Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BS202 > 20.2 Oncogenes > Flashcards

20.2 Oncogenes Flashcards

1
Q

specific genes that can induce cell transformation (process of converting normal cells to tumor cells) → they can induce cancer

A

oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

studies of () led to identification of cellular oncogenes involved in developement of non-virus-induced cancers

A

retroviral oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

() transforms chicken embryo fibroblasts in culture and induces sarcomas

A

Rous sarcoma virus (RSV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

RSV is closely related to () replicates in the same cells without inducing transformation → RSV contained specific genetic information for transformation

A

avian leukosis virus (ALV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

studies of RSV mutants revealed a single gene called () responsible for RSV tumor induction

A

src

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

many oncogenes encode components of signaling pathways that stimulate ()

A

cell proliferation (e.g. src, encoding Ras and Raf)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

studies involving the () found that even though a mouse was injected only with viral genes responsible for replication (i.e. no genes inducing transformation), it developed leukemia

A

Abelson leukemia virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

the Abelson leukemia virus was found to induce leukemia due to the presence of an oncogene called ()

A

abl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

explain how viral oncogenes can have cellular origins

A

a host cell gene that can drive cell proliferation occasionally becomes incorperated into a viral genome → yields a highly oncogenic virus with an oncogene derived from the host cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

normal genes from which retroviral oncogenes originated

A

proto-oncogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

oncogenes are () of the proto-oncogenes

A

abnormally expressed or mutated forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

proto-oncogenes often encode proteins in the signaling pathways that () → these genes are triggered by growth factors

A

control normal cell proliferation (e.g. src, ras, raf)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

retroviral oncogenes differ from proto-oncogenes in the ff aspects:

A
  1. transcription in viral oncogenes is controlled by viral promoters and enhancers
  2. oncogenes often encode proteins that differ in structure and function from normal proteins
  3. loss of regulatory domains generates in oncogenes proteins that function in an unregulated manner
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

transcription in viral oncogenes is controlled by viral promoters and enhancers; this results in the oncogenes being ()

A

expressed at much higher levels than proto-oncogenes or in the wrong cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

oncogenes such as Raf are expressed as fusion proteins with () at the amino terminus

A

viral sequences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

deletion of () leads to raf protein kinase hyperactivity → drives abnormal cell proliferation and then cell transformation

A

regulatory domain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

many oncogenes differ from proto-oncogenes by () → single amino acid substitutions in proteins, which then lead to unregulated protein activity

A

point mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

gene transfer experiments found evidence for involvement of cellular oncogenes in human tumors (not induced by viruses)

A

DNA from a human bladder carcinoma was found to induce transformation of mouse cells in culture → tumor contained an oncogene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

the first human oncogene identified was the homolog of the (1) of the (2)

A
  1. rasH oncogene
  2. Harvey sarcoma virus
20
Q

three members of the ras gene family () are the oncogenes most frequently encountered in human tumors

A

rasH, rasK, rasN

21
Q

mutations of ras oncogenes maintain the ras proteins in the ()

A

active GTP-bound conformation

22
Q

mutated ras proteins do not respond to GAP (GTPase-activating protein) → ()

A

GTP bound to Ras is not hydrolyzed to GDP to inactivate Ras

23
Q

many cancer cells have () → lead to generation of oncogenes

A

abnormal chromosome structures, including translocations, duplications, and deletions

24
Q

in Burkitt’s lymphoma, chromosome translocation inserts () oncogene into an (2), where it is expressed in an unregulated manner

A
  1. c-myc
  2. immunoglobulin locus
25
Q

translocation of abl proto-oncogene leads to production of a () → unregulated activity of Abl tyrosine kinase → cell transformation

A

bcr/abl fusion protein

26
Q

oncogenes can be activated by () → results in elevated expression

A

gene amplification

27
Q

amplification of the oncogene () (encodes RTK) is related to rapid growth of breast and ovarian tumors

A

erbB-2

28
Q

the main purpose of oncogene protein production is to (1), as well as to (2)

A
  1. promote cell proliferation and survival
  2. prevent programmed cell death
29
Q

functions of oncogene products include:

A
  1. activation of the ERK pathway
  2. transcriptional activation
  3. increasing cell proliferation
  4. inhibition of cell differentiation
  5. promotion of cell survival
30
Q

all the components of ERK pathway () can serve as oncogene proteins

A
  1. polypeptide growth factors
  2. growth factor receptors
  3. intracellular signaling proteins
  4. transcription factors
31
Q

give an overview of how the receptor for platelet-derived growth factor (PDGFR) can act as an oncogenic product (due to chromosome translocation)

A
  1. translocation results in PDGFRs with amino terminal sequences of the transcription factor Tel
  2. PDGFR+Tel oncogene proteins have a dimerization domain that constitutively keeps the receptor active → even without PDGF stimulation, pathway is activated and cell continuously proliferates
32
Q

transcription of the () is induced by phosphorylation of Elk-1 by the ERK pathway

A

fos proto-oncogene

33
Q

explain how transcription of the fos proto-oncogene can lead to tumor formation

A
  1. fos encodes for Fos, which dimerizes with Jun to form the AP-1 transcription factor
  2. AP-1 transcription factor then activates transcription of cyclin D1 → promotes cell proliferation
34
Q

Fos dimerizes with Jun to form ()

A

AP-1 transcription factor

35
Q

() were identified as oncogenes in mouse breast cancers

A

Wnt proteins

36
Q

explain how Wnt proteins serve as oncogenes

A
  1. Wnt signaling pathway triggers degradation of beta-catenin
  2. mutations convert beta-catenin (downstream target of the Wnt pathway) to an oncogene called CTNNB1
  3. CTNNB1 is more stabilized than beta-catenin → it is not degraded and can cause unregulated transcription of the c-myc oncogene as well as cycD1 (in coordination with the transcription factor Tcf)
37
Q

mutations convert beta-catenin (downstream target of the Wnt pathway) to an oncogene called ()

A

CTNNB1

38
Q

CTNNB1 is more stablized that beta-catenin → it is not degraded and can cause unregulated transcription of the c-myc oncogene as well as cycD1 in coordination with the transcription factor ()

A

Tcf

39
Q

gene encoding cycD1 (it is a proto-oncogene) can become an oncogene called () by chromosome translocation or gene amplification

A

CCND1

40
Q

catalytic partners of cycD1: () are also activated as oncogenes by point mutations, gene amplification, and chromosome translocation

A

Cdk4 and Cdk6

41
Q

mutated form of thyroid hormone receptor that can lead to maintaining leukemic cells in an actively proliferating state

A

ErbA

42
Q

mutated form of retinoic acid receptor that can lead to maintaining leukemic cells in an actively proliferating state due to blocking of cell differentiation

A

PML/RAR(alpha)

43
Q

acute promyelocytic leukemia can be treated with high doses of () → induces differentiation because effect of PML/RAR(alpha) oncogene is overridden

A

retinoic acid

44
Q

failure of cancer cells to () is a critical factor in tumor development

A

undergo programmed cell death

45
Q

PI 3-kinase and Akt act as oncogenes if they () → preventing cell death

A

constitutively keep the pathway active

46
Q

elevated expression of the antiapoptotic protein Bcl-2 also causes to serve as an oncogene by ()

A

blocking apoptosis

BS202 (36 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions