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PoD topics > Tumours 5 > Flashcards

Tumours 5 Flashcards

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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?

Study These Flashcards
A
  1. some breast cancers
  2. some ovarian cancers
  3. non- FAP colon cancers
25
what is the function of APC gene?
involved in signal transduction (polarising the cell) and controls cell-cell adhesion/attachment
26
where does the somatic mutation occur in APC gene? (4)
- gastric - colon - pancreas - melanoma
27
what is the inherited mutation from an APC mutation?
FAP colon cancer
28
what is the function of p.53 gene?
Cell cycle/apoptosis after DNA damage, acts as a tumour suppressor and repairs damaged DNA
29
Where does the somatic mutation occur in p.53 gene?
occurs in most cancers
30
what is the inherited mutation form a p.53 mutation?
Li-Fraumeni syndrome: multiple carcinomas and sarcomas
31
what is the role of Rb gene?
controls and regulates cell cycle
32
where does the somatic mutation occur in Rb gene? (4)
- retinoblastoma - colon - lung - breast carcinomas
33
what is the inherited mutation from an Rb mutation? (2)
retinoblastoma and osteosarcoma
34
what is the function of p16(INK4a) gene?
inhibits CDKs
35
where does the somatic mutation occur in p16(INK4a) gene? (2)
-pancreatic and oesophageal carcinomas
36
what is the inherited mutation from a p16(INK4a) mutation?
malignant melanoma
37
what is the function of BRCA-1/2 genes?
DNA repair
38
what is the inherited mutation from a BRCA-1/2 mutation? (2)
breast and ovarian cancers
39
what are proto-oncogenes?
normal genes coding for normal proteins that regulate normal growth
40
what 3 factors do proto-oncogenes work closely with to regulate a normal cell growth?
1. growth factors 2. growth factor receptors 3. signal transduction
41
what are onco-genes derived from?
proto-oncogenes
42
what are oncogenes activated by? (2)
1. alteration of proto-oncogene structure (point mutation or chromosome rearrangements and translocations) 2. dysregulation of proto-oncogene expression (gene amplification or overexpression)
43
what are oncoprotein products which are made by oncogenes? (5)
1. growth factors 2. growth factor receptors 3. proteins involved in signal transduction 4. nuclear regulatory proteins 5. cell cycle regulators
44
What are the 2 chromosomal re-arrangements which involve translocation and overexpression?
1. Burkitt lymphoma | 2. Mantle cell lymphoma
45
what can the chromosome rearrangement involving recombination to form chimeric proteins lead to?
Chronic mueloid leukemia
46
what happens to the viral genome in viral carcinogenesis?
Virus genome insterts near a host proto-oncogene
47
where do retroviruses insert their oncogene?
Into host DNA causing cell division
48
what cancer can HPV cause?
cervical cancer
49
what cancer can Hepatitis B cause?
liver cancer
50
what cancer can EBV cause?
Burkitt lymphoma
51
what 2 bases in DNA are critical cellular targets for damage by radiation and various oxidising and alkylating agents?
Purine and pyrimidine
52
what are formed when chemical carcinogens and their active metabolites react with DNA to form covalently bound products?
DNA adducts
53
What can adduct formation at particular DNA sites lead to activation of?
Oncogenes (and suppression of tumour suppressors)
54
what 2 mechanisms occur in most cancers in terms of genes?
1. activation of oncogenes | 2. loss of 2 or more tumour suppressors (anti-oncogenes)
55
What are 3 DNA-damaging environmental agents?
1. chemicals 2. radiant energy 3. viruses
56
What are the 4 key regulators which are mutated in majority of cancers?
1. p16 2. cyclin D 3. CDK4 4. Rb
57
loss or mutation to which gene allows genetically damaged cells to proliferate forming malignant neoplasms?
p.53
58
what cell cycle phases play the key role in maintaining a normal cell cycle and are often affected in cancer formation?
G1/S (by binding E2F transcription factors) More E2F, less pRb= mutations occur (no brake on cell cycle)

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