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PM3B copy (dvw) > (PM3B) Introduction to Cancer > Flashcards

(PM3B) Introduction to Cancer Flashcards

1
Q

What features do all cancers share?

A

Uncontrolled cell growth + invasion

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2
Q

How are cancers classified?

A

Usually based on:

(1) Where the cancer arises in the body

(2) The type of cell affected

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3
Q

What is cancer of epithelial tissue?

A

Carcinoma

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4
Q

What is cancer of connective tissue?

A

Sarcoma

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5
Q

What is cancer of bone marrow?

A

(1) Myeloma – plasma cells

(2) Leukaemia – RBCs + WBCs

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6
Q

What is cancer of the lymph nodes or glands?

A

Lymphoma

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7
Q

What does the suffix ‘oma’ refer to?

A

Benign tumours

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8
Q

What does the prefix adeno- mean?

A

Of a gland

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9
Q

What does the prefix chondro- mean?

A

Of cartilage

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10
Q

What does the prefix erythro- mean?

A

Of RBCs

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11
Q

What does the prefix hemangio- mean?

A

Of the blood vessels

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12
Q

What does the prefix hepato- mean?

A

Of the liver

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13
Q

What does the prefix lipo- mean?

A

Of the fat

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14
Q

What does the prefix lympho- mean?

A

Of the lymph nodes

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15
Q

What does the prefix melano- mean?

A

Of the pigment cells (melanocytes)

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16
Q

What does the prefix myelo- mean?

A

Of the bone marrow

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17
Q

What does the prefix myo- mean?

A

Of the muscle

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18
Q

What does the prefix osteo- mean?

A

Of the bone

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19
Q

Name some of the cancers with the best prognosis.

A

(1) Nonmelanoma of the skin

(2) Prostate

(3) Testis

(4) Melanoma

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20
Q

What does neoplasm mean?

A

A new disorganised growth

Excessive + uncontrolled growth

Synonymous with tumour

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21
Q

What is a tumour?

A

An abnormal mass of cells

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22
Q

What are benign tumours?

A

Enlarge but do not spread beyond their initial site

Do not invade surrounding tissues

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23
Q

What are malignant tumours?

A

Spread beyond their initial site

Can be very dangerous

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24
Q

What is metastasis?

A

Invasion of tumour to surrounding tissue

Spread beyond initial site

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25
Q

What is carcinogenesis?

A

Process of forming a cancer

via carcinogens

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26
Q

What are the stages of tumorigenesis?

A

(1) Normal tissue

(2) Initiated tumour growth

(3) Mild tumour growth

(4) Moderate tumour growth

(5) Severe tumour growth

(6) Carcinoma in situ

(7) Cancer

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27
Q

What are the phases of the cell cycle?

A

(1) M Phase – mitosis + cytokinesis

(2) GAP 0 –resting cells

(3) GAP 1 – RNA + protein synthesis required for S phase

(4) S Phase – DNA synthesis

(5) GAP 2 – RNA + protein synthesis required for M phase

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28
Q

What stages are included in the M phase?

A

(1) Prophase

(2) Metaphase

(3) Anaphase

(4) Telophase

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29
Q

What are the stages of mitosis?

A

(1) Prophase

(2) Metaphase

(3) Anaphase

(4) Telophase

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30
Q

What is prophase?

A

Stage of mitosis (M Phase)

(1) Chromosomes condense

(2) Centrosomes assemble

(3) Nuclear membrane begins to break down

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31
Q

What is metaphase?

A

Stage of mitosis (M Phase)

(1) Chromosomes align and attach to spindle

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32
Q

What is anaphase?

A

Stage of mitosis (M Phase)

(1) Chromotids pull apart and migrate to poles

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33
Q

What is telophase?

A

Stage of mitosis (M Phase)

(1) Chromotids de-condense

(2) New nuclear membrane forms

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34
Q

What is cytokinesis?

A

Stage of mitosis (M Phase)

(1) Nuclear membrane completely surrounds decondensed chromosomes

(2) Contractile ring pinches off

(3) Divides cytoplasm of mother and daughter cells

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35
Q

When is the cell cycle regulated?

A

Midpoint of GAP 1 (G1) phase

By extracellular signals

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36
Q

How is the cell cycle regulated?

A

Extracellular signals

In the GAP 1 (G1) phase

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37
Q

What are the cell cycle checkpoints?

A

(1) M Phase – anaphase – blocked if chromatids are not correctly assembled on mitotic spindle

(2) Late GAP1 (G1) Phase – DNA damage checkpoint – entrance to S phase is blocked if genome is damaged

(3) Mid S Phase: DNA damage checkpoint – DNA replication is halted if genome is damaged

(4) Late GAP 2 (G2) Phase – entrance into M Phase is blocked if replication is not complete

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38
Q

What protein complex is required to progress to S phase from GAP 1 (G1)?

A

D-CDK4/6

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39
Q

What protein complex is required to progress to GAP 2 (G2) phase from S Phase?

A

A-CDC2

40
Q

What protein complex is required to progress to M Phase from GAP 2 (G2) Phase?

A

B-CDC2

41
Q

Which stage of the cell cycle can be influenced by extracellular signals?

A

GAP 1 – G1 phase

42
Q

What role does cyclin play in the cell cycle?

A

Regulation relies on cyclin and cyclin-dependent kinases

43
Q

Which factors control regulatory cyclin expression?

A

(1) E2F transcription factors

(2) pRB proteins

44
Q

Which factors control regulatory cyclin CDK complexes?

A

Phosophorylation + dephosphorylation by other cyclin-dependent kinases

45
Q

How can cyclin-dependent complexes be inhibited?

A

Directly inhibited by cyclin-dependent kinase inhibitors

e.g. protein 27 (p27)

46
Q

Who established the hallmarks of cancer?

A

Robert Weinberg

47
Q

What are the hallmarks of cancer?

A

(1) Sustaining proliferative signalling

(2) Evading growth suppressors

(3) Activating invasion + metastasis

(4) Enabling replicative immortality

(5) Inducing angiogenesis (development of new blood vessels)

(6) Resisting cell death (apoptosis)

48
Q

How do cancer cells gain growth factor independence?

A

Gain an oncogene, lose necessity for external growth factors

Can be in a number of ways:
(1) Secretion of growth factor normally secreted by surrounding tissue

(2) Mutation in growth factor receptor so it is constantly activated

(3) Mutation of components of signalling pathways

(4) Mutation of transcription factors activated by growth factors

49
Q

What is an oncogene?

A

Genes which, when mutated or overexpressed, can cause cancer

Mutations in proto-oncogenes lead to a gain of function

Often involved in the regulation of cell proliferation

50
Q

How can oncogenes lead to a potential gain in function?

A

Mutations in proto-oncogenes lead to a gain of function

51
Q

Give an example of a proto-oncogene.

A

Ras

52
Q

What role does Ras play in cell proliferation?

A

(1) In presence of growth factors is activated

(2) Triggers other signalling events

(3) Signalling events lead to cell proliferation

53
Q

Give some examples of oncogenes, other than Ras.

A

(1) Bcr-Abl

(2) Myc

(3) Src

(4) PI3 kinase

54
Q

What is HER2?

A

Human epidermal growth factor receptor 2

55
Q

What can be said about HER2 positive cancers?

A

Typically more aggressive

Associated with early progression + recurrence + poor prognosis

56
Q

Name an inhibitor of HER2.

A

Trastuzumab (Herceptin)

57
Q

What is trastuzumab?

A

Herceptin

Inhibitor of HER2

58
Q

How may cell insensitivity to growth inhibitors arise?

A

Result from alterations in cell cycle regulation
- Loss of tumour suppression genes
- Upregulation of positive cell cycle regulators, e.g. cyclins

59
Q

How many ‘hits’ are typically required to inactivate a tumour suppressor gene?

A

2 hits

60
Q

Name some examples of tumour suppressor genes.

A

(1) pRB

(2) p53

(3) BRCA

61
Q

How do tumour suppressor genes function?

A

Detection of DNA damage + mutations

Triggers apoptosis or DNA repair

62
Q

What is the most common human mutated gene in cancer?

A

Protein53

p53

63
Q

What signalling roles does p53 have in the body?

A

(1) Cell cycle arrest

(2) DNA repair

(3) Block of angiogenesis

(4) Apoptosis

64
Q

What shortens with every cell division?

A

Telomere

65
Q

Why can cells only proliferate 40-60 times?

A

Telomere length shortens

66
Q

In which cell types do telomeres not shorten, following proliferation?

A

(1) Stem cells

(2) Cancers

67
Q

Why does the telomere of a cancerous cell not shorten?

A

Rebuild telomeres

Using telomerase

68
Q

Which mechanism do radiotherapy and chemotherapy exploit to kill cancer cells?

A

Apoptosis

69
Q

How are cancer cells able to avoid apoptosis?

A

(1) Gain of function (over-expression) of pro-survival factors (i.e. IGF)

(2) Loss of function of pro-apoptotic factors (i.e. p53)

70
Q

Give an example of a pro-apoptotic factor.

A

p53

Protein53

71
Q

How does IGF1 promote cancer development?

A

(1) Inhibits apoptosis

(2) Stimulates cell proliferation

72
Q

Which types of cancer may be more resistant to therapy?

A

Cancers which are able to avoid apoptosis

73
Q

What keeps tumours small initially?

A

Lack of blood supply

74
Q

How do cancer cells promote blood vessel growth (angiogenesis)?

A

Secretion of angiogenic factors

e.g. Vascular Endothelial Growth Factor (VEGF)

(OR)

Fibroblast growth Factor (FGF)

75
Q

How do cancer cells reach the blood supply?

A

‘Crawl’

Through the extracellular matrix (ECM)

76
Q

What are some potentially emerging hallmarks of cancer?

A

(1) Deregulating cellular energetic

(2) Avoiding immune destruction

(3) Genome stability + mutation

(4) Tumour-promoting inflammation

77
Q

What are some ways that cancer is able to kill?

A

(1) Muscle wasting

(2) Interferes with metabolic processes

(3) Interferes with normal organ function

78
Q

What are some ways that cancer interferes with normal organ function?

A

(1) Blockage/ obstruction

(2) Deprivation of nutrients

(3) Pressure

79
Q

What are some ways that cancer interferes with metabolic processes?

A

(1) Malnutrition

(2) Calcium changes

(3) Liver enzyme function

(4) Production of blood cells

(5) Hormone production

80
Q

What is the Knudson hypothesis?

A

That cancer is the result of an accumulation of mutations to DNA of a cell

81
Q

Which hallmarks does a cell need to meet to progress to cancer?

A

Most/ all of the hallmarks

82
Q

Which key types of gene, that when mutated, can lead to cancer?

A

(1) Proto-oncogenes

(2) Tumour suppressor genes

83
Q

What are the nucleotide base pairs?

A

Cytosine–Guanine (3 bonds)

Thymine–Adenine (2 bonds)

84
Q

What types of mutation can occur in a cell?

A

(1) Point mutations or small insertions/deletions in gene coding regions

(2) Alterations in transcription/splicing

(3) Amplifications/deletions of chromosomal regions

(4) Chromosomal translocations

(5) Gains and losses of whole chromosomes

(6) Changes in DNA modification, e.g. DNA methylation

85
Q

What are some potential causes of mutations?

A

(1) UV/ radiation

(2) Free radicals from metabolic processes

(3) Viruses

(4) Chemicals – smoking/ asbestos etc

(5) Copying/ repair errors (inheritable)

86
Q

What are the stages in cancer development?

A

(1) Initiation –first mutations promoting proliferation (carcinogenesis)

(2) Promotion – additional mutations promote further proliferation (carcinogenesis)

(3) Tumour progression – growth + invasion of tumour

87
Q

What is carcinogenesis?

A

First 2 stages of cancer progression

Initiation + promotion

88
Q

Why is identification of tumour progression important?

A

Determination of treatment + prognosis

89
Q

What are the stages that cancer tumours are put into?

A

(1) Stages 1-4

(2) TNM scheme

90
Q

What is the TNM scheme?

A

(1) T = Tumour –how far the tumour has grown locally; score 1-4

(2) N = Nodes – is there any invasion to lymph nodes; score 0-2

(3) Metastasis – has the tumour spread to distant sites; score 0 or 1

91
Q

Which organs have the lowest survival rates in cancer development?

A

(1) Pancreas

(2) Lung

(3) Oesophagus

92
Q

Why are cancer survival rates improving?

A

Earlier diagnosis due to:
- Screening
- Scanning
- Biomarkers

Better treatment due to:
- Surgery
- Radiotherapy
- Chemotherapy

93
Q

Name some cancers that can be self-checked for early diagnosis.

A

(1) Breast cancer

(2) Skin cancer

(3) Testicular cancer

94
Q

What are some current NHS screening programmes?

A

(1) Bowel cancer (60-75yrs old)

(2) Cervical cancer (25-65yrs old women)

(3) Breast cancer (50-70yrs old women)

95
Q

What are some risk factors for cancer?

A

(1) Smoking

(2) Alcohol

(3) Obesity

(4) Inactivity

(5) Poor diet

(6) Infections – cause 18% of cancers globally

PM3B copy (dvw) (31 decks)

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