Brainscape's Knowledge GenomeTM

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


See full index

Principles Of Disease Year 1 > Cancer > Flashcards

Cancer Flashcards

1
Q

What is the ectoderm?

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

What is the ectoderm?

A

Outer most layer of cells including the epidermis and nerve tissue

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

What is the endoderm ?

A

The innermost layer of tissue and cells often form a the lining of gut

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

What is the middle layer of tissue called?

A

Mesoderm

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

What are the type of cancer cells?

A

Glandular - breast
Epithelial - squamous
Mesoderm - bone and muscle

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

What are adenocarcinomas?

A

Glandular cancers

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

What are sarcomas?

A

Mesoderm cell cancer

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

What are carcinomas?

A

Epithelial cell cancers

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

How does invasion and metastasis allow for cancer cell growth?

A

Able to migrate to different areas and metastasis due to lack of cell to cell adhesison

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

How do cancer cells survive?

A

Evade growth signals
Avoid immune destruction
They have unlimited replication potential
They promote inflammation
Evades cell death
Angiogenesis
Frequent mutation
Reprogrammed metabolism
Increased growth factors
Invade and metastasis

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

How do cancer cells continually get growth factors?

A

They sustain proliferative signals by bypassing normal growth factor pathways

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

How do cancer cells avoid growth signals?

A

They use gene silencing to ignore the homeostatic mechanisms

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

What is gene silencing?

A

Interruptiom of a gene at transcriptional levels

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

How do cancer cells avoid immune destruction?

A

They hijack the immune checkpoint
They modulate STING

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

What is STING?

A

It’s an important signalling molecule which is important in controlling the transcription of body defence genes

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

What is an immune checkpoint?

A

Mechanism that maintains self tolerance during an immune response

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

What is PDL1 and PDL2?

A

Programme cell death protein
They surpress the adaptive immune system during pregnancy or autoimmune diseases
Give the opportunity for cancer to invade the immune system

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

What is a telomere?

A

The end of chromosomes

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

How do cancer cells survive using their replicative potential?

A

Telomeres normally decide when the cell has reached the normal number of divisions and causes the cell to enter senescencebut cancer cells don’t shorten their chromosomes after fission

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

How does tumour promoting inflammation help the cancer survive?

A

Inflammatory cells release growth factors which stimulate cancer cell growth, This creates new blood vessels for the cancer.

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

How does necrosis benefit cancer cells?

A

Necrosiss causes inflammation and releases bioactive regulatory factors which stimulates viable cells to proliferate
Radical oxygen speciesrae released by inflammatory cells which increases the risk of mutation

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

How does angiogenesis help cancer cells?

A

New route for nutrients to reach cancer but also for cancer to metastasis

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

What does caspases do?

A

Triggers apoptosis
Mutation in the gene allow cancer cells to go unchecked and continue growing

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

All mutations are somatic.
True or false

A

False
Most are somatic so DNA in cells is damaged due to an acquired muatation
Only egg or sperm mutations are inherited this u a germline mutation

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

What is haploinsufficiency ?

A

Only 1 of the mutated alleles can lead to cancer rather than two.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the basemnte membrane made of?

A

Extracellular matrix proteins
Which are proteoglycans and collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the seed and soil theory?

A

Cancer spreads via cell surface by providing an ideal microbe environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is E cadherin?

A

Type of calcium dependant CAM involved in epithelial cell adhesion
Often epithelial cancers down regulate or mutate e cadherin

29
Q

What does sub clonal mean?

A

They are genetically identical but differed by mutations

30
Q

What are the 2 types of mechanism of metastasis?

A

Monoclonal or polyclonal

31
Q

What are the 2 patterns of metastasis?

A

Linear or Branched

32
Q

What are epithelial mesenchymal transition?

A

When epithelial cells become independent mesenchymal cells with the ability to move and invade their local environment.
Loss of cell polarity destroys cell junctions, alongside this there is a down regulation of e chadherin

33
Q

What are the 5 steps of metastais?

A

Invasion
Intravasation
Transport
Extravasation
Colonisation

34
Q

What is invasion?

A

Entry into ECM
Mutations in cadherins which are glycoprotein
Integrins enable cells to become mobile by modifying membrane distribution so the cell can leave the ECM
Protease can degrade components of the ECM

35
Q

What are mesenchymal cells?

A

Typically stem cells in the bone marrow

36
Q

Where does EMT happen?

A

Embryogenesis
Cancer

37
Q

All cells in the tumour have the ability to metastasis
True or false

A

False
Tumour stroma

38
Q

What are integrins?

A

-Modify membrane distribution here allow cells to break free

39
Q

How do protease help in metastasis?

A

Degrade components of ECM

40
Q

What is intravasation?

A

Entry into blood or lymph

41
Q

What is the stoma side of the basal membrane ?

A

The side which faces the ECM and blood vessels

42
Q

What is autocrine stimulation?

A

Cells which release their own growth factors to combine with the cell surface proteins like sarcomas

43
Q

How does intravasation happen?

A

Protease enzyme breaks down the basement membranes hence enabling tumour cells to pass between endothelial cells And into the bloodstream

44
Q

What is transendothelial migration?

A

Movement of tumour cells into the bloodstream

45
Q

What is transport?

A

Circulating tumor cells travelling unidirectionally
And infect the first organ they reach

46
Q

What is the first pass organ?

A

The first organ that CTCs in the bloodstream reach after leaving the primary tumor

47
Q

What is extravasation?

A

It’s how tumor cells leave the blood into new organs
E selectin binds the cancer cell to the endothelium
Transendothelial migration
The basement membrane degrades

48
Q

What is colonisation.

A

Cells can spread and remain dormant till they reach favourable conditions to colonies taking into account blood vessels and nutrients

49
Q

What is micrometastases?

A

When cancer cells spread around the body but are dormant because of unfavorable condition or kept at bay by the immune system

50
Q

What is sprouting?

A

Growth of endothelial cells using a balance of inhibitor and inducer factors (angiogenesis switch)

51
Q

What is chemotherapy?

A

Chemicals which target DNA RNA and proteins
Forces cell to undergo apoptosis
Non specific to cancer cells

52
Q

How is chemotherapy delivered?

A

Orally or using IV
Done in cycles (frequency of administration)

53
Q

What 3 settings can chemotherapy be given?

A

Neoadjuvant
Adjuvant
Disease Control Palliative

54
Q

What is neoadjuvant?

A

Before surgery with the aim to reduce cancer aigns

55
Q

What is adjuvant?

A

Reduce risk of cancer returning

56
Q

What is disease control palliative?

A

Control the disease for as long as possible

57
Q

What are the 3 types of chemotherapy?

A

Alkylating agents and pt drugs?
Antimetabolites
Organic drugs

58
Q

What is an alkylating agent and pt drugs?

A

Blocks DNA replication
Create cross links hence change the structure of the DNA helix
All phases of cell cycle

59
Q

What are the 3 organic drugs?

A

Vince alkaloids
Taxanes
Anthracyclines

60
Q

What are antimetabolites?

A

Structurally mimic essential molecules requires so it blocks the enzyme and doesn’t cause cell division
Act on S and G phase

61
Q

What do vinca alkaloids do?

A

Bind to tubulin to prevent formation of mitotic spindle

62
Q

What are taxanes?

A

Prevent tubulin polymerisation hence prevents mititic spindle formation

63
Q

What do anthracyclines do?

A

Inhibits an enzyme for mitotic torsion

64
Q

What are personalised systemic therapies?

A
65
Q

What are hormonal therapies?

A

Oestrogen plays a key role in increasing cellular replication hence a greater chance of mutation
We are targeting these hormones by blocking them or preventing their formation

66
Q

How does tamoxifen work?

A

Binds to oestrogen receptors

67
Q

What are the types of organic drugs?

A

Vinca alkaloids
Taxanes
Anthracyclines

68
Q

What is the most common side effects of chemo?

A

Nausea

69
Q

What are the personal system therapies?

A

Hormonal therapies
Targeted therapies
Immunotherapies

Principles Of Disease Year 1 (16 decks)

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