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Cell Biology > W11 Cancer > Flashcards

W11 Cancer Flashcards

1
Q

what are 4 cancer cell features

A

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

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2
Q

what is the mechanism of cancer cell plasticity

A

-

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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)
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4
Q

what is EMT

A

changes in cell shape and size from epithelial to mesenchymal

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5
Q

what are cells called when they are proliferating

A

epithelial cells

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6
Q

what is MET

A

changes in cell shape and size from mesenchymal to epithelial cells

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7
Q

what is intravasion

A

mesenchymal cells trying to enter neighbouring tissue

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8
Q

what are cancer cells able to bypass

A

normal proliferation controls

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9
Q

what is anchorage independent growth

A

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

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10
Q

what is density dependent inhibition

A

cell sense contact can stop growth

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11
Q

what type of growth are cancer cells

A

anchorage independant

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12
Q

what does cancer cell metabolism rely on

A

oxidative phosphorylation + aerobic glycolysis

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13
Q

which stages of mitosis do cancer cells bypass

A

G1 to S phase restriction points

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14
Q

what are cancer cells conditions that allow for dividing

A

abnormal stress responses

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15
Q

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

A

no apotosis

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16
Q

what do cancer cells escape

A

replicative cell senescence

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17
Q

why are cancer cells DNA able to last this long

A

telomeres don’t shortern

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18
Q

which genes are expressed more during cancer cells

A

increased oncogenes

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19
Q

what are the 6 most common cancers

A

lung
breast
colon
prostate
stomach
liver

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20
Q

what is carcinomas

A

cancer from epithelial cells that cover body surfaces

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21
Q

what is sarcomas

A

development of cancer from connective tissues like bones

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22
Q

where does lymphomas/leukaemia’s begin

A

cells of lymphatic and blood origin

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23
Q

what is blastomas

A

cancer from blasts of embryonic tissue

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24
Q

what is osteosarcoma

A

cancer development in growing bones

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25
Q

how is osteosarcoma stained

A

H and E

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26
Q

what are symptoms of interest for lymphomas

A

enlarged lymph nodes + spleen

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27
Q

what are the requirements of cancer spreading

A
  • brake off primary tumour
  • invade local tissue
  • spread to rest of body via blood vessels or lymph channels
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28
Q

what is angiogenesis

A

growth of blood vessels

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29
Q

what is metastasis

A

entering of cancer cells into bloodstream

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30
Q

what do tumour microenvironments do

A

influence cancer development

31
Q

what does the microenvironment contain

A

endothelial cells
bone marrow cells
macrophages
monocytes
mesenchymal stem cells

32
Q

how do tumour microenvironments promote cancer growth

A
  • 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
Q

how is angiogenesis regulated

A

endogenous angiogenesis inhibitors

34
Q

what are the 2 main activators of angiogenesis

A

basic fibroblast GF (VEGF)
vascular endothelial GF (FGF)

35
Q

what are the 3 main inhibitors of angiogenesis

A

angiostatin
endostatin
thrombospondin

36
Q

what does cell invasion rely on

A

cell adhesion changes
increased motility
protease production

37
Q

what happens to cancer cells when they undergo metastasis

A

intravascular growth and adhesion to organ membrane

38
Q

what are the 3 internal causes of cancer

A

oncogene activation
TSG loss
UV radiation

39
Q

what is lung cancer linked to

A

asbestos

40
Q

how does benzidine cause cancer

A

metabolise in liver
can cause bladder cancer

41
Q

what do cancer cells do to DNA

A

crosslinks between 2 strands of double helix causing breaks in DNA strands

42
Q

what cancer does the HPV cause

A

cervical cancer

43
Q

which bacteria’s cause liver cancer

A

hepatitis B/C

44
Q

what cancers can UV radiation cause

A

melanoma + carcinomas

45
Q

what is changed in oncogenes to cause cancer

A

change in the Ras protein

46
Q

how can oncogenes be activated

A

Point mutation
Gene amplification
Chromosomal translocation
Local DNA rearrangements
Insertional mutagenesis

47
Q

what can chromosomal translocation lead to

A

increased oncogene expression
fusion proteins

48
Q

what is Burkitt’s lymphoma caused by

A

chromosomal translocation affecting B lymphocytes

49
Q

what are 3 mutations that disrupt proto-oncogenes

A

insertions
deletions
inversions

50
Q

what is insertional mutagenesis

A

viral DNA integrated into host chromosome
stimulate expression of proto-oncogenes for too much proteins

51
Q

what are proto-oncogenes

A

genes that control cell growth

52
Q

how many human oncogenes are there

A

224-246

53
Q

what are the 6 categories of oncogenes

A

growth factors
receptors
GTP-binding proteins
non-receptor kinases
transcription factors
apoptosis/cell cycle regulators

54
Q

what do cell hybridization experiments do

A

supress malignancy by cell fusion

55
Q

what does the Rb gene do

A

regulates progression of G1/S phase

56
Q

where are Rb genes found

A

retinoblastomas

57
Q

which is the most commonly mutated TSG and its job

A

p53 -> responds to DNA damage to trigger apoptosis

58
Q

where are BRCA1/2 expressed

A

in breast

59
Q

what are the jobs of BRCA1/2

A

repair DDSB

60
Q

what are screening techs used for cancer

A

biopsy + pathology

61
Q

what are 3 treatments of cancer

A

surgery
radio therapy
chemo

62
Q

what do antimetabolites do as a chemo drug

A

inhibit DNA synthesis

63
Q

what do alkylating agents/antibiotics do as a chemo drug

A

inhibit DNA function

64
Q

what do plant derived drugs do as a chemo drug

A

block specific cell cycle progressions

65
Q

what is hyperthermia treatment

A

using high temps to kill cancer cells

66
Q

what is photodynamic therapy

A

treatment using photosensitizing agents

67
Q

what does herceptin do

A

binds and deactivates HER-2 GF

68
Q

how does inhibiting CTLA4 stop tumours

A

more activation of T cells to attack cancer cells

69
Q

what is ipilimumab (anti-CTL4) used on

A

metastatic melanoma

70
Q

where are PD-1 receptors expressed

A

cell surface of TILs

71
Q

what is the oncolytic virus for

A

immunotherapy -> thrive in cancer cells to break open tumour cells

72
Q

what does imatinib do

A

treats chronic myelogenous leukaemia (CML)

73
Q

what does the inhibition of BRAF and MEK do

A

activates MAPK pathway

74
Q

when is adjuvant therapy used

A

after primary treatments are used

Cell Biology (11 decks)

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