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CLS > Cancer first half.. > Flashcards

Cancer first half.. Flashcards

1
Q

Difference between well differentiated tumour and a poorly differentiated tumour and prognosis

A

Well differentiated = closely resembles origin ( better)
poorly - little resemblance (worst)
undiff = cells of origin unknown

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2
Q

Name 4 properties of a benign tumour

A

grows by expansion
compresses adjacent tissue
DOES NOT infiltrate
stays at the site of origin

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3
Q

name 4 properties of a malignant tumour

A

expands and infiltrates
compresses and invades adjacent tissue
metastasises in the blood
irregular outline

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4
Q

carcinoma

A

malignant epithelial

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5
Q

adenoma

A

benign epithelial

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6
Q

leiomysarcoma

A

malignant smooth muscle

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7
Q

osteoma

A

benign bone

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8
Q

rhabdomyloma

A

benign striated muscle

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9
Q

lipoma

A

benign adipose

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10
Q

chrondrosarcoma

A

malignant cartilige

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11
Q

tetratomas

A

germ cell 3 laters

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12
Q

embryonal

A

embryogenic blast tissue

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13
Q

how does a benign tumour grow in a solid organ and on epithelial surface

A

1 - expands and compresses grows spherically

2- direction of least resistance , papillary shape

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14
Q

5 properties of malignant tumour

A 
nuclear hyperchromatism 
high nuclear:cytoplasmic ratio 
pleomorphism
high mitotic count 
abnormal mitosis
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15
Q

difference between malignant tumour and dysplasia

A

loss of differentiation is dysplasia differentiation varies in malignant

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16
Q

what is a carcinoma in situ

A

dysplasia in epithelium has signs of a malignant tumour but not invading

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17
Q

describe 3 ways cancers spread

A

1) serosal surfaces
2) lymph - in lumen of lymph, into lymph draining system, proliferate in the subscapularsinus and replace node
3) blood - invade vessel wall and into lumen, get stuck in small capillary and grows (distal metastasis)

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18
Q

name 5 effects of a benign tumour

A 
can metastasise 
pressure on adjacent vital structures
can get stuck in bronchioles 
interfere with endocrine (pituitary)
bleeding
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19
Q

name some common sites of BBM

A

brain, liver, adrenals, bone, lungs

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20
Q

name the 5 ways of diagnosing cancer

A 
tumor marker
history
imaging
physical exam 
biopsy
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21
Q

What do HCG, AFP and PSA detect

A

HCG - trophoblast tumours
AFP - liver and germ cell tumours
PSA - pituitary tumors

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22
Q

3 places you can detect tumour markers

A

csf, blood, urine

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23
Q

what do you asses in histology of a tumour

A

degree of differentiation and how far spread

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24
Q

common cancer cytogenetics test

A

cervical smear - exfoliate top layer

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25
Q

3 things that determine the stage of a tumour

A

if it has metastasised
invasion
size of primary origin

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26
Q

Dukes colorectal staging?

A

A doesn’t pass muscle
B passes
C infiltrate nodes

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27
Q

describe a cells entry back into the cell cycle

A

PDGF and FGF stimulate TFs c-cos c-jun and c-myc. These are all competency factors and immediate early genes. (G1a)
TFs transribe proteins CYCLIN D and EZE which stimulate the cell to go into re entry.
(delayed responce) (G1b)
progression factors finally cause the cell to reenter G1

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28
Q

which cyclins are expressed where in the cell cycle

A

DE in G1 cdk 6 and 4
A in S cdk 2
B in M and G2 cdk 1

29
Q

name 3 things that can activate oncogenes

A

mutation
gene amplification
translocation

30
Q

what are protooncogenes and oncogenes

A
  • protooncogenes any component of the growth signalling cascade
  • oncogenes are protooncogenes that dont need a signal to activate - mutated
31
Q

what do p53 and Rb check

A

TSG. they prevent progression of the cell cycle,
all DNA replicated?
favourable environment?

32
Q

RNA virus tumour 4 types

A

B eccentric core C centric code (90%) D bullet shaped core

A- intracellularly

33
Q

viral genes and what they code for

A

gag - G antigens (core protein )
pol - polmerase (enzymes)
env - envelope
scr - silent

34
Q

describe -ve RNA virus replication

A

1) RNA virus lysis with cell and releases 2 single stranded RNA into virus
2) Reverse transcription of RNA - proviral DNA
3) RNA depredates and used to make new DNA complementary strand. Contains identicle LTRs
4) proviral DNA integrated into cells DNA and transcribed into mRNA (DNA polymerase)
5) viral proteins made
6) proteins and RNA bud off to make new virus particle

35
Q

how does sarcoma and leukaemia virus replicate

A

sarcoma - SRC contains silent oncogene
leukaemia - integrates next to silent human protooncogene. rightward LTR has a strong promoter so protooncogene is expressed

36
Q

name 4 functions of oncogene products (how they cause cancer)

A

hormones - monkey virus makes PDGF which tells all cells to divide
receptors - think theyve got a ligand attached - constant signals to divide
g proteins - GTAase mutation therefor GTP constantly bound
TF switch on cell growth

37
Q

descrive monkeyvirus

A

-in non permissive cells e.g. human can only do early phase
this means early phase proteins e.g. T antigens are produced and the cell can not progress
-in permissive cells e.g. monkey cells can do early and late phase. this means late phase proteins e.g. VP123 can be produced. new virus buds off and cell is lysed

38
Q

two types of DNA virus life cycle

A

lytic- early and late phase. permissive cells. cell lysis

transforming - only early phase, non permissive causes cell to divide

39
Q

how do DNA virus replicate

A

DNA gets transcribed to mRNA then viral proteins made from that

40
Q

how to DNA virus cause cancer

A

early phase viral proteins e,g, E6.

E6 can bind to p53 and Rb and cause them to be inactive therefor no defence against abnormal division

41
Q

what increases a families risk of Rb

A

loss of normal chromosome
loss and reduplicate of abnormal Ch13
mitotic crossing over
inderpendant mutation

= loss of hetrozygosity - usually have 1 mutated 1 norm if lose normal then only have 1 mutated

42
Q

Name 5 characteristics of cancer

A 
disturb cellular arrangements = pain
disturb normal pleomorphism - anaplasia
metastasis - cell heterotopia 
new growth 
invasion adjacent tissue
43
Q

How does the body respond to carcinogens once inhaled

A

phase 1 - makes it more reactive

phase 2 - couples with more water soluble so body can excrete

44
Q

how does the reactivity of a compound relate to how carcinogenic it is

A

unreactive more carcinogenic as, more reactive react quicker so are rid quicker however these persist in cells

45
Q

explain how BP is a carcinogen

A

phase one .. BP —AHH—> BP=o —EH—> HO–BP–OH —–AHH—> O=BP -OH-OH
phase 2 .. detoxified and excreted . conjugated with glutathione, sulfate, glucaronic acid

OR
attracted to e- on G. causes either
1) G - T not C as BP uses one of bonding positions - if in an oncogene can cause cancer
2) induces SOS repair (not always effective so can cause errors and mutations

46
Q

effect of radiation on DNA

A 
DIRECT
- excitation and ionisation electrons causing ions 
- dimerisation of pyramiding in uv 
INDIRECT 
free radical formation
47
Q

name 2 types of cancer that are limited to white peple sun exposed areas

A

squamous and basal cell carcinoma

48
Q

what is XP and symptoms

A

recessive, unusual response to sunlight, loads of freckles, pigmentation abnormalities, skin cancer

49
Q

explain how XP causes cancer

A

uv light causes free rad formation and TT dimers in DNA. These are usually cleaved by endonuclease but XP has definitional endonuclease. This means during dna replication DNA polymerase has to leave a gap in the dna where the TT dimer is. This causes SOS repair which isnt faithful and can cause errors + mutations

50
Q

Name 5 things that can alter apoptosis of a cell

A 
GF levels
GIF environment
secreted growth inhibitors 
intrinsic program of differentation/ apoptosis, 
tumour immune responce
51
Q

name 5 things that a malignant cell must have

A 
insensitivity to antigrowth signals
sensitivity to growth signals 
evading apoptosis 
VEGS new blood vessels growth
tissue evasion and metastasis
52
Q

3 ways a cell evades apoptosis

A

upregs anti apoptotic
downregs apoptotic
loss of func of apoptotic factors

53
Q

what does Wilfs tumour caused by

A

upref of GFs

54
Q

what can breast cancer be caused by

A

increased TK receptors

55
Q

what can cause GI stromal tumours and how do you treat

A 
mutation in TK domain of c-kit.
TK inhibitor (gleevec)
56
Q

non hodgekins lymphonma is caused by?

A

B cells and T ells

57
Q

Name the 2 main types of hodgekins lymphoma

A 
nodular lymphocyte (good)
neoplastic cells - classic hodge
58
Q 
describe...
nodular sclerosing 
lymphocyte depleted
lymphocyte rich 
mixed cellularity
A

1 - RS and lymph equal (diff architecture)
2 - more RS low LYMPH
3- low RS more LYMPH
4 - RS and lymph equal

59
Q

describe embryonal tumour

A

blast tissue remnants. increased likely young children, highly malignant, can spread early by lymph and vv

60
Q

where is a neuroblastoma

A

adrenal gland

61
Q

whats special about a astrocytoma

A

its malignant but does not metastasise as cant adhere to any other body surfaces

62
Q

describe the two types of tetroma

A

OVIAN - young woman - cysys. contains keratin . good prognosis
TESTIS - young men. painless swelling of testes, malignant . can use tumour markers and tests

63
Q

describe variable expression

A

mutation in a single cancer gene can predispose to loads of diff tumours

64
Q

describe age related penetrance

A

takes time for individual to accumulate ‘hits’

65
Q

name 2 genes and cancers that are caused by mutations in protoncogenes

A

MET - hereditory papillary renal carcinoma

RET - multiple endocrine neoplasia

66
Q

name 2 cancers that are caused by TS gene mutation

A

breast and ovarian BRCA1 BRCA2

APC 0 FAP

67
Q

what are genes hMLH1

A

mutator genes, held repair DNA if get a mutation

68
Q

outcome of being a high AHH inducer

A

high risk induce - diol made quicker, increase chances of it binding to dna

CLS (17 decks)

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