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
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
3
Q
name 4 properties of a malignant tumour
A
expands and infiltrates
compresses and invades adjacent tissue
metastasises in the blood
irregular outline
4
Q
carcinoma
A
malignant epithelial
5
Q
adenoma
A
benign epithelial
6
Q
leiomysarcoma
A
malignant smooth muscle
7
Q
osteoma
A
benign bone
8
Q
rhabdomyloma
A
benign striated muscle
9
Q
lipoma
A
benign adipose
10
Q
chrondrosarcoma
A
malignant cartilige
11
Q
tetratomas
A
germ cell 3 laters
12
Q
embryonal
A
embryogenic blast tissue
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
14
Q
5 properties of malignant tumour
A
nuclear hyperchromatism high nuclear:cytoplasmic ratio pleomorphism high mitotic count abnormal mitosis
15
Q
difference between malignant tumour and dysplasia
A
loss of differentiation is dysplasia differentiation varies in malignant
16
Q
what is a carcinoma in situ
A
dysplasia in epithelium has signs of a malignant tumour but not invading
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)
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
19
Q
name some common sites of BBM
A
brain, liver, adrenals, bone, lungs
20
Q
name the 5 ways of diagnosing cancer
A
tumor marker history imaging physical exam biopsy
21
Q
What do HCG, AFP and PSA detect
A
HCG - trophoblast tumours
AFP - liver and germ cell tumours
PSA - pituitary tumors
22
Q
3 places you can detect tumour markers
A
csf, blood, urine
23
Q
what do you asses in histology of a tumour
A
degree of differentiation and how far spread
24
Q
common cancer cytogenetics test
A
cervical smear - exfoliate top layer
25
3 things that determine the stage of a tumour
if it has metastasised
invasion
size of primary origin
26
Dukes colorectal staging?
A doesn't pass muscle
B passes
C infiltrate nodes
27
describe a cells entry back into the cell cycle
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
28
which cyclins are expressed where in the cell cycle
DE in G1 cdk 6 and 4
A in S cdk 2
B in M and G2 cdk 1
29
name 3 things that can activate oncogenes
mutation
gene amplification
translocation
30
what are protooncogenes and oncogenes
- protooncogenes any component of the growth signalling cascade
- oncogenes are protooncogenes that dont need a signal to activate - mutated
31
what do p53 and Rb check
TSG. they prevent progression of the cell cycle,
all DNA replicated?
favourable environment?
32
RNA virus tumour 4 types
B eccentric core C centric code (90%) D bullet shaped core
| A- intracellularly
33
viral genes and what they code for
gag - G antigens (core protein )
pol - polmerase (enzymes)
env - envelope
scr - silent
34
describe -ve RNA virus replication
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
how does sarcoma and leukaemia virus replicate
sarcoma - SRC contains silent oncogene
leukaemia - integrates next to silent human protooncogene. rightward LTR has a strong promoter so protooncogene is expressed
36
name 4 functions of oncogene products (how they cause cancer)
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
descrive monkeyvirus
-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
two types of DNA virus life cycle
lytic- early and late phase. permissive cells. cell lysis
| transforming - only early phase, non permissive causes cell to divide
39
how do DNA virus replicate
DNA gets transcribed to mRNA then viral proteins made from that
40
how to DNA virus cause cancer
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
what increases a families risk of Rb
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
Name 5 characteristics of cancer
```
disturb cellular arrangements = pain
disturb normal pleomorphism - anaplasia
metastasis - cell heterotopia
new growth
invasion adjacent tissue
```
43
How does the body respond to carcinogens once inhaled
phase 1 - makes it more reactive
| phase 2 - couples with more water soluble so body can excrete
44
how does the reactivity of a compound relate to how carcinogenic it is
unreactive more carcinogenic as, more reactive react quicker so are rid quicker however these persist in cells
45
explain how BP is a carcinogen
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
effect of radiation on DNA
```
DIRECT
- excitation and ionisation electrons causing ions
- dimerisation of pyramiding in uv
INDIRECT
free radical formation
```
47
name 2 types of cancer that are limited to white peple sun exposed areas
squamous and basal cell carcinoma
48
what is XP and symptoms
recessive, unusual response to sunlight, loads of freckles, pigmentation abnormalities, skin cancer
49
explain how XP causes cancer
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
Name 5 things that can alter apoptosis of a cell
```
GF levels
GIF environment
secreted growth inhibitors
intrinsic program of differentation/ apoptosis,
tumour immune responce
```
51
name 5 things that a malignant cell must have
```
insensitivity to antigrowth signals
sensitivity to growth signals
evading apoptosis
VEGS new blood vessels growth
tissue evasion and metastasis
```
52
3 ways a cell evades apoptosis
upregs anti apoptotic
downregs apoptotic
loss of func of apoptotic factors
53
what does Wilfs tumour caused by
upref of GFs
54
what can breast cancer be caused by
increased TK receptors
55
what can cause GI stromal tumours and how do you treat
```
mutation in TK domain of c-kit.
TK inhibitor (gleevec)
```
56
non hodgekins lymphonma is caused by?
B cells and T ells
57
Name the 2 main types of hodgekins lymphoma
```
nodular lymphocyte (good)
neoplastic cells - classic hodge
```
58
```
describe...
nodular sclerosing
lymphocyte depleted
lymphocyte rich
mixed cellularity
```
1 - RS and lymph equal (diff architecture)
2 - more RS low LYMPH
3- low RS more LYMPH
4 - RS and lymph equal
59
describe embryonal tumour
blast tissue remnants. increased likely young children, highly malignant, can spread early by lymph and vv
60
where is a neuroblastoma
adrenal gland
61
whats special about a astrocytoma
its malignant but does not metastasise as cant adhere to any other body surfaces
62
describe the two types of tetroma
OVIAN - young woman - cysys. contains keratin . good prognosis
TESTIS - young men. painless swelling of testes, malignant . can use tumour markers and tests
63
describe variable expression
mutation in a single cancer gene can predispose to loads of diff tumours
64
describe age related penetrance
takes time for individual to accumulate 'hits'
65
name 2 genes and cancers that are caused by mutations in protoncogenes
MET - hereditory papillary renal carcinoma
| RET - multiple endocrine neoplasia
66
name 2 cancers that are caused by TS gene mutation
breast and ovarian BRCA1 BRCA2
| APC 0 FAP
67
what are genes hMLH1
mutator genes, held repair DNA if get a mutation
68
outcome of being a high AHH inducer
high risk induce - diol made quicker, increase chances of it binding to dna
