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Human Sciences > Cancer > Flashcards

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
Q

What is the extrinsic cancer causing pathway?

A
  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
Q

Which cells does cancer thrive in?

A

Domains of high growth:
• Intestinal cells
• Some white blood cells
• Skin cells

27
Q

Where does cancer not thrive?

A

Areas of no growth- stable cells- can live all of an animals life

28
Q

Which cell types can cancer be very dangerous in?

A

Highly mobile/ invasive cell types

29
Q

Which cell types are particularly vulnerable to cancer?

A

Those that readily produce GFs, remodel extracellular matrix and promote blood flow- hence inflamed regions are susceptible

30
Q

Which tissues are more resilient against cancer?

A

Those producing:
• anti-proliferative factors (angiogenin, endostation)
• Protease inhibitors
• Anti-angiogenesis factors

31
Q

What are the stages of a tumour?

A
  • 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
Q

What are Rb and p53?

A

Crucial tumour suppressors

Most human tumours deregulate one or both

33
Q

What does the Rb pathway involve?

A

Cyclin D, CDK4, p16^INK4A, Rb

34
Q

How is the Rb pathway affected in breast cancer?

A

CyclinD elevated

35
Q

How is the Rb pathway affected in melanoma?

A

CD4K elevated

P16^INK4A deleted/silenced

36
Q

How is the Rb pathway affected in pancreatic cancer?

A

P16^INK4A deleted/silenced

37
Q

How is the Rb pathway affected in retinoblastoma and soft tissue carcinomas?

A

Rb lost or mutated

38
Q

What does p53 normally do?

A

Arrests cell cycle and promoted apoptosis in response to DNA damage, hypoxia, unscheduled oncogene activation

39
Q

Which mediators of p53 can be targeted in cancers?

A

p21^CIP1 & ARF

  • > Activate MDM2
  • > Inhibits p53
40
Q

What is the Hayflick limit?

A

A cell can only divide a certain number of times

41
Q

How does telomere attrition induce senescence?

A

Engages:
ARF-p53-p21^CIP1 (p53 pathway)

Or:
p16^INK4A (Rb pathway)

42
Q

How do cancer cells avoid senescence?

A

Telomerase expression is induced

43
Q

What is an arrested state?

A
  • No proliferation in response to GFs

* Enlarged with flattened morphology

44
Q

What can be used to assess senescence in cultured cells?

A

Senescence associated beta-galactosidase
(SA beta-gal)

-biochemical marker

45
Q

What is the ECM?

A

Extracellular matrix:
layer of proteins- collagen, glycosaminoglycans (as proteoglycans) that form supportive mesh work underlying endo/epithelial cells

46
Q

What are the functions of the ECM?

A
  • 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
Q

How do tumour cells use the ECM?

A
  • Attack basement (encapsulating membranes)
  • Migrate along ECM fibres to find blood vessels
  • Aquire direction from GFs in ECM
48
Q

What percentage of cancer sufferers does metastatic spread kill?

A

90%

49
Q

What is the epithelial/mesenchymal transition?

A

De-differentiation of epithelial cells to a fibroblastoid, migratory and more malignant phenotype.

Must occur for metastasis

50
Q

What does hTERT do?

A

Telomerase activity

51
Q

What does SV40 large T antigen do?

A

Lost cell cycle suppression

Escape from apoptosis

52
Q

What does vRas do?

A

Drives proliferation

53
Q

Where does skin cancer most commonly spread to?

A

Lungs

54
Q

Where does colon cancer most commonly spread to?

A

Liver

55
Q

Where does lunch cancer most commonly spread to?

A

Adrenal glands

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Human Sciences (8 decks)

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