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Cancer Flashcards

1
Q

A definition of cancer

A

Cancer is a term used for diseases in which abnormal cells divide without control and are able to invade other tissues. Cancer cells can spread to other parts of the body

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2
Q

Kinds of benign neoplasias

A

Hyperplasia

Metaplasia

Dysplasia

Adenomas/polyps/warts

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3
Q

Hyperplasia

A

Over proliferation of cells that appear otherwise normal

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4
Q

Metaplasia

A

Normal in appearnace but in the wrong place, usual from an adjacent tissue

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5
Q

Dysplasia

A

Cells that appear abnormal; often increased nuclear to cytoplasmic ratio

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6
Q

Adenomas/polyps/warts

A

Larger growths of dysplastic cells

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7
Q

Driver mutations vs Passenger mutations

A

driver mutations do affect function of genes that reegulate proliferation, apoptosis, immortality

Passenger mutations are ones not relevant to promotion of cancer

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8
Q

Function of proto-oncogenes

A

Promote cell proliferation

Gain of function mutations in cancer

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9
Q

Function of tumour supressor genes

A

Inhibit events leading to cancer

Loss of function mutations in cancer

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10
Q

Main characteristics of cancer

A

Proliferation: grow independantly of signals

Immortality: Avoid senescene/telomere shortening

Avoid cell death: Avoid apoptosis

Angiogenesis: They must be fed

Metastasis

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11
Q

At which cell cycle checkpoint do oncogenes work

A

Restriction point

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12
Q

Which two processes normally limit life of cell

A

Senescence: Cells in G0, dont proliferate

Apoptosis: programmed cell death

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13
Q

Define senescence

A
  • Metabolically active, irreversibly lost ability to re-enter cell cycle, stay in G0
  • Normal cells have finite proliferative capcity (Hayflick limit)
  • Cancers must avoid senscence to continue growing
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14
Q

Role of P53 in Telomeres/cancer

A

P53 normally warns about short ends and initiates senescence

Excess telomere shortening leads to crisis and apoptosis

Crisis

  • Normall cells will undergo apoptosis
  • In cancer cells TERT is reactivated; repairs broken ends, but creates faulty chormosomes
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15
Q

Which factor induces angiogenesis

A

Hypoxia-inducible factor 1-alpha is a hypoxia induced factor

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16
Q

Different word for tumour

A

Neoplasia

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17
Q

Define neoplasia

A

An abnormal mass of tissue, the growth which exceeds, and is uncoordinated with, that of normal tissue, and which presents in the same excessive manner after the cessation of the stimulus which has evoked the change

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18
Q

Cancer is colloqial speak for

A

A malignant tumour

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19
Q

Meaning of differntiation in tumours

A

Described how close in appearance the cells of a tumour are to the cell type from which they are derived. Important in predicting likely behaviour of a tumour

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20
Q

Different tumour types based on differentiation

A

Well-differentiated

  • Composed of cells which very closely resemble the cell of origin

Poorly differentiated

  • Bear little resemblance to the cell of origin, but just enought for original cell type to be indentified

Undifferntiated/Anaplastic tumour

  • Composed of cells which are so undifferntiated that cell of origin is unknown
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21
Q

Benign vs Malignant tumours

A

Benign

  • Grow by expansion
  • Compress adjacent tissue
  • DO NOT infiltrate/spread

Malignant

  • Grow by expansion AND INFILTRATION
  • Compress and invade adjacent tissue
  • INFILTRATE
  • Can spread to different sites = metastasis
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22
Q

Define Adenomas

A

Tumour of glandular epithelium

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23
Q

Define Papilloma

A

Tumour of squamous and transitional epithelium

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24
Q

Define Carcinoma

A

A malignant epithelial tumour

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25
Suffix for benign _mesenchymal tumuors_
- OMA e. g. osteoma, lipoma
26
Suffix for malignant mesenchymal tumours
- OSARCOMA e. g. osteosarcoma Liposarcoma
27
Define Teratomas
Tumours derived from ferm cells, containin representatives from all 3 germ layers
28
Difference in benign tumour growth in solid organs vs epithleium
**Solid organs** Expand, compress adjacent tissue. Look circumscribed and give a spherical mass **Epithelial surfaces** Form papillary outgrowths in directino of least resistance=**papilomas**
29
Cytological characteristics of malignancy
* High nucleus to cytoplasm ratio * Pleomorphism * Nuclear hyperchromatism * High mitotic count * Abnormal mitoses
30
Cellular vs nuclear pleomorphism
Variation in size/shape of tumour cells vs Variation in size/shape of nuclei in tumour cells
31
What is a high mitotic count
Increasednumbers of cells in mitosis, including abnormal mitotic forms Indicative of malignancy
32
Define Dysplasia and its causes
Abornam cell structure, due to: * Loss of differntiation * Pleomorphism * Nuclerar hyperchromatism * High nucleus/cytoplasm ratio
33
Carcinoma in-situ
A dysplastic epithelium showing cytological characteristics of malignancy _but no evidence of invasion_
34
Modes od spreak for malignant tumours
**Lymphatics,** transported to node, can proliferate within nodes **Blood stream**, Clumps break off and enter circulation, can cause tumour embolisms and procue a _distant metastasis_
35
Effects/problems from _benign_ tumours
Not alway harmless, can cause illnes and death by: * Bleeding e.g. gut, bladder * Pressure on adjacent vital structures e.g. in brain * Obstruction e.g. in brain, bronchus * Hormone secretion e.g. pituitary adenoma * Conversion to malignant tumour
36
3 Tumour markers
HCG AFP PSA
37
What is the tumour marker HCG indicative of
From tumour cells with trophoblast elements
38
What is the tumour marker alpha feotprotein idicative of?
Liver cancer, germ cell tumours
39
What is tumour marker PSA indicative of
Prostate-specific antigen from carcinoma of prostate
40
How are tumours graded?
* The degree of differntiation of tumour cells realtive to normal tissue of origin * Cariation in size and shape of constituent cells of the tumour (pleomrophism) * The proportion of cells containing mitotic figures (mitotic index)
41
What is considered in TNM staging
Tumour Nodes Metasteses * Based upon extent of local tumour spread, regional lymph node involvment and presence of distant metasteces
42
Which staging system is used in colorectal cancers?
Dukes staging for colorectal cancers
43
Describe stages in Dukes staging
A: Any tumour which does not extend beyond muscularis propria. _no nodal ivolvment_ B: Tumour extends beyond muscle. _no nodal involvment_ C: Any dpeth of tumour, **present in nodes**
44
Tumours with excellent prognosis
Thyroid
45
Tumours with moderate prognosis
Kidney, prostate, cervix, breast
46
Tumours with poor prognosis
Pancreas, brain, oesophagus
47
Define Generation time
Time it takes for acell to double its contents(population doubles in size)
48
Components involves in control of cell cycle/proliferation
* CDKs * Checkpoints * Intrinsic proteins * Tumour supressors
49
Role of CDKs in cell cycle
Have to be bound to cycline for active kinase effect Activation causes progression in cell cycle
50
Role of Intrisic proteins in cell-cycle control
1. Normal: **proto-Oncogenes** * Positive regulators of cell cycle * Promote growth 2. Abnormal: **oncogenes** * **​​**mutated/upregulated * No longer wait fro activating signal
51
Role of tumour supressors in contorlling cell cycle/proliferation
**Normal**: Prevent progression of cell cycle if there are problems with DNA
52
Mode of action fro Tumour supressor pRB
Workst at START checkpoint
53
Mode of action for tumour supressor p53
* Works at p53 * START checkpoint * G/M checkpoint * Detects DNA damage * Perharps repariable(separate pthway) * Extenseive damage; Bax stimulated; apoptosis * Only active if theres a fault * Transient, removed once repair completed
54
Pathway activated if repairable damge recognised by P53 in G/M checkpoint
1. Stimulates p21 CKI 2. Inhibits cyclin E/cdk2 3. Cells arrests at G1/S or G2 4. Gives cell an opportunity to repair DNA/progress to apoptosis
55
What causes Cells to stay in G0
Proliferation inhibited Maintained by TGF-b
56
How do G0 cells re-enter cell cycle
* Need growth factors e.g. PDGF or _fibroblast growth factors_ In 3 stages 1. **Competency**: Immediate early genes * C-jun * C-fos/C-myc: Increase cyclin D1 expression, and decrease degredation 2. **Re-entry:** Delayed response genes * E2F * Cyclin D-CDK4/CDK6, allows progression past START 3. **Progression**
57
What is monitored at G1/S
Size DNA integrity
58
What is monitored at START/restriction point
Favourable enviroment? Mediated by: **pRB & p53**
59
CDK complex involved in S phase
Cyclin A-CDK2 7.5hrs
60
CDK complexes involved in G2
cyclin A-CDK1 cyclin B-CDK1
61
What is monitored at G2/M point
DNA synthesis, succesful? Meidated by **P53**
62
CDK complexes involved in M phase
Cyclin A-CDK1 Cyclin B-CDK1 * Peaks, then has to be completely eradicated to exit M phase * Degradede by proteolysis at M/A poin
63
What is monitored at M/A checkpoint?
Spindle formation
64
65
Which mutations cause *gain of function*
* Overexpression: amplification/regulatory regions change * Point mutations/fusions
66
Which mutations cause *loss-of function*
Point mutation, deletion(frameshift), loss of allele
67
Difference between sporadic and familial retinoblastoma
Sporadic is unilateral Familial is bilateral
68
Inheritence pattern of retinoblastoma
Autosomal Dominant
69
2-hit hypothesis
* Familial tumours due to a single random somatic event * Sporadic tumors require two random somatic events
70
2-hit hypothesis for _retinoblastoma_
* Phenotype of Rb allele is _dominant at the level of the whole organism, one hit_ * However - The phenotype of mutant allele is recessive at cellular level, requirst two hits * Characteristic of TS genes
71
Explain how TS genes are associated with loss of heterozygosity in tumours
72
How do the tumour supressors Rb and P53 act? Cell cycle checkpoints
73
What happens in loss of TS function
Normal: TS porteins detect errors, mediate repair, inhibit replaication or initiate apoptosis Cancer: Loss of TS function means errors not repaired but cell continues to proliferate
74
Prevelance of oncogene mutations in familial cancers
Generally, mutant ocogenes cannot be tolerated in germ line - their action would be dominant * Disrupt normal embryonic development
75
Eaxmple of a deletion oncogene mutation
ErbB: the EGFR with its external domain deleted
76
Example of point mutation oncogene mutation
EGFR - Actiavte kinase activity in non-small cell lung cancer
77
How do translocational oncogene mutations work?
78
Example of oncogene mutation by translocation to an actively transcribing region
79
How does an amplificiation mutation of oncogen work
Tumours end up containing many copies of said gene(100-150 copies) e.g. Myc in neuroblastoma
80
how do carcinogens cause mutations?
* Reaction with free radicals * Mechanisms of mutation, adducts, cross links breaks etc * Increase rate of mutation, DNA breaks or base chnges
81
Li-Fraumeni inheritance and mutation
* Autosomal dominant inheritance * High suceptibility to cancers from early age * Mutations in TP53: Another tumout supressor gene that codes for P53
82
Lifetime risk of breast cancer with BRCA1/BRCA1 genes
60-90%
83
Age groups screened for: Breast Colon Prostate Cervical
Breast: 47-73 Colon: 60-74 Prostate: 50+ Cervical: 25-65
84
Different screening methods for bowel cancer
* Foecal occult blood test * Colonospy, 4-5x more polyps detected than FOBT
85
Mechanisms by which cancer therapies can exert their impact
86
Ways by which chemotherapy work
87
READ CLINICAL CANCER GENETIC LECTURE AND SELF STUDY ON CARCINOGENS
88
Define lymphomas
Neoplastic proliferation of lymphoid cells of various types
89
Two main categories of lymphomas
Hodgkin's and

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