Hallmarks of Cancer 1,2,3

Question 1

normal cell division is _____

Answer 1

controlled

Question 2

cancer is a ______ process

Answer 2

multistep

Question 3

what do cancer cells develop characteristics to do?

Answer 3

move from the primary mass to around the body- metastasise

Question 4

what types of cancer are the hardest to treat? why?

Answer 4

metastasis- aggressive and hard to control

Question 5

most common cancer in men? women?

Answer 5

men- prostate

women- breast

Question 6

6 hallmarks of cancer?

Answer 6

1: self sufficiency in proliferative growth signals
2: insensitive to growth inhibitory signals
3: evasion of apoptosis
4: limitless replicative potent;l
5: induction of angiogenesis
6: induction of metastasis

Question 7

TME is highly ________. meaning?

Answer 7

interconnected

cross talk between lots of cells

Question 8

examples of non cancer cells in the ME?

Answer 8

endothelial cells
fibroblasts
immune cells

Question 9

what enables communication in the TME?

Answer 9

CYTOKINES

growth factors

Question 10

what is the role of non-cellular solid material in the TME?

Answer 10

structure and support

Question 11

TF: the tumour ME is hypoxic? explain? what does this lead to?

Answer 11

yes, depravation of oxygen. leads to differences in cell characteristic

Question 12

what pH is the TME?

Answer 12

acidic

Question 13

what types of inflammation exist in the TME?

Answer 13

pro and anti tumour inflammation

Question 14

TF: immune cells have help tumour cells evade immune surveillance?

Answer 14

TRUE

Question 15

what do IDO positive dendritic cells do?

Answer 15

suppress T-cell function and anti-cancer immune response

Question 16

4 additional hallmarks of cancer?

Answer 16

evading immune destruction
reprogramming energy metabolism to pro tumour
tumour promoting inflammation
genome instability and mutation

Question 17

5 steps of cancer from normal to metastatic

Answer 17

normal
hyperplasia (normal cells in excess
carcinoma in situ (localised) 
invasive cancer (surrounding tissue)
metastatic cancer

Question 18

what is a carcinoma?

Answer 18

cancer associated changes but staying local

Question 19

what happens to the cells at the cancer differentiated stage?

Answer 19

cells still resemble normal cells.

Question 20

what is dedifferentiation in cancer?

Answer 20

cells differentiate but in cancer the reverse happens so they no longer resemble the tissue

Question 21

what underpins dedifferenciation?

Answer 21

DNA changes-

Question 22

what are epigenetic changes?

Answer 22

changes that influence gene expression

switch genes on and off

Question 23

are epigenetic changes mutations?

Answer 23

NO

just changes transcription level

Question 24

3 gene classes involved in cancer development

Answer 24

oncogenes
TSGs
modifying genes

Question 25

role of oncogenes

Answer 25

GO signal- gain in function

Question 26

TF: oncogenes are recessive

Answer 26

false, mainly dominant

Question 27

what are protooncogenes

Answer 27

normal genes that mutate to form oncogenes

Question 28

TSGs role

Answer 28

loss of function, STOP signal

Question 29

TSGs are dominant or recessive?

Answer 29

recessive

Question 30

are modifying genes a gain or loss in function?

Answer 30

either

Question 31

phenotypic hallmarks of cancer

Answer 31

increased proliferation inappropriate survival/ no apoptosis immortalisation invasion, angiogenesis and metastatis

Question 32

TF: most cancers are familial

Answer 32

FALSE most are sporadic

Question 33

TF: the mutations seen in familial cancers are often the same as in sporadic cancers

Answer 33

true

Question 34

why are you more likely to get cancer if you have it in your family?

Answer 34

familial cancer mutations in one allele that's inherited. therefore you only need one more mutation to get cancer in sporadic you need 2 random mutations

Question 35

signs of retinoblastoma

Answer 35

white pupil squint inflamed eye enlarged pupil

Question 36

if retinoblastoma is inherited how many eyes does it tend to effect vs sporadic onset if familial vs sporadic

Answer 36

both eyes, mutation is in every cell in the body. tends to occur earlier in life

Question 37

so why is sporadic retinoblastoma rare?

Answer 37

you need two random events to occur simultaneously in the same cell. in familial you only need one in any cell as they all possess the single mutant allele

Question 38

what phase of the cell cycle can apoptosis occur?

Answer 38

G1 | can stop and go into a inhibited phase

Question 39

what protein is important in regulating the transition between G1 and S

Answer 39

pRb

Question 40

effect of pRB on G1--> S transition? effect?

Answer 40

inhibits | stops proliferation

Question 41

what does phosphorylation of pRb do?

Answer 41

can no longer bind to E2F. E2F switches on genes which enable G1-S transition therefore phosphorylation. leads to proliferation

Question 42

how else can pRb be taken away from binding E2F?

Answer 42

bound to viral proteins

Question 43

cells which mutate in colon cancer?

Answer 43

``` APC MLH1 and MSH2 N-CAM K-ras p53 ```

Question 44

APC change in colon cancer? function of this gene?

Answer 44

LOSS cell adhesion cell proliferation

Question 45

K-ras change in colon cancer? gene function?

Answer 45

GAIN | oncogene

Question 46

N-CAM change in colon cancer? gene function?

Answer 46

loss | cell adhesion

Question 47

p-53 change in colon cancer? gene function?

Answer 47

LOSS | DNA damage réponse, apoptosis

Question 48

MSH2 MLH1 change in colon cancer? gene function?

Answer 48

loss | DNA repair

Question 49

APC in normal cells?

Answer 49

in a complex consequently there's a degradation of proteins e.g. beta catenin keeps a check on function

Question 50

APC in tumour cells?

Answer 50

cant bind in its complex, meaning B-catenin and other proteins start to function results in gene transcription changes towards metastatic state

Question 51

TF: K-ras doesn't work by signal transduction

Answer 51

false- it does | receptors on surface which respond to signals outside the cells

Question 52

2 pathways off the TK receptor?

Answer 52

MAPK | PI3K-AKT

Question 53

MAPK and PI3K pathways are drivers of?

Answer 53

proliferation

Question 54

PTEN effects on PI3K

Answer 54

PTEN is a TSG which puts the breaks on PI3K

Question 55

effects of K-RAS changes?

Answer 55

mutated becomes hyperactivated- drives MAPK pathway irrespective of TK receptor ligand binding on outside of cell proliferation

Question 56

p53 has an active response to?

Answer 56

DNA damage

Question 57

what 2 things do p53 do after DNA damage?

Answer 57

1. stop transition from G1-S phase- allows time for DNA repair 2. apoptosis activation

Question 58

p53 is lost in ____% of tumours

Answer 58

50

Question 59

the rate of genomic instability and DNA repair deficiencies ______ during carcinogenesis

Answer 59

INCREASES

Question 60

What is mismatch repair? what can mutations do to this? | which genes does this involve?

Answer 60

removes incorrectly matched base pairs in the new strand of DNA upon replication mutations: loss of function of mismatch repair proteins MSH2 and MLH1