W11 Cancer Flashcards

1
Q

what are 4 cancer cell features

A

large nuclei
many dividing cells
variation in shape/size
disorganised arrangement

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

what is the mechanism of cancer cell plasticity

A

-

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

what do cancer cells need to become invasive

A
  • break off from primary tumour -> change cell adhesion molecules + release proteases
  • undergo EMT
  • enter local endothelia’s
  • can form a 2ndary tumour back to epithelial cells (MET)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is EMT

A

changes in cell shape and size from epithelial to mesenchymal

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

what are cells called when they are proliferating

A

epithelial cells

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

what is MET

A

changes in cell shape and size from mesenchymal to epithelial cells

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

what is intravasion

A

mesenchymal cells trying to enter neighbouring tissue

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

what are cancer cells able to bypass

A

normal proliferation controls

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

what is anchorage independent growth

A

doesn’t require a matrix -> can grow in suspension

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

what is density dependent inhibition

A

cell sense contact can stop growth

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

what type of growth are cancer cells

A

anchorage independant

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

what does cancer cell metabolism rely on

A

oxidative phosphorylation + aerobic glycolysis

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

which stages of mitosis do cancer cells bypass

A

G1 to S phase restriction points

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

what are cancer cells conditions that allow for dividing

A

abnormal stress responses

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

what process is limited in cancer cells to allow them to live for longer

A

no apotosis

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

what do cancer cells escape

A

replicative cell senescence

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

why are cancer cells DNA able to last this long

A

telomeres don’t shortern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

which genes are expressed more during cancer cells

A

increased oncogenes

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

what are the 6 most common cancers

A

lung
breast
colon
prostate
stomach
liver

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

what is carcinomas

A

cancer from epithelial cells that cover body surfaces

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

what is sarcomas

A

development of cancer from connective tissues like bones

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

where does lymphomas/leukaemia’s begin

A

cells of lymphatic and blood origin

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

what is blastomas

A

cancer from blasts of embryonic tissue

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

what is osteosarcoma

A

cancer development in growing bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how is osteosarcoma stained
H and E
26
what are symptoms of interest for lymphomas
enlarged lymph nodes + spleen
27
what are the requirements of cancer spreading
- brake off primary tumour - invade local tissue - spread to rest of body via blood vessels or lymph channels
28
what is angiogenesis
growth of blood vessels
29
what is metastasis
entering of cancer cells into bloodstream
30
what do tumour microenvironments do
influence cancer development
31
what does the microenvironment contain
endothelial cells bone marrow cells macrophages monocytes mesenchymal stem cells
32
how do tumour microenvironments promote cancer growth
- communication between tumour cells and stroma - stroma provides framework for tumour - during carcinoma cells secrete signal proteins for stromal cells - stomal cells will turn on tumour cells
33
how is angiogenesis regulated
endogenous angiogenesis inhibitors
34
what are the 2 main activators of angiogenesis
basic fibroblast GF (VEGF) vascular endothelial GF (FGF)
35
what are the 3 main inhibitors of angiogenesis
angiostatin endostatin thrombospondin
36
what does cell invasion rely on
cell adhesion changes increased motility protease production
37
what happens to cancer cells when they undergo metastasis
intravascular growth and adhesion to organ membrane
38
what are the 3 internal causes of cancer
oncogene activation TSG loss UV radiation
39
what is lung cancer linked to
asbestos
40
how does benzidine cause cancer
metabolise in liver can cause bladder cancer
41
what do cancer cells do to DNA
crosslinks between 2 strands of double helix causing breaks in DNA strands
42
what cancer does the HPV cause
cervical cancer
43
which bacteria's cause liver cancer
hepatitis B/C
44
what cancers can UV radiation cause
melanoma + carcinomas
45
what is changed in oncogenes to cause cancer
change in the Ras protein
46
how can oncogenes be activated
Point mutation Gene amplification Chromosomal translocation Local DNA rearrangements Insertional mutagenesis
47
what can chromosomal translocation lead to
increased oncogene expression fusion proteins
48
what is Burkitt's lymphoma caused by
chromosomal translocation affecting B lymphocytes
49
what are 3 mutations that disrupt proto-oncogenes
insertions deletions inversions
50
what is insertional mutagenesis
viral DNA integrated into host chromosome stimulate expression of proto-oncogenes for too much proteins
51
what are proto-oncogenes
genes that control cell growth
52
how many human oncogenes are there
224-246
53
what are the 6 categories of oncogenes
growth factors receptors GTP-binding proteins non-receptor kinases transcription factors apoptosis/cell cycle regulators
54
what do cell hybridization experiments do
supress malignancy by cell fusion
55
what does the Rb gene do
regulates progression of G1/S phase
56
where are Rb genes found
retinoblastomas
57
which is the most commonly mutated TSG and its job
p53 -> responds to DNA damage to trigger apoptosis
58
where are BRCA1/2 expressed
in breast
59
what are the jobs of BRCA1/2
repair DDSB
60
what are screening techs used for cancer
biopsy + pathology
61
what are 3 treatments of cancer
surgery radio therapy chemo
62
what do antimetabolites do as a chemo drug
inhibit DNA synthesis
63
what do alkylating agents/antibiotics do as a chemo drug
inhibit DNA function
64
what do plant derived drugs do as a chemo drug
block specific cell cycle progressions
65
what is hyperthermia treatment
using high temps to kill cancer cells
66
what is photodynamic therapy
treatment using photosensitizing agents
67
what does herceptin do
binds and deactivates HER-2 GF
68
how does inhibiting CTLA4 stop tumours
more activation of T cells to attack cancer cells
69
what is ipilimumab (anti-CTL4) used on
metastatic melanoma
70
where are PD-1 receptors expressed
cell surface of TILs
71
what is the oncolytic virus for
immunotherapy -> thrive in cancer cells to break open tumour cells
72
what does imatinib do
treats chronic myelogenous leukaemia (CML)
73
what does the inhibition of BRAF and MEK do
activates MAPK pathway
74
when is adjuvant therapy used
after primary treatments are used