Lecture 15: cancer 33 Flashcards

(38 cards)

1
Q

Identified tumour suppressor genes:

A
  • Rb
  • P53
  • WT-1
  • Ptc
  • BRCA-1
  • APC
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2
Q

Inherited cancer predisposition diseases

A
  • Retinoblastoma
  • Li Fraumeni
  • Wilm’s tumour
  • Gorlin’s syndrome
  • Breast cancer
  • Familial adenomatous polyposis coli (FAP)
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3
Q

Oncogenes vs tumour suppressor genes: number of alleles mutated to exert effect

A

oncogenes: one

TSG: 2

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4
Q

Oncogenes vs tumour suppressor genes: effect on the function of the protein

A

oncogene: Enhanced

TSG: reduced

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5
Q

Oncogenes vs tumour suppressor genes: inherited mutations:

A

oncogenes: RET, Abl

TSG: p53, RB, WT-1, Ptc, APC

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6
Q

Oncogenes:

A

activate, gain of function, dominant

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7
Q

TSG:

A

inactivating, loss of function, recessive

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8
Q

normal cell division, normal apoptosis:

A

HOMEOSTASIS

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9
Q

INCREASED cell division, normal apoptosis :

A

TUMOUR

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10
Q

Normal cell division, DECREASED apoptosis :

A

TUMOUR

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11
Q

cell cycle

A

G1 - growth 1
S - replicate genome
G2 - growth phase 2
M - cell division

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12
Q

Many genes control cell division:

A
  • Many Genes Promote Cell Division

- Many Genes Block Cell Division

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13
Q

DNA detected by stable, active p53

A
  • Hyperproliferative signals
  • DNA damage
  • Telomere shortening
  • Hypoxia
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14
Q

outcome from p53 detecting DNA damage

A
  • cell cycle arrest
  • senescence
  • apoptosis
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15
Q

p53 has been called the

A

‘guardian of the genome’

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16
Q

p53

A

• arrests cells when DNA is damaged

• turns on transcription of DNA repair genes and
genes that arrest cell cycle

• turns on apoptosis when all else fails

17
Q

many cancers arise from defects in the machinery that regulates

A

cell growth and/or cell death

18
Q

most cancer cells are defective in apoptotic response
⇑anti-apoptotic or
⇓ pro-apoptotic proteins

19
Q

Cancer cells have tricks to avoid apoptosis:

B-cell leukemias and lymphomas express

A

high levels of Bcl-2

20
Q

Cancer cells have tricks to avoid apoptosis: Lung and colon cancer cells
secrete

A

“decoy” molecules that bind and inactivate MHC type1 receptors

⇓T cell recognition sites
—Cytotoxic T-lymphocytes & NK cannot kill the cancer cells

21
Q

routes of tumour spread

A
  • direct
  • via lymphatics
  • transcoelomic
  • field change
  • via bloodtsream
22
Q

Metastasis mechanism

A

still poorly understood

23
Q

metastasis is promoted by

A
  • ⇓ adherence between cells
  • Synthesis of defective basement membrane
  • Tumour angiogenesis
  • ⇑cell motility
  • Secrete growth factors
  • Secrete alternative extracellular matrix
  • Secrete proteinases
  • Evade host immune system
24
Q

treatment for cancer:

A
  • Surgery
  • Radiotherapy
  • -Chemotherapy
  • Endocrine-related treatments
  • Immunotherapy
  • –Interferons, vaccination
  • Molecular mechanism-based
25
an effective screening should be
-Be affordable to the healthcare system --Be acceptable to all social groups -Have good discrimination between benign & malignant lesions -Show a reduction in mortality from the cancer
26
Herceptin as mode of action
=monoclonal antibody binds to erbB2 receptor sites Inhibits receptor function 1.Cell cycle arrest blocks cell cycle in G1 2. Suppresses angiogenesis ⇑antiangiogenic factors ⇓proangiogenic factors
27
cancer is a ___ of diseases
group
28
cancer is controlled / uncontrolled cell division
uncontrolled | - aberrant differentiation & cell interactions
29
2 types of tumours:
benign & malignant
30
cancer affects
a large proportion of the population (but is rare from the cells perspective)
31
Many carcinogens act as
mutagens - cancer not usually become apparent until years after exposure
32
_____ in cellular function need to occur before a cell can become malignant
MULTIPLE CHANGEs include defects in the machinery that regulates cell growth and death
33
Gain of function mutations occur in
oncogenes
34
loss of function mutations associated with
tumour suppressors
35
many cancers display
genomic instability
36
cancer may arise from
'stem cells'
37
__ treatments are availble
variable - often used in combination
38
New insights into tumour biology is providing
new therapies