Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

JC articles > T&H7 Oncogenes and TSGs > Flashcards

T&H7 Oncogenes and TSGs Flashcards

1
Q

TSG or oncogene: p110

A

oncogene

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

TSG or oncogene: EGFR

A

oncogene

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

TSG or oncogene: ERBB2/HER2

A

oncogene

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

TSG or oncogene: B-RAF

A

oncogene

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

TSG or oncogene: K-RAS

A

oncogene

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

TSG or oncogene: myc

A

oncogene

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

TSG or oncogene: BCR-ABL

A

oncogene

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

TSG or oncogene: IDH1/2

A

oncogene

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

TSG or oncogene: JAK2

A

oncogene

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

TSG or oncogene: KIT

A

oncogene

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

TSG or oncogene: MET

A

oncogene

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

TSG or oncogene: FLT-3

A

oncogene

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

TSG or oncogene: p53

A

TSG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

TSG or oncogene: PTEN

A

TSG

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

TSG or oncogene: p16

A

TSG

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

TSG or oncogene: p14

A

TSG

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

TSG or oncogene: BRCA1/2

A

TSG

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

TSG or oncogene: LKB1

A

TSG

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

TSG or oncogene: VHL

A

TSG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

TSG or oncogene: APC

A

TSG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

TSG or oncogene: FBXW7

A

TSG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

TSG or oncogene: Rb

A

TSG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

TSG or oncogene: NF1/2

A

TSG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How long are miRNAs?

A

20-30 nucleotide RNA molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ABL kinase normally shuffles between nucleus and cytoplasm. Whenever it is mutated and forms fusion gene BCR-ABL, it is constitutively active and permanently found in the ______.

A

cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How does imatinib target BCR-ABL?

A

binds in the vicinity of ATP-binding site and locks BCR-ABL in an inhibited conformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What cancers are associated with BCR-ABL fusion oncoprotein?

A

most CML patients, ~30% adult ALL, ~10% pediatric ALL, occasionally AML

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Myc promotes cell cycle progression by influencing a variety of targets, including downregulation of _______ and upregulation of _______, ____, ____, and _____.

A
  • CDK inhibitors
  • cyclin D1, CDK4, CDC25A, and E2F transcription factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the paradoxical effect of myc?

A

upregulation can trigger apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe chromosomal translocation event in Burkitt LSA.

A

Chromosomal translocation between chromosome 8 (where myc resides) and chromosomes where IgH and light-chain genes reside, leading to overexpression of myc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

myc targets _____ to cause tumor promoting inflammation in tumorigenesis.

A

IL-1beta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

myc targets ____ to cause avoidance of immune destruction in tumorigenesis.

A

ICAM-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

myc targets _____ and _____ to deregulate cellular energetics in tumorigenesis.

A

GLUT-1 and LDHA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

myc targets _______ and _____ to cause genomic instability in tumorigenesis.

A

MAD2 and BUBR1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

myc targets _____ to activate metastasis in tumorigenesis.

A

ezrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

myc targets ____ to induce angiogenesis in tumorigenesis.

37
Q

myc targets ____ to enable replicative immortality in tumorigenesis.

38
Q

What EGF family member cannot bind ligand, so it needs to be activated by dimerization with other family members?

A

ERBB2/HER2

39
Q

An activating point mutation of EGFR leads to the receptor attaining an intermediate phosphorylation status, which activates ______ and ______ signaling at expense of other downstream pathways.

A

PI3K and MAPK

40
Q

ERBB2/ERBB3 heterodimeric receptor complex is a potent signal transducer of which pathway and why?

A
  • PI3K pathway
  • ERBB3 receptor directly recruits PI3K rather than using intermediary adaptor proteins
41
Q

ERBB2/HER gene is amplified in roughly ___% of all human breast cancers. What other cancers are associated with this amplification at a lower frequency?

A

25%
gastric and ovarian cancers

42
Q

Amplification of ______ is generally an early event in breast cancer progression and is associated with poor prognosis in breast and gastric cancers.

A

ERBB2/HER2

43
Q

Class IA PI3 kinases convert _____ to ____. This recruits PH domain-containing proteins, such as _____ and ______, to the plasma membrane for activation. _____ contributes to activation of _______, which then transmits signals downstream by phosphorylating a range of targets.

A
  • PIP2 to PIP3
  • AKT/PKB and PDK1
  • PDK1
  • AKT
44
Q

_____ is a negative regulator of PI3K pathway by what mechanism?

A
  • PTEN
  • Acts as lipid phosphatase for PIP3
45
Q

Activating mutations have been identified in the ______ gene, which encodes what subunit of PI3K?

A
  • PIK3CA
  • catalytic subunit p110
46
Q

PIK3CA mutations result in what 3 outcomes?

A
  • constitutive activation of PI3 kinase
  • buildup of PIP3
  • increased mobilization of downstream pathways
47
Q

80% of all somatic PI3K mutations occur at 3 hotspot residues. Name them.

A
  • E542K and E545K in helical domain
  • H1047R in kinase domain
48
Q

PI3 kinase pathway is generally overstimulated in cancers through ______, ________, and ____________.

A
  • aberrant activation of receptors
  • activating mutations of PI3 kinase catalytic subunit p110
  • loss of PTEN
49
Q

AKT can downregulate TSC1-TSC2 complex, which modulates what pathway?

A

RHEB GTPase - TORC1 signaling

50
Q

______ is the most frequently mutated RAF family member. It it mutated in ____% of malignant melanomas in people.

51
Q

_____ substitution in the kinase activation loop accounts for _____ of all B-RAF mutations in people.

52
Q

_______ is an agent that targets BRAF mutation and shows marked improvement in patients with malignant melanoma.

A

vemurafenib

53
Q

RAS and RAF lie downstream of ______ and upstream of _____ and ____.

A
  • RTKs (primarily EGFR and PDGFR)
  • MEK and MAPK
54
Q

Ras can be activated by single point mutations in up to ___% of human cancers.

55
Q

What Ras gene is most commonly mutated?

56
Q

What cancers are associated with K-RAS mutations?

A

pancreatic, lung, colon, endometrial, and ovarian

57
Q

What cancers are associated with N-RAS mutations?

A

Neuronal cancer, melanoma, and myeloid malignancies

58
Q

What cancers are associated with H-RAS mutations?

A

bladder cancer

59
Q

The most common Ras mutations are gain of function substitutions in codons ___, ___, and ____. How is this mutations distinct?

A
  • codons 12, 13, and 61
  • Ras-GTPase enzymatic turnover is blocked by oncogenic mutations –> locks protein into activated GTP-bound signaling state –> upregulation of downstream effectors
60
Q

What is the active Ras bound state?

A

GTP-bound Ras

61
Q

What is the inactive Ras bound state?

A

GDP-bound Ras

62
Q

____ is a novel oncogene which encodes isocitrate dehydrogenase, a Kreb cycle enzyme

63
Q

IDH oncogene activation is seen in what type human cancers?

A

AML and glioblastoma multiforme

64
Q

Most mutations in TP53 are _______ mutations.

65
Q

In response to DNA damage, _____ targets ___ which leads to phosphorylation of p53, thus blocking MDM2 and leading to its downstream effects.

66
Q

In response to oncogene activation, ________ inhibits MDM2 to allow p53 to do its job.

67
Q

In response to cell stress, ___ targets ______ which phosphorylates p53, thus blocking MDM2 and leading to its downstream effects.

A

ATR
Casein kinase II

68
Q

p53 targets ____ for DNA repair.

69
Q

p53 targets ____ for cell cycle arrest or senescence.

70
Q

p53 targets ____ to inhibit angiogenesis.

A

thrombospondin

71
Q

What pro-apoptotic proteins does p53 target?

A
  • Bax
  • PUMA
  • p53AIP1
  • NOXA
72
Q

p53 targets what receptor, which leads to apoptosis.

73
Q

p53 targets ____ which inhibits survival signaling.

74
Q

p53 downregulates what anti-apoptotic protein?

75
Q

BRCA1 is involved in the resection step of DNA DSB by ____ via interaction with _____.

A

HR
MRN complex

76
Q

BRCA2 is a large protein that contains several regions. One region binds ____ and the other binds interacts with ____. What is its primary function?

A
  • RAD51
  • ssDNA
  • Facilitate DNA repair by HR through recruitment of RAD51 to resected ssDNA
77
Q

Tumors lacking BRCA1/2 are deficient in what repair pathway? These tumors can be targeted by _____, which is a good example of synthetic lethality.

A
  • HR
  • PARP inhibitors (involved in an alternative DNA repair pathway - BER)
78
Q

_______ Rb binds E2F which prevents cell cycle progression.

A

hypophosphorylated

79
Q

__________ phosphorylate Rb, which releases _____ allowing for cell cycle progression.

A

Cyclin/CDK complexes
E2F

80
Q

Which RTK is activated in canine MCT and GISTs and how does it differ in these two tumors?

A
  • c-kit
  • c-kit mutations are common in GIST (60-70%) and minority in high-grade MCTs (20-30%)
  • exon 9 and 11 for GIST (exon 11 highest for GIST)
  • DOG1 only expressed in GIST
81
Q

_____ phosphorylate GDP to GTP on RAS for activation while ___ de-phosphorylate to inactivate.

A
  • GEFs (ie, SOS)
  • GAPs
82
Q

Name 2 transcription factors that when deregulated are associated with cancer in humans and dogs.

A

p53, myc
- myc: diffuse large B cell LSA and prostatic carcinoma, tvt in dogs

83
Q

What is the critical step in the initiation of the apoptotic pathway? Hows does Bcl-2 influence this?

A
  • critical step: creation of pores in mitochondria to release cytochrome C
  • Bcl-2 is an anti-apoptotic protein that prevents apoptosis by sequestering caspases or by preventing release of mitochondrial apoptotic factors such as cytochrome C and AIF into the cytoplasm
84
Q

Name the anti-apoptotic proteins

A
  • Bcl-2
  • Bcl-xl
  • Bcl-w
  • A1
  • Mcl-1
  • Boo
85
Q

What are mechanisms of LOH?

A
  1. Mitotic recombination
  2. Gene conversion
  3. Hemizygosity
  4. Chromosomal translocations
  5. Chromosomal non-disjunction
86
Q

In canine lymphoma, abnormal p53 was associated with worse prognosis (MST _______ vs. ______).

A

MST 9 months
MST 2 months

87
Q

What is the correlation between PTEN gene expression and biologic behavior in canine mammary tumors?

A

decreased levels of PTEN associated with malignancy and lymph node mets

JC articles (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions