(PM3B) Introduction to Cancer Flashcards
1
Q
What features do all cancers share?
A
Uncontrolled cell growth + invasion
2
Q
How are cancers classified?
A
Usually based on:
(1) Where the cancer arises in the body
(2) The type of cell affected
3
Q
What is cancer of epithelial tissue?
A
Carcinoma
4
Q
What is cancer of connective tissue?
A
Sarcoma
5
Q
What is cancer of bone marrow?
A
(1) Myeloma – plasma cells
(2) Leukaemia – RBCs + WBCs
6
Q
What is cancer of the lymph nodes or glands?
A
Lymphoma
7
Q
What does the suffix ‘oma’ refer to?
A
Benign tumours
8
Q
What does the prefix adeno- mean?
A
Of a gland
9
Q
What does the prefix chondro- mean?
A
Of cartilage
10
Q
What does the prefix erythro- mean?
A
Of RBCs
11
Q
What does the prefix hemangio- mean?
A
Of the blood vessels
12
Q
What does the prefix hepato- mean?
A
Of the liver
13
Q
What does the prefix lipo- mean?
A
Of the fat
14
Q
What does the prefix lympho- mean?
A
Of the lymph nodes
15
Q
What does the prefix melano- mean?
A
Of the pigment cells (melanocytes)
16
Q
What does the prefix myelo- mean?
A
Of the bone marrow
17
Q
What does the prefix myo- mean?
A
Of the muscle
18
Q
What does the prefix osteo- mean?
A
Of the bone
19
Q
Name some of the cancers with the best prognosis.
A
(1) Nonmelanoma of the skin
(2) Prostate
(3) Testis
(4) Melanoma
20
Q
What does neoplasm mean?
A
A new disorganised growth
Excessive + uncontrolled growth
Synonymous with tumour
21
Q
What is a tumour?
A
An abnormal mass of cells
22
Q
What are benign tumours?
A
Enlarge but do not spread beyond their initial site
Do not invade surrounding tissues
23
Q
What are malignant tumours?
A
Spread beyond their initial site
Can be very dangerous
24
Q
What is metastasis?
A
Invasion of tumour to surrounding tissue
Spread beyond initial site
25
What is carcinogenesis?
Process of forming a cancer
via carcinogens
26
What are the stages of tumorigenesis?
(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
27
What are the phases of the cell cycle?
(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
28
What stages are included in the M phase?
(1) Prophase
(2) Metaphase
(3) Anaphase
(4) Telophase
29
What are the stages of mitosis?
(1) Prophase
(2) Metaphase
(3) Anaphase
(4) Telophase
30
What is prophase?
Stage of mitosis (M Phase)
(1) Chromosomes condense
(2) Centrosomes assemble
(3) Nuclear membrane begins to break down
31
What is metaphase?
Stage of mitosis (M Phase)
(1) Chromosomes align and attach to spindle
32
What is anaphase?
Stage of mitosis (M Phase)
(1) Chromotids pull apart and migrate to poles
33
What is telophase?
Stage of mitosis (M Phase)
(1) Chromotids de-condense
(2) New nuclear membrane forms
34
What is cytokinesis?
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
35
When is the cell cycle regulated?
Midpoint of GAP 1 (G1) phase
By extracellular signals
36
How is the cell cycle regulated?
Extracellular signals
In the GAP 1 (G1) phase
37
What are the cell cycle checkpoints?
(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
38
What protein complex is required to progress to S phase from GAP 1 (G1)?
D-CDK4/6
39
What protein complex is required to progress to GAP 2 (G2) phase from S Phase?
A-CDC2
40
What protein complex is required to progress to M Phase from GAP 2 (G2) Phase?
B-CDC2
41
Which stage of the cell cycle can be influenced by extracellular signals?
GAP 1 – G1 phase
42
What role does cyclin play in the cell cycle?
Regulation relies on cyclin and cyclin-dependent kinases
43
Which factors control regulatory cyclin expression?
(1) E2F transcription factors
| (2) pRB proteins
44
Which factors control regulatory cyclin CDK complexes?
Phosophorylation + dephosphorylation by other cyclin-dependent kinases
45
How can cyclin-dependent complexes be inhibited?
Directly inhibited by cyclin-dependent kinase inhibitors
e.g. protein 27 (p27)
46
Who established the hallmarks of cancer?
Robert Weinberg
47
What are the hallmarks of cancer?
(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
How do cancer cells gain growth factor independence?
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
What is an oncogene?
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
How can oncogenes lead to a potential gain in function?
Mutations in proto-oncogenes lead to a gain of function
51
Give an example of a proto-oncogene.
Ras
52
What role does Ras play in cell proliferation?
(1) In presence of growth factors is activated
(2) Triggers other signalling events
(3) Signalling events lead to cell proliferation
53
Give some examples of oncogenes, other than Ras.
(1) Bcr-Abl
(2) Myc
(3) Src
(4) PI3 kinase
54
What is HER2?
Human epidermal growth factor receptor 2
55
What can be said about HER2 positive cancers?
Typically more aggressive
Associated with early progression + recurrence + poor prognosis
56
Name an inhibitor of HER2.
Trastuzumab (Herceptin)
57
What is trastuzumab?
Herceptin
Inhibitor of HER2
58
How may cell insensitivity to growth inhibitors arise?
Result from alterations in cell cycle regulation
- Loss of tumour suppression genes
- Upregulation of positive cell cycle regulators, e.g. cyclins
59
How many 'hits' are typically required to inactivate a tumour suppressor gene?
2 hits
60
Name some examples of tumour suppressor genes.
(1) pRB
(2) p53
(3) BRCA
61
How do tumour suppressor genes function?
Detection of DNA damage + mutations
Triggers apoptosis or DNA repair
62
What is the most common human mutated gene in cancer?
Protein53
p53
63
What signalling roles does p53 have in the body?
(1) Cell cycle arrest
(2) DNA repair
(3) Block of angiogenesis
(4) Apoptosis
64
What shortens with every cell division?
Telomere
65
Why can cells only proliferate 40-60 times?
Telomere length shortens
66
In which cell types do telomeres not shorten, following proliferation?
(1) Stem cells
| (2) Cancers
67
Why does the telomere of a cancerous cell not shorten?
Rebuild telomeres
Using telomerase
68
Which mechanism do radiotherapy and chemotherapy exploit to kill cancer cells?
Apoptosis
69
How are cancer cells able to avoid apoptosis?
(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
Give an example of a pro-apoptotic factor.
p53
Protein53
71
How does IGF1 promote cancer development?
(1) Inhibits apoptosis
| (2) Stimulates cell proliferation
72
Which types of cancer may be more resistant to therapy?
Cancers which are able to avoid apoptosis
73
What keeps tumours small initially?
Lack of blood supply
74
How do cancer cells promote blood vessel growth (angiogenesis)?
Secretion of angiogenic factors
e.g. Vascular Endothelial Growth Factor (VEGF)
(OR)
Fibroblast growth Factor (FGF)
75
How do cancer cells reach the blood supply?
'Crawl'
Through the extracellular matrix (ECM)
76
What are some potentially emerging hallmarks of cancer?
(1) Deregulating cellular energetic
(2) Avoiding immune destruction
(3) Genome stability + mutation
(4) Tumour-promoting inflammation
77
What are some ways that cancer is able to kill?
(1) Muscle wasting
(2) Interferes with metabolic processes
(3) Interferes with normal organ function
78
What are some ways that cancer interferes with normal organ function?
(1) Blockage/ obstruction
(2) Deprivation of nutrients
(3) Pressure
79
What are some ways that cancer interferes with metabolic processes?
(1) Malnutrition
(2) Calcium changes
(3) Liver enzyme function
(4) Production of blood cells
(5) Hormone production
80
What is the Knudson hypothesis?
That cancer is the result of an accumulation of mutations to DNA of a cell
81
Which hallmarks does a cell need to meet to progress to cancer?
Most/ all of the hallmarks
82
Which key types of gene, that when mutated, can lead to cancer?
(1) Proto-oncogenes
| (2) Tumour suppressor genes
83
What are the nucleotide base pairs?
Cytosine–Guanine (3 bonds)
Thymine–Adenine (2 bonds)
84
What types of mutation can occur in a cell?
(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
What are some potential causes of mutations?
(1) UV/ radiation
(2) Free radicals from metabolic processes
(3) Viruses
(4) Chemicals – smoking/ asbestos etc
(5) Copying/ repair errors (inheritable)
86
What are the stages in cancer development?
(1) Initiation – first mutations promoting proliferation (carcinogenesis)
(2) Promotion – additional mutations promote further proliferation (carcinogenesis)
(3) Tumour progression – growth + invasion of tumour
87
What is carcinogenesis?
First 2 stages of cancer progression
Initiation + promotion
88
Why is identification of tumour progression important?
Determination of treatment + prognosis
89
What are the stages that cancer tumours are put into?
(1) Stages 1-4
| (2) TNM scheme
90
What is the TNM scheme?
(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
Which organs have the lowest survival rates in cancer development?
(1) Pancreas
(2) Lung
(3) Oesophagus
92
Why are cancer survival rates improving?
Earlier diagnosis due to:
- Screening
- Scanning
- Biomarkers
Better treatment due to:
- Surgery
- Radiotherapy
- Chemotherapy
93
Name some cancers that can be self-checked for early diagnosis.
(1) Breast cancer
(2) Skin cancer
(3) Testicular cancer
94
What are some current NHS screening programmes?
(1) Bowel cancer (60-75yrs old)
(2) Cervical cancer (25-65yrs old women)
(3) Breast cancer (50-70yrs old women)
95
What are some risk factors for cancer?
(1) Smoking
(2) Alcohol
(3) Obesity
(4) Inactivity
(5) Poor diet
(6) Infections – cause 18% of cancers globally
