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Pathobiology > Lecture 15: cancer 33 > Flashcards

Lecture 15: cancer 33 Flashcards

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

A

CANCER

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
Q

an effective screening should be

A

-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
Q

Herceptin as mode of action

A

=monoclonal antibody binds to erbB2 receptor sites
Inhibits receptor function
1.Cell cycle arrest
blocks cell cycle in G1

  1. Suppresses angiogenesis
    ⇑antiangiogenic factors
    ⇓proangiogenic factors
27
Q

cancer is a ___ of diseases

A

group

28
Q

cancer is controlled / uncontrolled cell division

A

uncontrolled

- aberrant differentiation & cell interactions

29
Q

2 types of tumours:

A

benign & malignant

30
Q

cancer affects

A

a large proportion of the population (but is rare from the cells perspective)

31
Q

Many carcinogens act as

A

mutagens - cancer not usually become apparent until years after exposure

32
Q

_____ in cellular function need to occur before a cell can become malignant

A

MULTIPLE CHANGEs

include defects in the machinery that regulates cell growth and death

33
Q

Gain of function mutations occur in

A

oncogenes

34
Q

loss of function mutations associated with

A

tumour suppressors

35
Q

many cancers display

A

genomic instability

36
Q

cancer may arise from

A

‘stem cells’

37
Q

__ treatments are availble

A

variable

  • often used in combination
38
Q

New insights into tumour biology is providing

A

new therapies

Pathobiology (12 decks)

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