19
Q

what are oncogenes

A

genes which drive neoplastic behavior in cells

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20
Q

what do oncogenes produce

A

oncoproteins

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21
Q

what are the 5 groups of onco(genes/protiens)

A
  1. growth factors
  2. receptors for growth factors
  3. DNA binding transcription factors
  4. signaling mediator with tyrosine Kinase activity
  5. signaling mediator with nucleotide binding activity
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22
Q

what are the 2 signaling mediators involved as oncogenes

A

signaling mediator with tyrosine Kinase activity
signaling mediator with nucleotide binding activity

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23
Q

Diploid

A

normal amount of DNA (2N)

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24
Q

Polyploidy

A

Exact multiples of diploid state (4N or 8N)

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25
Q

Aneuploidy

A

Inexact multiples

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26
Q

low risk HPV forms…..

A

warts

27
Q

high risk HPV forms…?

A

squamous cell carcinoma

28
Q

where can HPV happen

A

head and neck region
anogenital

29
Q

What are transformation zones and what does this mean

A

Areas of transition from one epithelial type to another (ie transformation zone) most prone to instability

30
Q

where is the p53 in terms of checkpoint

A

G2-M

31
Q

what gene is at checkpoint G1-S

A

pRB - retinoblastoma protein

32
Q

what viral HPV oncoprotein acts on TP53

A

E6

33
Q

E6 viral oncoprotein acts on what

A

TP53

34
Q

what does TP53 make

A

p53

35
Q

what does p53 do

A

Activates DNA repair proteins, holding cell cycle to allow repair, initiating apoptosis of badly damaged cells
Is at G2-M checkpoint

36
Q

what viral HPV oncoprotein acts on RB

A

E7

37
Q

E7 acts on what

A

RB

38
Q

what is RB

A

retinoblastoma protein that inhibits cell cycle progression until cell is ready to divide

39
Q

RB or TP53 first

A

RB

40
Q

what virus is associated with some lymphomas and carcinoma (HINT- EBV)

A

Epstein Barr Virus (EBV) is a type of herpesvirus (“glandular fever”)

About 90% of the population end up with some kind of (usually transient) EBV infection

41
Q

What can EBV cause

A

EBV driven lymphoproliferative disorder

42
Q

what are EBVs associated with

A

Burkitt Lymphoma
Hodgekin Lymphomas
primary effusion lymphoma

43
Q

what promotes nasopharyngeal carcinoma

A

smoking. inactivation of p16/CDKN2A and TGFBR2

44
Q

major cause of radiation skin cancer

A

UV (ultraviolet)

45
Q

which UV is most common for skin cancer

A

UVB

46
Q

what cancers are UV most associated

A

malignant melanoma
basal cell carcinoma

47
Q

melanoma is cancer of which cells

A

melanocytes (produce melanin pigment)

48
Q

what is the scale of UV damage and melanin

A

fitzpatrick scale - Pale people are more susceptible to UV damage

49
Q

what increases risk of UV damage

A

tanning beds, sunburns

50
Q

what is ionising radiation (give examples)

A

radiation which detaches electrons from atoms or molecules. Gamma rays, x rays and nuclear radiation

51
Q

what is radiation which detaches electrons from atoms or molecules

A

Ionising Radiation

52
Q

which tissues are sensitive to carcinogenic effects of ionising radiation

A

thyroid, bone, breast, haematopoetic tissue

53
Q

name a bacteria carcinogen

A

Helicobacter Pylori

54
Q

what is Helicobacter Pylori linked with

A

Gastric adenocarcinomas and some lymphomas
They releases toxins which activate oncoproteins such as CagA at SHP2 binding site

55
Q

what Hormones are carcinogens

A

excess oestrogen (linked to excess adipose tissue)
anabolic steroids
growth hormones IGF1

56
Q

Is age a factor in tumour development?

A

Older you are the more likely you are to get cancer

57
Q
A
58
Q

does diet impact as a carcinogen. If yes elaborate.

A

Yes.
Obesity - excess adipose tissue means higher levels of growth hormones
Processed meats - Nitrate ->Nitrosameine (chemical carcinogen)
Alcohol - acetaldehyde cause cell damage esp. when paired with smoking

59
Q

Some people have inherited mutations which predispose them to certain types of cancer. which ones.

A

BRCA1, BRCA 2, MEN syndromes (endocrine)

60
Q

what makes cancer cells ‘behave’ badly

A
  • Invasiveness determined by the neoplastic cell
  • Decreased cellular adhesion (become unstuck from eachother)
  • Secretion of proteolytic enzymes(damage surrounding tissue)
  • increased cellular motility (they move around)
61
Q

What is metastasis?

A

The process by which tumour cells get from their site of origin (primary) to another part of the body (secondary)

62
Q

how many steps of metastasis

A

6

63
Q

what are the 6 steps of metastasis

A
  1. detachment
    2.Invasion of surrounding tissue
  2. Intravasation into vessels
  3. Evasion of host cell defenses
  4. Adherence to endothelium else where
  5. Extravasation of cells from vessel into surrounding tissue
64
Q

what are some of the routes of metastasis

A

Haematogenous (by blood)
Lymphatic
Transcoelomic
across a body cavity (ie peritoneum)

First Year med - dundee (41 decks)

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