tumors and oncogenes Flashcards

1
Q

oncogenes

A

genes that contribute to tumorigenesis by obtaining activating mutants, pushes cells towards its replicating stage for viruses to make copies

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2
Q

sacroma

A

mesodermal tissue cancer

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3
Q

carcinoma

A

endo/ectodermal tissue cancer

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4
Q

nauroblastoma, glioblastoma, melanoma

A

neural cancer

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5
Q

leukimia

A

blood cancer

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6
Q

lymphoma, myeloma

A

lymph nodes, solid tumors

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7
Q

LTR gene

A

carried by RNA tumor viruses, acts as promotor

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8
Q

pol gene

A

by RNA viruses, reverse transcriptase, to transcribe RNA into DNA for integration in the hosts’
genome

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9
Q

env gene

A

rna virus, is an envelop protein (host specific, e.g. specific for surface proteins of chick cells)

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10
Q

gag

A

rna virus, structural rna binding protein

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11
Q

onc

A

rna virus, viral oncogen transorms host making it oncogenic

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12
Q

Ras

A

rat sarcoma, dominant mutation

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13
Q

raf

A

rat fibrosacroma

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14
Q

fos

A

feline osteosarcoma

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15
Q

sis

A

simina (monkey) sarcoma,codes for PDGF B chain: results in increased levels of PDGF B and increased activation of receptor, c-SIS is human homolog and does not contain activating mutations, v‐SIS also does
not contain activating mutations, but its expression is increased in host cell via the LTR regions, v and c onc

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16
Q

rna viruses

A

obtained oncogenic features, infect host with envelop proteins (gag, pol, env) and have them take up proto-oncogenes in their own viral genome

17
Q

3 types of oncogenes

A

‐ c‐onc with v‐onc homolog e.g. RAS, FOS, JUN
‐ c‐onc without v‐onc homolog e.g. kFGF, ErbB2
‐ v‐onc without c‐onc homolog  DNA tumor viruses

18
Q

DNA tumor viruses

A

bigger genome than RNA viruses, contain transforming genes
 Adenoviruses (E1A)
 SV40 virus (large T)
 Human Papillomavirus (E6; E7);
+ E1A, large T and E6/E7 are proteins that bind other proteins encoded by tumor
suppressor genes, proteins inactivate tumor supressor genes

19
Q

v onc

A

viral oncogens

20
Q

c onc

A

human or cellular oncogenes

21
Q

kKGF gene

A

activating mutations in promotor region of the gene, c onc

22
Q

EGFR mutations

A
  1. no ligand domain -> ligand independent, activated by spontaneous dimer formation,
  2. mutations in TK domain -> it keeps phosphorylating, keeps dividing
23
Q

RAS mutations

A

often mutated in human tumors, but also in other diseases/syndromes, such as
Costello syndrome, In tumor:
 mutations in intrinsic GTPase activity
 No return to GDP bound form
 RAS constitutively active

24
Q

RAF mutations

A

Mutations in V600E (Valine to glutamic acid) in melanoma
+ Valine has a neutral charge, while
glutamic acid has a negative charge
+ When proteins are phosphorylated,
they also obtain a negative charge
 The amino acid switch results in a
phosphorylation mimic.
 The protein is ‘activated’

25
Q

Vemurafenib

A

kinase inhibitor, interrupts RAF/MEK step, patient specific treatment, vemurafenib inhibits mutant RAF V600E specifically, however it activates other
RAF mutants!

26
Q

FOA + JUN mutations

A

 truncation of mutation of regulating sequences (especially in RNA) making them
constitutive active: FOS and JUN mRNAs are usually degraded quickly due to
destabilizing elements in noncoding part of RNA, during oncogenesis these can
be deleted
 Gene duplication: multiple copies of the gene present in the genome

27
Q

tumor suppressor genes

A

 Genes that encode for proteins involved in suppressing oncogenesis,
for example by inhibiting the cell cycle or inducing apoptosis
 Three key examples RB, p53 and PTEN

28
Q

Retinoblastoma RB

A

retina/eye tumor, RB protein is a transcription repressor inhibiting gene activation, RB gene  inactivation
1 allele makes sufficient RB protein.
both RB genes need mutations for mutation to show

29
Q

p53 gen/protein

A

tumor supressor gene, nuclear transcription factor, tumour cells have elevated expression of p53, makes other cells ongogenic, when mutated it becomes stable, complex of 4 copies of itself and needs only one of them mutated for the complex to inactivate, no genes will be transcribed, genes for growth inhibition, dominant negative mutation

30
Q

haplo insufficiency

A

1 allele is not enough for funcion, both allels are needed, VEGF mutations

31
Q

VEGF

A

needed to generate blood vessels, 2 alleles needed, but with one allele mutated phenotype visable -> aberrant blood vessel formation, dose from one allel = 90% and 100% is needed to be healthy