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PoD topics > Tumours 5 > Flashcards

Tumours 5 Flashcards

1
Q

what are 6 disorders of cell growth?

A
  1. tumour suppressor genes affected (anti-oncogenes)
  2. inherited factors in carcinogenesis
  3. oncogens
  4. viral carcinogenesis (HIV)
  5. precursors of cancer
  6. multistep process of tumour development
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2
Q

what 3 factors stimulate carcinogenesis?

A
  1. geographic and environmental factors
  2. age
  3. genetics/ heredity
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3
Q

On a molecular basis, what are the 2 genes which undergo disruptions of its normal regulatory genes?

A
  1. tumours suppression genes (anti-oncogenes)

2. proto-oncogenes

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4
Q

what do tumour suppressors do? what 2 cellular processes do they regulate?

A

Inhibit abnormal cell growth (genes regulate apoptosis and halt cell division for DNA repair)

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5
Q

what are proto-oncogenes?

A

Normal genes which promote normal cell growth and mitosis

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6
Q

what are the genes which negatively regulate mitosis?

A

pRb

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7
Q

before normal cell transforms to a cancer cell, how many mutations are needed?

A

several mutations (MANY)

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8
Q

what are the 3 key events which occur in tumour formation?

A
  1. uncontrolled cell proliferation
  2. cell cycle dysregulation
  3. loss of tumour suppressor gene function
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9
Q

what is a retinoblastome gene?

A

A tumour suppressor (anti-oncogene)

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10
Q

What do mutations in the Rb gene favour?

A

Cell proliferation (excessive cell division)

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11
Q

Mutations where else mimic the effect of pRb loss?

A

Mutations in other genes controlling pRb phosphorylation

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12
Q

what are the mutations of the other genes which control pRb phosphorylation?

A
  1. mutational activation of cyclin D or CDK4

2. mutational inactivation of CDKIs also drive proliferation

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13
Q

what does pRb on its own act as in the cell cycle?

A

cell cycle “brake”

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14
Q

what does absent or inactive pRb lead to?

A

cell cycle brake being released (stimulating cell proliferation)

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15
Q

In what 2 ways can mutations occur in tumour suppressors (anti-oncogenes) such as retinoblastomas?

A
  1. somatic (spontaneous)

2. inherited

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16
Q

What is the “two-hit hypothesis” of oncogenesis?

A
  1. Inherited form: one defected copy of pRb and somatic point mutation of other copy occurs
  2. Sporadic form: both hits occur in a SINLGE cell
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17
Q

Loss/inactivation of both normal allelic copies of pRb gives a rise to what?

A

cancer

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18
Q

what percentage of cancers does heredity account for?

A

5-10%

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19
Q

What are 3 heredity factors which can be inherited resulting in cancer?

A
  1. inherited cancer syndromes
  2. familial cancers
  3. autosomal recessive syndromes of defective DNA repair
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20
Q

What does inherited cancer syndrome indicate about family history?

A

Strong family history of UNCOMMON and SITE SPECIFIC cancers

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21
Q

What type of inheritance needs to occur to inherit a cancer syndrome?

A

autosomal dominant inheritance of a single mutant gene

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22
Q

what are 5 of the most common inherited cancer syndromes?

A
  1. Familial retinoblastoma
  2. familial adenomatous polyposis of colon (FAP)
  3. multiple endocrine neoplasia
  4. neurofibromatosis
  5. Van-Hippel- Lindau syndorme
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23
Q

What are 3 main characteristics of familial cancers? (family clustering of cancers bud individual predisposition is unclear)

A
  1. multifunctional inheritance
  2. early age of onset
  3. multiple/bilateral tumours
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24
Q

What are 3 main familial cancers?

A
  1. some breast cancers
  2. some ovarian cancers
  3. non- FAP colon cancers
25
Q

what is the function of APC gene?

A

involved in signal transduction (polarising the cell) and controls cell-cell adhesion/attachment

26
Q

where does the somatic mutation occur in APC gene? (4)

A
  • gastric
  • colon
  • pancreas
  • melanoma
27
Q

what is the inherited mutation from an APC mutation?

A

FAP colon cancer

28
Q

what is the function of p.53 gene?

A

Cell cycle/apoptosis after DNA damage, acts as a tumour suppressor and repairs damaged DNA

29
Q

Where does the somatic mutation occur in p.53 gene?

A

occurs in most cancers

30
Q

what is the inherited mutation form a p.53 mutation?

A

Li-Fraumeni syndrome: multiple carcinomas and sarcomas

31
Q

what is the role of Rb gene?

A

controls and regulates cell cycle

32
Q

where does the somatic mutation occur in Rb gene? (4)

A
  • retinoblastoma
  • colon
  • lung
  • breast carcinomas
33
Q

what is the inherited mutation from an Rb mutation? (2)

A

retinoblastoma and osteosarcoma

34
Q

what is the function of p16(INK4a) gene?

A

inhibits CDKs

35
Q

where does the somatic mutation occur in p16(INK4a) gene? (2)

A

-pancreatic and oesophageal carcinomas

36
Q

what is the inherited mutation from a p16(INK4a) mutation?

A

malignant melanoma

37
Q

what is the function of BRCA-1/2 genes?

A

DNA repair

38
Q

what is the inherited mutation from a BRCA-1/2 mutation? (2)

A

breast and ovarian cancers

39
Q

what are proto-oncogenes?

A

normal genes coding for normal proteins that regulate normal growth

40
Q

what 3 factors do proto-oncogenes work closely with to regulate a normal cell growth?

A
  1. growth factors
  2. growth factor receptors
  3. signal transduction
41
Q

what are onco-genes derived from?

A

proto-oncogenes

42
Q

what are oncogenes activated by? (2)

A
  1. alteration of proto-oncogene structure (point mutation or chromosome rearrangements and translocations)
  2. dysregulation of proto-oncogene expression (gene amplification or overexpression)
43
Q

what are oncoprotein products which are made by oncogenes? (5)

A
  1. growth factors
  2. growth factor receptors
  3. proteins involved in signal transduction
  4. nuclear regulatory proteins
  5. cell cycle regulators
44
Q

What are the 2 chromosomal re-arrangements which involve translocation and overexpression?

A
  1. Burkitt lymphoma

2. Mantle cell lymphoma

45
Q

what can the chromosome rearrangement involving recombination to form chimeric proteins lead to?

A

Chronic mueloid leukemia

46
Q

what happens to the viral genome in viral carcinogenesis?

A

Virus genome insterts near a host proto-oncogene

47
Q

where do retroviruses insert their oncogene?

A

Into host DNA causing cell division

48
Q

what cancer can HPV cause?

A

cervical cancer

49
Q

what cancer can Hepatitis B cause?

A

liver cancer

50
Q

what cancer can EBV cause?

A

Burkitt lymphoma

51
Q

what 2 bases in DNA are critical cellular targets for damage by radiation and various oxidising and alkylating agents?

A

Purine and pyrimidine

52
Q

what are formed when chemical carcinogens and their active metabolites react with DNA to form covalently bound products?

A

DNA adducts

53
Q

What can adduct formation at particular DNA sites lead to activation of?

A

Oncogenes (and suppression of tumour suppressors)

54
Q

what 2 mechanisms occur in most cancers in terms of genes?

A
  1. activation of oncogenes

2. loss of 2 or more tumour suppressors (anti-oncogenes)

55
Q

What are 3 DNA-damaging environmental agents?

A
  1. chemicals
  2. radiant energy
  3. viruses
56
Q

What are the 4 key regulators which are mutated in majority of cancers?

A
  1. p16
  2. cyclin D
  3. CDK4
  4. Rb
57
Q

loss or mutation to which gene allows genetically damaged cells to proliferate forming malignant neoplasms?

A

p.53

58
Q

what cell cycle phases play the key role in maintaining a normal cell cycle and are often affected in cancer formation?

A

G1/S (by binding E2F transcription factors)

More E2F, less pRb= mutations occur (no brake on cell cycle)

PoD topics (34 decks)

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