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Cellulaire Oncologie > HC2 - Viruses, oncogenes & growth factors > Flashcards

HC2 - Viruses, oncogenes & growth factors Flashcards

1
Q

cancer as infectious disease

A

until late 19th century, Rous sacroma virus (RSV)

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2
Q

virus

A

genetic material encapsulatedv

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3
Q

viruses and cancer

A

viruses can transform infected cells in culture

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4
Q

formation of foci

A

loss of contact inhibition

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5
Q

permissive host

A

allow virus replication and are killed quickly

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6
Q

non-permissive host

A

does not allow virus replication and causes transformation

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7
Q

intergration of viral DNA into host genome

A
  • exploit replication machinery
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8
Q

HPV

A

99.7% of cervical carcinomas

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9
Q

episomal virus

A

outside of host genome, hitchhike during mitosis

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10
Q

retrovirus

A

reverse transcription to intergrate genetic material

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11
Q

kidnapping and exploiting host genes

A

v-src and c-src

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12
Q

existing normal genes

A

can be oncogenic

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13
Q

a single gene

A

sufficient for oncogenic transformation

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14
Q

virus vector

A

to deliver foreign DNA

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15
Q

kidnapped genes

A

most are silent, over 30 proto-oncogenes

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16
Q

induction of transformation

A

viral intergration next to proto-oncogene c-myc

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17
Q

insertional mutagenesis (mechanism c-myc)

A

strong viral promotor forces overexpression of c-myc gene > uncontrolable cell proliferation

18
Q

viruses as carcinogenes

A

in 20% of cancers, HPV, Hep. B and C

19
Q

not all cancers caused by virusses

A
  • cancers don’t propagrate between humans
  • no outbreaks
  • non-biological reagents can be carcinogenic > chemicals and radiation
20
Q

latent viruses

A

inactive proviruses can be reactivated by some chemicals > BrdU

21
Q

mutations as drivers for transformation

A
  • transfection of foreign DNA to test oncogenic potential of genes
  • oncogens act across species = evolutionary conserved
22
Q

cellular oncogenes

A
  • often amplified in cancers
  • multiple copies > increased protein production
23
Q

HER2 in 30% of breast cancers

A

correlated with poor patient prognosis

24
Q

tumor suppressor genes

A

counteract oncogenic transformation

25
Q

deletion or mutation tumor suppressor genes

A

releases breaks on cell proliferation

26
Q

proto-oncogenes

A

activated by genetic changes affecting protein expression or structure

27
Q

H-ras bladder carcinoma oncogene

A

identical in length to normal human DNA, somatic point mutation

28
Q

Burkitt’s lymphoma

A

-chromosome translocation fusing regions of chromosomes 2, 14, 22 to a region of chromosome 8
- places myc proto-oncogene under control of transcriptional activators of immunoglobulines

29
Q

epidermal growth factor receptors (EGFR)

A

recognizes EGF and initiates intracellular signaling to promote growth

30
Q

trunction EGFR

A
  • in some carcinomas and glioblastomas
  • lacks extracellular domain > sends growth-stimulatory signals even in absence of EGF
31
Q

hybrid proteins in chronic myelogenous leukemia (CML)

A

abl proto-oncogene kinase (ch. 9) fuses with bcr region (ch 22.) > deregulation of abl protein > emits strong growth-promoting signals

32
Q

MLL1 (ALL1) gene

A
  • histone methylase participates in >50 fusions
  • affects chromatin structure and function
33
Q

different mechanisms for transformation

A
  • changes in proto-oncogene expression level - changes in proto-oncogene structure
  • complex cellular control systems
34
Q

changes in proto-oncogene expression levels

A
  • amplification
  • insertional mutagenesis = control by an external promotor
  • translocation = control by an active promotor of another gene
35
Q

changes in proto-oncogene structure

A
  • truncation
  • hybrid protein
  • mutation
36
Q

complex cellular control systems

A

regulating levels of proteins posttranscriptionally

37
Q

coordination of cell behavior

A

growth-stimulatory signals from their environment

38
Q

cell membrane

A

barrier in cell transduction

39
Q

growth factors (GF)

A
  • convey signals between cells in a tissue
  • dimerization and transphosphorylation
40
Q

cancer alters growth factor metabolism

A
  • overexpression or change of receptors
  • enhanced autocrine signaling
41
Q

EGFR amplication glioblastomas

A

increased levels of receptors can trigger activation

42
Q

membrane-permeable ligands (small, hydrophobic)

A
  • steroid sex hormones, retinoids, vitamin D
  • bind directly to nuclear recpetor

Cellulaire Oncologie (14 decks)

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