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Cancer Flashcards

1
Q

What are polymorphic alleles?

A

More than one allele occupies that genes locus in a population

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2
Q

What are carcinogenesis and tumourigenesis?

A

An interplay between genetics and the environment.

Constant rate of mutation followed by testing for advantage.

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3
Q

What is the Hanahan-Weinberg definition of cancer?

A
  • Capacity to proliferate irrespective of mitogens
  • Unbounded proliferative potential
  • Failure to respond to growth inhibiting signals
  • Resistance to apoptosis
  • Ability to recruit vasculature
  • Ability to invade nearby and distant tissue
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4
Q

What is neoplasm?

A

New growth

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5
Q

What is hyperplasia?

A

Increase in cell number

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6
Q

What is metastasis?

A

Dissemination to give secondary tumours

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7
Q

What is an ectopic tumour?

A

Develops inappropriate capacities

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8
Q

What is a benign tumour?

A
  • Hyperplasia- may be a lump
  • Retains original morphology and functions
  • No infiltration of surrounding tissues
  • Little risk- often encapsulated
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9
Q

What is a malignant tumour?

A
  • Perversion of normal function
  • Odd morphology
  • Abnormal organs
  • Increasingly well adapted to unbounded growth
  • Infiltration
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10
Q

Describe the physical appearance of a cancer cell

A
  • Larger nucleus, denser nucleoli
  • Less cytoplasm
  • Wrong morphology- often more rounded
  • Less contact with neighbours- disordered tissues
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11
Q

Describe the functional characteristics of a cancer cell

A
  • May not need exogenous GFs
  • Insensitive to inhibitory signals- cell division checkpoints fail
  • Evasion of apoptosis- self-rescue
  • Immortal with unlimited replication- no eroded telomeres
  • Invadopodia
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12
Q

What are invadopodia?

A

Actin-rich protrusions of plasma membrane that are associated with degradation of extracellular matrix

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13
Q

What percentage of human genes are cancer genes?

A

1%

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14
Q

What percentage of cancers show somatic mutations (sporadic cancers)?

A

90%

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15
Q

What percentage of cancers are germline mutation (predisposition)?

A

20%

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16
Q

What percentage of cancers have somatic and germline mutations?

A

10%

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17
Q

What are the most and second most common protein domains coded for by cancer genes?

A
  1. Kinases

2. DNA binding

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18
Q

Which three types of gene are targets in causing cancer?

A
  1. Proto-oncogenes (over expression, hyperactive forms)
  2. Tumour suppressor genes (inactivated)
  3. Housekeeping genes (normally protect genome integrity)- most tumours lack one or more DNA repair mechanisms
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19
Q

What are catalytic mutations?

A

Encourage genomic instability and facilitate further mutations
-Especially housekeeping genes

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20
Q

Give two caretaker genes that mutations of cause cancers and name the cancers

A

Rb tumour suppressor- retinoblastoma- childhood eye cancer

p53 tumour suppressor- Li-Fraumeni syndrome

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21
Q

What is haplo insufficiency?

A

When only one copy of the sensitive gene need be mutated as the second is non-functional or can’t compensate

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22
Q

How do polymorphisms affect cancer?

A

They modify responses to carcinogens

Eg. Those that confer susceptibility to cigarette smoke.

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23
Q

Where can cancer cells originate from?

A
  • Stem cells that partially differentiate

* Differentiated cells that partially de-differentiate (stemness)

24
Q

What is the intrinsic cancer forming pathway?

A
  1. Inherited mutation- susceptibility or resistance
  2. Initiation- spontaneous mutation/suppression failure
  3. Promotion- growth advantage/apoptosis avoidance
  4. Progression- additional growth advantages, lost differentiation
  5. Metastatic spread
25
What is the extrinsic cancer causing pathway?
1. Carcinogens increase risk of DNA damage and mutations somatic and stromal cells 2. Carcinogens act on stroma to support growth- survival/GFs/angiogenesis
26
Which cells does cancer thrive in?
Domains of high growth: • Intestinal cells • Some white blood cells • Skin cells
27
Where does cancer not thrive?
Areas of no growth- stable cells- can live all of an animals life
28
Which cell types can cancer be very dangerous in?
Highly mobile/ invasive cell types
29
Which cell types are particularly vulnerable to cancer?
Those that readily produce GFs, remodel extracellular matrix and promote blood flow- hence inflamed regions are susceptible
30
Which tissues are more resilient against cancer?
Those producing: • anti-proliferative factors (angiogenin, endostation) • Protease inhibitors • Anti-angiogenesis factors
31
What are the stages of a tumour?
* 2nm diameter= steady state, fed by diffusion * Recruits a blood supply- produce angiogenic factors or recruit local cells to (bFGF, TGFalpha, VEGF) * Size increase increases likelihood of further advantageous mutation
32
What are Rb and p53?
Crucial tumour suppressors | Most human tumours deregulate one or both
33
What does the Rb pathway involve?
Cyclin D, CDK4, p16^INK4A, Rb
34
How is the Rb pathway affected in breast cancer?
CyclinD elevated
35
How is the Rb pathway affected in melanoma?
CD4K elevated | P16^INK4A deleted/silenced
36
How is the Rb pathway affected in pancreatic cancer?
P16^INK4A deleted/silenced
37
How is the Rb pathway affected in retinoblastoma and soft tissue carcinomas?
Rb lost or mutated
38
What does p53 normally do?
Arrests cell cycle and promoted apoptosis in response to DNA damage, hypoxia, unscheduled oncogene activation
39
Which mediators of p53 can be targeted in cancers?
p21^CIP1 & ARF - > Activate MDM2 - > Inhibits p53
40
What is the Hayflick limit?
A cell can only divide a certain number of times
41
How does telomere attrition induce senescence?
Engages: ARF-p53-p21^CIP1 (p53 pathway) Or: p16^INK4A (Rb pathway)
42
How do cancer cells avoid senescence?
Telomerase expression is induced
43
What is an arrested state?
* No proliferation in response to GFs | * Enlarged with flattened morphology
44
What can be used to assess senescence in cultured cells?
Senescence associated beta-galactosidase (SA beta-gal) -biochemical marker
45
What is the ECM?
Extracellular matrix: layer of proteins- collagen, glycosaminoglycans (as proteoglycans) that form supportive mesh work underlying endo/epithelial cells
46
What are the functions of the ECM?
* Proteins sequester water-> turgor in soft tissues * Minerals give rigidity to skeletal tissues * Reservoir for GFs controlling proliferation * Cell to cell interaction * Substratum for adherence, migration and proliferation
47
How do tumour cells use the ECM?
* Attack basement (encapsulating membranes) * Migrate along ECM fibres to find blood vessels * Aquire direction from GFs in ECM
48
What percentage of cancer sufferers does metastatic spread kill?
90%
49
What is the epithelial/mesenchymal transition?
De-differentiation of epithelial cells to a fibroblastoid, migratory and more malignant phenotype. Must occur for metastasis
50
What does hTERT do?
Telomerase activity
51
What does SV40 large T antigen do?
Lost cell cycle suppression | Escape from apoptosis
52
What does vRas do?
Drives proliferation
53
Where does skin cancer most commonly spread to?
Lungs
54
Where does colon cancer most commonly spread to?
Liver
55
Where does lunch cancer most commonly spread to?
Adrenal glands | Brain

Human Sciences (8 decks)

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