Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cancer Biology and Therapy > Hallmarks of Cancer 1,2,3 > Flashcards

Hallmarks of Cancer 1,2,3 Flashcards

You may prefer our related Brainscape-certified flashcards:
AP® Biology flashcards Biology 101 flashcards
1
Q

normal cell division is _____

A

controlled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

cancer is a ______ process

A

multistep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do cancer cells develop characteristics to do?

A

move from the primary mass to around the body- metastasise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

metastasis- aggressive and hard to control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

most common cancer in men? women?

A

men- prostate

women- breast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

6 hallmarks of cancer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

TME is highly ________. meaning?

A

interconnected

cross talk between lots of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

examples of non cancer cells in the ME?

A

endothelial cells
fibroblasts
immune cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what enables communication in the TME?

A

CYTOKINES

growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

structure and support

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what pH is the TME?

A

acidic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what types of inflammation exist in the TME?

A

pro and anti tumour inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what do IDO positive dendritic cells do?

A

suppress T-cell function and anti-cancer immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

4 additional hallmarks of cancer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

5 steps of cancer from normal to metastatic

A 
normal
hyperplasia (normal cells in excess
carcinoma in situ (localised) 
invasive cancer (surrounding tissue)
metastatic cancer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is a carcinoma?

A

cancer associated changes but staying local

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what happens to the cells at the cancer differentiated stage?

A

cells still resemble normal cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is dedifferentiation in cancer?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what underpins dedifferenciation?

A

DNA changes-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are epigenetic changes?

A

changes that influence gene expression

switch genes on and off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

are epigenetic changes mutations?

A

NO

just changes transcription level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

3 gene classes involved in cancer development

A

oncogenes
TSGs
modifying genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

role of oncogenes

A

GO signal- gain in function

26
Q

TF: oncogenes are recessive

A

false, mainly dominant

27
Q

what are protooncogenes

A

normal genes that mutate to form oncogenes

28
Q

TSGs role

A

loss of function, STOP signal

29
Q

TSGs are dominant or recessive?

A

recessive

30
Q

are modifying genes a gain or loss in function?

A

either

31
Q

phenotypic hallmarks of cancer

A

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

32
Q

TF: most cancers are familial

A

FALSE most are sporadic

33
Q

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

A

true

34
Q

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

A

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

35
Q

signs of retinoblastoma

A

white pupil
squint inflamed eye
enlarged pupil

36
Q

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

A

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

37
Q

so why is sporadic retinoblastoma rare?

A

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

38
Q

what phase of the cell cycle can apoptosis occur?

A

G1

can stop and go into a inhibited phase

39
Q

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

A

pRb

40
Q

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

A

inhibits

stops proliferation

41
Q

what does phosphorylation of pRb do?

A

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

42
Q

how else can pRb be taken away from binding E2F?

A

bound to viral proteins

43
Q

cells which mutate in colon cancer?

A 
APC 
MLH1 and MSH2
N-CAM 
K-ras
p53
44
Q

APC change in colon cancer? function of this gene?

A

LOSS
cell adhesion
cell proliferation

45
Q

K-ras change in colon cancer? gene function?

A

GAIN

oncogene

46
Q

N-CAM change in colon cancer? gene function?

A

loss

cell adhesion

47
Q

p-53 change in colon cancer? gene function?

A

LOSS

DNA damage réponse, apoptosis

48
Q

MSH2 MLH1 change in colon cancer? gene function?

A

loss

DNA repair

49
Q

APC in normal cells?

A

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

50
Q

APC in tumour cells?

A

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

51
Q

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

A

false- it does

receptors on surface which respond to signals outside the cells

52
Q

2 pathways off the TK receptor?

A

MAPK

PI3K-AKT

53
Q

MAPK and PI3K pathways are drivers of?

A

proliferation

54
Q

PTEN effects on PI3K

A

PTEN is a TSG which puts the breaks on PI3K

55
Q

effects of K-RAS changes?

A

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

56
Q

p53 has an active response to?

A

DNA damage

57
Q

what 2 things do p53 do after DNA damage?

A
  1. stop transition from G1-S phase- allows time for DNA repair
  2. apoptosis activation
58
Q

p53 is lost in ____% of tumours

A

50

59
Q

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

A

INCREASES

60
Q

What is mismatch repair? what can mutations do to this?

which genes does this involve?

A

removes incorrectly matched base pairs in the new strand of DNA upon replication

mutations: loss of function of mismatch repair proteins

MSH2 and MLH1

Cancer Biology and Therapy (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions