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Phase I Medicine > Principles of Cancer > Flashcards

Principles of Cancer Flashcards

1
Q

What are the hallmarks of cancer?

A 
Sustenance of proliferative signalling
Enabling replication immortality
Resisting cell death
Evasion of growth suppressors
Invasion and metastasis of tissues
Inducing angiogenesis
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2
Q

How can DNA be damaged?

A 
Chemical exposure
Replication errors
Radiation
Viral infection
Metabolic processes
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3
Q

What is p53 responsible for?

A

Cell cycle arrest.

This allows for DNA repair and when this is not possible, apoptosis.

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4
Q

Why does p53 trigger apoptosis?

A

If DNA can’t be fixed, you don’t want the damage being propagated to daughter cells.

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5
Q

What is the difference between exogenous and endogenous factors?

A

Exogenous - extracellular

Endogenous -intracellular

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6
Q

What are examples of exogenous DNA damaging factors?

A

UV light
X-rays
Natural isotopes
Chemicals

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7
Q

What are examples of endogenous DNA damaging factors?

A

Oxygen
Water
Reactive metabolism intermediates

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8
Q

How do exogenous factors damage DNA?

A

Alkylating agents add methyl groups to the DNA helix

They act as bulky lesions causing DNA distortion

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9
Q

How do endogenous factors damage DNA?

A

Biotransformation- metabolism of chemicals may lead to damaging intermediates.

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10
Q

For what condition is ATM low-absent?

A

Ataxia-telangiectasia (A-T)

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11
Q

What is ataxia-telangiectasia?

A
  • Autosomal recessive disorder
  • Progressive neurodegeneration
  • Impairment triggering cell cycle checkpoints in response to DNA damage (double strand breaks)
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12
Q

What allows for the accumulation of P53 protein?

A

ATM

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13
Q

How can p53 be mutated?

A

UV light
Aflatoxin B1 in diet
Benzo[a]pyrene in tobacco smoke

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14
Q

Where is p53 mutated most of the time?

A

CpG sites

Methylation of C

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15
Q

What is the MGMT enzyme responsible for?

A

Repair of alkylation damage

Transfer of alkyl group from modified base to cysteine residue

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16
Q

What is the function of DNA glycosylases?

A

Base removal

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17
Q

What is the function of AP endonucleases?

A

Repairing AP sites after base removal

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18
Q

What is the difference between base excision repair and nucleotide excision repair?

A

Base- use of DNA glycosylases and AP endonucleases to remove a single base

Nucleotide- removal of a nucleotide fragment that contains damaged base(s). Works on bulkier lesions

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19
Q

How are cut fragments repaired in NER?

A

The gap is filled by DNA polymerase

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20
Q

What is a possible consequence of NER defects with respect to UV damage

A

Xeroderma pigmentosum (XP) - extreme sensitivity to sunlight and 1000x higher risk of skin cancer

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21
Q

What kind of DNA damage does ionising radiation cause?

A

Double strand break

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22
Q

Why is a double strand break dangerous?

A

The broken bits are cleaned up and stuck together via ligation- no memory of bases lost

23
Q

What genetic instability is commonly responsible for HNPCC?

A

Inappropriate DNA repair

hMSH2 hMLH1 mismatch

24
Q

What genetic instability is commonly responsible for early breast and ovarian cancer?

A

Inappropriate repair of double strand break

Problems with checkpoint signalling

25
Q

What is the importance of APC with respect to bowel cancer?

A

The absence of this DNA repair gene is responsible for FAP.

26
Q

What is microsatellite instability?

A

Contraction/ elongation of a repeated sequence on replication

27
Q

What is a tumour/ neoplasm?

A

Abnormal mass of cells resulting from poorly regulated cell proliferation and growth in the absence of a distinct initiating event

28
Q

What are the normal regulatory genes for a cell?

A

Proto-oncogenes
Tumour suppressor genes
Apoptosis control genes
DNA repair genes

29
Q

What is penetrance?

A

The number of people who will show the effects of their inherited mutations

30
Q

What is expressivity with respect to mutations?

A

Severity of symptoms of the same mutation may vary from person to person

31
Q

How does HPV go on to cause cervical cancer?

A

Strains 16 and 18
Infects cervical epithelial cells -> E1-7 viral protein production
E6 and 7 reduce pRb and p53 levels
Promotion of DNA synthesis
Interruption of p53 mediated cell cycle arrest and apoptosis

32
Q

What strains of HPV are low risk?

A

6 and 11

These cause anogenital warts

33
Q

Is metaplasia reversible?

A

Yes

34
Q

What is osseous metaplasia?

A

Areas of fibrous tissues exposed to chronic trauma forming bone

35
Q

What is dysplasia?

A

Disordered growth of cells
Increased cell division
Incomplete maturation
Loss of architectural relationship between cells

36
Q

What is the difference between ‘oma’ and ‘sarcoma’?

A

Oma- benign neoplasm

Sarcoma- malignant neoplasm

37
Q

What is a teratoma?

A

Cancer containing elements of all three embryological germ cell layers.
The cancer tissue type is not normally found in the space the cancer is occupying.

38
Q

What is the difference between lymphomas and leukaemias?

A

Lymphoma - solid tumour mass

Leukaemia- circulating tumour cells

39
Q

What is a hamartoma?

A

Disorganised mass of mature specialised cells indigenous to the site

40
Q

What is a choristoma?

A

Collection of normal cells in an abnormal location

41
Q

What is the difference between benign and malignant neoplasms?

A

Benign:
Localised
Expansile
Fibrous capsule

Malignant:
Ill defined bordered
Margins for infiltration

42
Q

What does metastasis mean?

A

Distant spread of neoplastic cells away from primary neoplasm.

43
Q

What are secondary neoplasms?

A

Subpopulations of neoplastic cells

44
Q

What are the routes of metastasis?

A

Haematogenous- venous
Lymphatic
Transcoelomic

45
Q

What is haematogenous metastasis?

A

Vein penetration-> tumour embolus follows flow of normal drainage

46
Q

What is lymphatic metastasis?

A

Lymphatic vessels draining the primary site into regional lymph nodes.

47
Q

What is transcoelomic metastasis?

A

Spreading across cavities and surfaces- through tumour penetration.

48
Q

How do ovarian cancers normally metastasise?

A

Transcoelomically

49
Q

What is differentiation with relation to cancer?

A

Extent to which neoplastic cells resemble normal ones

50
Q

What is anaplasia?

A

Malignant neoplasm composed of undifferentiated cells

51
Q

What is pleomorphism?

A

Variation in cell shape and size

52
Q

What is intussusception?

A

The bowel folds in on itself like a telescope.

53
Q

What are the hormonal effects of neoplasms?

A

Endocrine insufficiency via gland destruction

Elaboration of hormones

54
Q

What is paraneoplastic syndrome?

A

Symptoms of hormone elaboration. This comes from tissues ‘over-expression’ that tumours have invaded.

Phase I Medicine (46 decks)

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