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Biology of Cancer > Unit 3 Exam Chapter (Stem Cells, Metastasis, Angiogenesis, Immunology) > Flashcards

Unit 3 Exam Chapter (Stem Cells, Metastasis, Angiogenesis, Immunology) Flashcards

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1
Q

RB1 Tumor Suppressor Gene

chromosome location

A

13q14

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2
Q

RB1 Gene function

A

Transcription Regulation

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3
Q

RB1 Tumor Type

A

Retinoblastoma, osteosarcoma

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4
Q

RB1 Cancer Syndrome

A

Familial Retinoblastoma

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5
Q

RB1 Tumor Phenotype

A

MTC, Pituitary adenocarcinoma, pheochromacytoma

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6
Q

p53 chromosome location

A

17q11

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7
Q

p53 gene function

A

Transcription regulation

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8
Q

p53 tumor type

A

Sarcoma

Breast/brain tumors

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9
Q

p53 Cancer syndrome

A

Li Fraumeni

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10
Q

p53 cancer phenotype

A

lymphomas, sarcomas

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11
Q

VHL gene function

A

Proteolysis regulator

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12
Q

VHL Tumor Type

A

Hemangioma
Renal
pheochromacytoma

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13
Q

VHL Cancer syndrome

A

Von-Hippel Lindau

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14
Q

APC Gene function

A

Regulates Beta-Catenin Activity

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15
Q

APC Tumor type

A

Colon Cancer

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16
Q

APC Cancer syndrome

A

Familial adenomatous polyposis

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17
Q

APC Tumor phenotype

A

Intestinal polyps

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18
Q

BRCA1 Gene function

A

Transcription regulator

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19
Q

BRCA1 Tumor Type

A

Breast/ovarian tumors

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20
Q

BRCA1 Cancer Syndrome

A

Familial Breast Cancer

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21
Q

BRCA2 Gene function

A

Transcription Regulator

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22
Q

BRCA2 Tumor Type

A

Breast/ovarian tumors

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23
Q

BRCA2 Cancer Syndrome

A

Familial breast cancer

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24
Q

PTEN Gene function

A

Dual specificity phosphatase

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25
Q

PTEN Tumor Type

A

Gliobastomas
Prostate
Breast

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26
Q

PTEN Cancer Syndrome

A

Cowden syndrome
BZN
Ldd

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27
Q

PTEN Cancer Syndrome

A

Lymphoma
thyroid
endometrium
prostate

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28
Q

Knudson’s two-hit hypothesis and its application to tumor suppressor genes

A

Explains mechanisms for tumor suppressor genes
Both alleles must be mutated to trigger carcinogenesis
Explains certain individuals have an increased risk for cancer
They inhibit tumor suppressor allele

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29
Q

Retinoblastoma

A

Rare childhood cancer
1 in 20,000
Familial and Sporadic

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30
Q

Familial Retinoblastoma

A

40% of cases
Germline mutation n RB gene is passed to child, mutation is present in all cells
Affects BOTH EYES

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31
Q

Sporadic Retinoblastoma

A

60% of all cases
Individual requires 2 somatic mutations in 2 alleles
Usually affects 1 eye

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32
Q

What is the role of the Retinoblastoma gene in tumor suppression?

A

RB protein controls cell proliferationby binding E2F transcription factor
When E2F is bound to Rb, the protein cannot activate transcription genes coding for enzymes and other proteins for initiating DNA replication (NO CELL DIVISION)

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33
Q

What is the role of Retinoblastoma in cell division?

A

Leads to production of cyclin-CDK complexes which catalyze the phosphorylation of Rb protein, which results in release of E2F- results in cell division.

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34
Q

What is the role played by viral gene products which interfere with tumor suppressor genes?

A

Several DNA viruses have been shown to be carcinogenic
Papillpmavirus, Adenovirus, Herpes Virus, and Hepatitis B
Coerces the cell into S phase

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35
Q

Interaction of DNA Viral protein products with Rb

A

Adenovirus EIA, Papillomavirus E7, and SV40 Large T antigen inactivate RB

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36
Q

E1A and E7 use what system when interacting with Rb?

A

ubiquitin-proteasome system

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37
Q

E7 binds ubiquitin-proteasome ligase that forms

A

a dimer and binds to Rb

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38
Q

Rb is tagged for recognition by

A

the proteasome for degredation

Adds a ubiquitin tag

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39
Q

Most important tumor suppressor gene
Most commonly mutated
P63 and P73 are homologs
Protects the cell from DNA Damage

A

P53 Gene

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40
Q

P53 is known as

A

The guardian of the genome

is tied to many processes

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41
Q

What gene regulates Over 300 different genes’ promoter regions

A

P53 Gene

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42
Q

P53 is located

A

On chromosome 17 and contains 11 exons

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43
Q

P53 contains 4 domains:

A

 Amino-terminal transactivation domain (transactivation domain and MDM2 binding site)
 DNA binding domain which binds to DNA
 Oligomerization domain
 Carboxy-terminal (regulatory domain)

44
Q

Upstream molecular pathways of P53 activation

A

Prevents degredation of P53 by MDM2

45
Q

CHK and Casein Kinase II disrupts

A

P53-MDM2 by phosphorylating P53

46
Q

DNA Damage-> P53 Activation

DNA Double-Stranded Breaks

A

DNA Damage
ATM
CHK2
P53 activation

47
Q

Cell stress-> P53 Activation

A

Cell Stress
ATR
Casein Kinase II
P53 Activation

48
Q

Downstream inhibition of the cell cycle and activation of DNA repair mechanisms

A

p53 suppresses tumors by
Causing cell cycle arrest
P35 acts as transcriptional activator for p21 gene
p21 acts as an inhibitor for cyclin-CDK complex, stopping cell cycle between G1-> S-> G2 -> M

49
Q

P53 acts as

A

a transcriptional activator for P21 gene

50
Q

P21 acts

A

as inhibitor for cyclin-cdk complex stopping cell cycle between G1  S and G2  M

51
Q

P21 also binds

A

PCNA (Proliferating Cell Nuclear Antigen) that has a role in DNA repair

52
Q

What regulates expression of XPC Gene which has a role in nucleotide excision repair (DNA repair mechanism)

A

P53

53
Q

NOXA, PUMA, P53, A1P1

A

Promote apoptosis by releasing cytochrome C from the mitochondria causing cell death

54
Q

____ regulates pro-apoptotic BAX and repressing Antiapoptotic BCL-2

A

P53

55
Q

____ Regulates expression of thrombospondin, an inhibitor of angiogenesis

A

P53

56
Q

Autoregulatory Feedback loop associated with P53 gene

A

A transcription factor transcribing a protein that inhibits transcription factors

57
Q

Germline mutation of P53 gene
Leads to predisposition to a wide range of cancers
25-fold increased risk of developing cancer before 50 years old
Develop cancer at a young age and have frequent occurrence of multiple primary tumors
Sarcomas, Breast Cancer, Leukemia, Brain Tumors

A

Li Fraumeni Syndrome

58
Q

Mutations of the P53 pathway and cancer (type of mutation)

A

Over 75% are missense mutations- different from classic tumor suppressor genes that are characterized by nonsense or frameshift mutations

59
Q

More than 90% of missense mutations located in

A

DNA binding domain and more than 30% of these affect only 6 codons and are therefore “hotspots”

60
Q

Common therapeutic strategies for treating cancers associated with tumor suppressor genes

A

Advexin
Onyx015
Ataluren
Nutlins

61
Q

Advexin

A

Gene therapy

P53 Restored

62
Q

Onyx 015 Virus

A

Viral replication, cell lysis

63
Q

APR-246 and PRIMA-1

A

Aberrant folding

Restores P53 function

64
Q

Atalauren

A

Read-through

Ignore the stop codon, make the normal protein

65
Q

Nutlins

A

Binds to MDM2

Target P53 inhibitor (MDM2) and activates P53

66
Q

Pifithrin-Alpha

A

Inhibits P53 transcription

May be used to limit side effects in normal cells

67
Q

When cancer cells are not dividing, what phase of the cell cycle are they in?

A

G0

68
Q

Cancer stem cells obligatory asymmetric replication

A

When a stem cell divides, it becomes another stem cell and a progenitor cell
Progenitor cell will divide rapidly, and their progeny divide and differentiate into a specific cell type

69
Q

A block in cell differentiation results in

A

a higher net number of cells and therefore is a mechanism for tumor formation

70
Q

True or False: DIfferentiated cells enter the cell cycle

A

FALSE

Differentiated cells withdraw from the cell cycle

71
Q

Normal Cells multiply only when needed

A

On activation by environmental input, the niche cells induce them to divide into a stem cell and progenitor cell

72
Q

Human Embryonic Stem Cells (hESC) types

A

Pluripotent
Ethical debate
Easy to grow and acquire

73
Q

Adult stem cells

A

includes umbilical cord blood stem cells
Amniotic fluid stem cells
Fetal Stem cells

74
Q

Fetal stem cells

A

Multipotent- Often used in bone marrow stem cell transplants in leukemias and lymphomas

75
Q

3 types of stem cell transplants

A

Autologous
Allogenic
Syngenic
(Avoids ethical issues)

76
Q

Autologous stem cells

A

your own bone marrow stem cells

More likely to avoid immune rejection

77
Q

Allogenic stem cells

A

From an HLA matched individual

78
Q

Syngenic Stem cells

A

From an identical twin

79
Q

Induced Pluripotent Stem Cells (iPSC)

A

Adult cells that have been reprogrammed
Core of regenerative medicine
Pluripotent

80
Q

Cancer stem cells

A

Rare
Located within the tumor and can self-renew
Can give rise to phenotypically diverse cancer cells

81
Q

Cancer stem cell Surface Protein Markers

A

Breast cancer stem cell markers CD44+, CD24-low

Colon cancer stem cells over-express the surface antigen CD133

82
Q

Feature of self-renewal shared with tumor cells

A

Self-Renewal provides increased opportunities for carcinogenic changes to occur
Altered regulation of self-renewal directly underlies carcinogenesis

83
Q

Cancer stem cell signaling pathways

A

Wnt

Hedgehog

84
Q

Wnt Pathway

A 
Plays a role in stem cell self-renewal
Stimulatory factor
19 Wt genes
Involved in embryonic development (Development of the heart)
Has a destruction complex
85
Q

Wnt Pathway Destruction complex

A

Axin
APC
CKI
GSK3Beta

86
Q

How is the Wnt pathway regulated in normal cells?

A

Wnt binds to frizzled and LRP is phosphorylated with Axin
(Activated) Beta Catenin Binds to TCF/LEF with BCL9 and pygopus
affects target genes like c-myc and cyclin
(Self-Renewal Proceeds)

87
Q

When beta catenin binds to TCF, what happens?

A

Self-Renewal proceeds

88
Q

When Beta Catenin is inhbited from binding to TCF, what happens?

A

No differentiation

89
Q

What goes wrong in tumors?

A

Abnormal activation of the Wnt/β-catenin pathway promotes CSC progression and thus leads to the deterioration and metastasis of cancer

90
Q

Hedgehog pathway is involved in

A 
Embryo development
Tissue Self-Renewal
Tissue Repair
Carcinogenesis
Digit formation in mammals
Neural tube, gut formation
91
Q

Proteins involved in the Hedgehog pathway

A 
Gli-1
Sufu
PKA
Smoothened
Patched
92
Q

How is the hedgehog pathway regulated in normal cells?

A

Cyclopamine suppresses the hedgehog pathway by inhibiting the activity of transmembrane protein SMOOTHENED

93
Q

Inactivating mutations in Patched and activating mutations of Smoothened are identified in what cancer?

A

Basal Cell Carcinoma (BCC)
Gli-1 Expression in BCC
Posesses an activated Hedgehog signaling pathway

94
Q

Gli (Zinc-Finger Transcription Factor) in Hedgehog pathway (HH ABSENT)

A

No hedgehog
Patched cannot bind to smoothened
Sufu binds to Gli and PKA
Target genes are inhibited in the nucleus

95
Q

Gli in Hedgehog pathway (HH Present)

A

Hedgehog protein binds to Patched, which binds to smoothened
Sufu dissociates from PKA and Gli
Gli activates target genes

96
Q

Hereditary Non-Polyposis Colorectal Cancer (HNPCC)

A 
Lynch syndrome
15% of colorectal cancers
Autosomal dominant
Only requires one abnormal gene
AD Mutation in in DNA mismatch repair
80% progress to cancer
Proximal Colon
Increase the risk of other cancers
97
Q

Familial Adenomatous Polyposis (FAP)

A 
85% of colon cancers
Chromosomal instability
Mutation in APC on chromosome 5q
Beta Catenin
Normal colon progression into carcinoma
100% of the time becomes cancerous
Pancolonic (the entire colon)
98
Q

FAP progression to Carcinoma

A

Normal colon-> Loss of APC gene-> Colon at risk-> K-RAS mutation-> Adenoma-> Loss of P53 gene-> Carcinoma

99
Q

Polycomb Group (PcG proteins)

A 
Guardians of stemness
Genes that control development and transcription
HOX
FOX
PAX
POU
SOX
100
Q

What is the role of PcG proteins in stem cell differentiation?

A

Stem cell differentiation is dependent on the polycomb group (PcG proteins)
Repress transcription by epigenetic modifications
Inhibit FOX and SOX
Suppress stem cell differentiation
AML translocation (t98;21)

101
Q

What is the role of lineage-specific transcription factors in stem cell differentiation (AML1, Pu.1, C/EBPalpha)

A

Shows how little we know about stem cells
Hscs-> Pu.1-> CMPs (Myeloid pathway)-> GMPs -> Pu.1-> Monocyte
OR GMPs-> C/EBPalpha-> Granulocytes

102
Q

New cancer therapeutics designed to target different aspects of differentiation pathways Cyclopamine and GDC-0499

A

involving administration of ABC inhibitors along with chemotherapies are being investigated
Stem cells express high levels of ATP-Binding Cassette (ABC) transporters, members of the multi-drug resistance gene family

103
Q

Knudson’s Two-Hit Hypothesis (Essay Question)

A

Explains the mechanism of tumor suppressor genes
States that both alleles must be mutated to trigger carcinogenesis
Explains certain individuals have increased risk of cancer
They inhibit tumor suppressor allele

104
Q

What are stem cells (essay question)

A

Cells of variable potency that can self-renew
Normally found in our bodies
Help in organ maintenance
Help in Organ repair
Somewhat committed to a cell lineage type
Have the ability to migrate to other tissues
High level of telomerase activity
Maintain a balance between self-renewal and differentiation

105
Q

HPCC (Hereditary Non-polyposis colorectal cancer)

A 
Lynch syndrome
15% of colorectal cancer
Autosomal dominant inheritance pattern
Only requires one abnormal gene
AD Mutation in DNA Mismatch repair
80% progress to cancer
Occurs in the proximal colon (Ascending, Transverse)
Increase the risk of other cancers
106
Q

Familial Adenomatous Polyposis Coli (FAP)

A 
85% of colon cancers
Chromosomal instability
Mutation in APC on chromosome 5q
Beta-Catenin
Normal colon-> loss of APC Gene-> Colon at risk-> K-RAS mutation-> adenoma-> Loss of P53-> Carcinoma
100% of the time becomes cancer
Pancolonic (Affects the entire colon)

Biology of Cancer (4 decks)

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