Week 4 - Cancer Biology Flashcards

1
Q

What is another name for a tumour

A

Neoplasm

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2
Q

Describe the growth of a benign tumour

A

Grows slowly and remains located to the site of origin

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3
Q

Describe the growth of a malignant tumour

A

They grow fast, invade and spread to different sites

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4
Q

Metastasis

A

A multistep process by which tumour cells move form a p to a s site

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5
Q

How does cancer cell morphology differ in cancer cells

A

They have large, variably shaped nuclei

Many dividing cells

Variation in size and shape

Loss of normal features

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6
Q

6 characteristics of cancer

A

Self-sufficiency in growth signals

Insensitivity to growth-inhibitory signals (inactivation of tumour suppressor genes)

Evasion of programmed cell death

Limited replication potential

Sustained angiogenesis (can draw blood supply)

Tissue invasion and metastasis

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7
Q

What are CDKs

A

enzymes

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8
Q

Cells receive which signal to enter the cell cycle

A

Growth factors

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9
Q

What is an oncogene

A

A gene who’s product in involved in inducing cancer

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10
Q

What is a proto-oncogene

A

A normal cellular gene that encodes a protein usually involved in regulation of cell growth/differentiation WHEN MUTATED causes ONCOGENE

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11
Q

Which two main factors cause formation of a tumour

A

Molecules that aree initiate/speed up proliferation are switched on

Molecules that slow down proliferation are switched off

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12
Q

Examples of receptors that when switched on, initiate/speed up proliferation

A

EGFR
HER2
c-Met

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13
Q

Examples of cytoplasmic signalling intermediates (transducers) when switched on, initiate/speed

A

Ras
BRAF
Abl, Src (kinases)

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14
Q

Examples of nuclear molecules when initiated/switched speed proliferation

A

Cyclin D
Myc (transcription factor)
Fos, Jun

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15
Q

Are mutations that cause molecules to initiate/speed up proliferation dominant or recessive

A

Dominant

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16
Q

What can proto-oncogene RAS cause

A

RAS -
NORMALLY
produces G protein that transduces signals from cell surface receptors

WHEN POINT MUTATION
‘Ras’ that is always on - repeated stimulation

e.g 30% of tumours

17
Q

What can proto-oncogene BRAF cause

A

NORMALLY
produces kinase that transduces signals from cell surface receptors

WHEN POINT MUTATION
Hyperactive kinase activity that is ‘on’ all the time

e.g >50% of all melanomas

18
Q

What can proto-oncogene EGFR cause

A

NORMALLY
produces a cell surface receptor that receives an extracellular signal

WHEN DELETION MUTATION
receptor is activated in absence of EGF

e.g non-small cell lung cancer

19
Q

What can ERB B2 (HER2) proto-oncogene cause

A

NORMALLY
Produces HER2

WHEN GENE AMPLIFICATION
More receptors equalling more stimulation

20
Q

What can proto-oncogenes BCR + ABL cause

A

Philadelphia translation causing bcr-abl hybrid gene - causing persistent activated kinase activity

Found in CML

21
Q

2 examples of cancers caused by Rb protein mutations

A

Retinoblastoma
Breast cancer

22
Q

2 examples of mutated p53 protein cancers

A

Brain tumours
Leukaemia

23
Q

Rb tumour supressor- dominant or recessive?

A

Recessive- two copies of mutated genes required for a cell to become cancerous

(germline + somatic)

24
Q

p53 tumour supressor - dominant or recessive?

A

Dominant negative

25
Q

What is the role of BCL-2

A

B-cell lymphoma-2 regulates apoptosis

26
Q

What is different about the BCL-2 gene of cancer cells

A

They have undergone a translocation mutation, causing increased expression of pro-survival BCL-2 proteins

27
Q

What do telomerase enzymes do

A

They add telomeres on which protect chromosome ends

28
Q

In cancer cells, what is different about telomerase enzymes

A

They express more telemorases which prevents chromosomes from shortening and results in limitless replicative potential

29
Q

What is angiogenesis

A

When tumour grows, cells further away from blood vessels receive insufficient nutrition and become hypoxic. This stimulates tumour cells to produce VEGF (vascular endothelial growth factor) which causes vessels to grow towards the tumour

30
Q

What happens to the tight junctions of epithelial tumours

A

They lose epithelial-cadherin which form part of the adherens junction

31
Q

Metastasis is aided by which group of 23 enzymes and what is their function

A

Matrix metalloproteinases (MMPs)

They use these specific enzymes to break through structures such as the basement membrane, which gives cancer cells easier access to blood vessels

32
Q

What does Herceptin target

A

ERBB2 gene (causes b cancer)

33
Q

What does Bevacizumab target

A

VEGF gene (colorectal cancer)

34
Q

Which gene does imatinib target

A

ABL (CML)

35
Q

Venmurafenib targets?

A

BRAF (melanoma)

36
Q
A