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Biology of Cancer > Unit 2 Chapter 4, 5,6 > Flashcards

Unit 2 Chapter 4, 5,6 Flashcards

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1
Q

Kinases

A

are enzymes that catalyze the
transfer of gamma phosphate group from
ATP/GTP to hydroxyl groups on a specific
amino acid in a target group

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2
Q

Phosphatase

A

an enzyme that removes
phosphate group from a specific amino acid in a
target group

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3
Q

EGFR’s belong to a family of

A

receptor tyrosine kinases

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4
Q

EGFR include 4 types of receptors

A

ErbB1 (HER1),
ErbB2(HER2)
ErbB3 (HER 3)
ErbB4 (HER4

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5
Q

Steps of EGF signaling

A
  1. Binding the growth factor to the receptor
  2. Receptor dimerization
  3. Autophosphorylation
  4. Activation of intracellular transducers
  5. A cascade of serine/ threonine kinases
  6. Regulation of transcription factors and gene expression
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6
Q

Steps 1 and 2 of EGF binding and dimerization

A

EGF binds to domain 1 and 2, Domain 3 binding to EGF

This exposes domain 2 and forms a dimer with another EGF bound to EGFR

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7
Q

Autophosphorylation in EGF/EGFR

A

Dimerization enables the kinase domains of one receptor to phosphorylate the other receptor and vice versa
▪ The change in receptor conformation permits access to ATP and substrate to the catalytic kinase domain

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8
Q

Why is autophosphorylation crucial in EGF/EGFR?

A

it’s crucial for recruitment of cytoplasmic proteins

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9
Q

RAS

A

responsible for integrating growth factor signals

from membrane to nucleus

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10
Q

Describe ras

A

GTP-binding proteins and are activated when

bound to GTP and inactivated when bound to GDP

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11
Q

RAS-GTP binds to and contributes to

the activation

A

serine/threonine kinase RAF

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12
Q

Describe the RAS to MAP Kinase signaling cascade

A

Ras-GTP Binds to activation of RAF
Activated RAF phosphorylates MEK
Activated MEK Phosphorylates MAP Kinase
MAPK affects activity of trancription factors by phosphorylation

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13
Q

Transcription Factor

A

group of proteins that bind to DNA and regulate

the expression of genes involved in growth, differentiation and death

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14
Q

AP-1 gene transcription factor is target of

A

Map Kinase

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15
Q

AP-1 gene products activate

A

cyclin D genes which are critical regulators of cell cycle

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16
Q

Star player in regulating growth

A

RAS

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17
Q

Describe RAS activation of AKT

A

Ras interacts with PI3K by activating PIP 2 to PIP 3
PIP3 recruits PDK-1 and AKT to the membrane
AKT translocates to the nucleus, phosphprylates nuclear transcription factors

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18
Q

AKT is involved in

A

anti-apoptotic and survival roles

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19
Q

In normal cells, activated RAS is

A

is inactivated

immediately by GAPS protein

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20
Q

inactivated RAS causes

A

conformational change in RAS and releases RAF which then is inactivated by phosphatase

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21
Q

Inactivation of RAS

A

Brings thecell back to normal non-proliferative state

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22
Q

In cancer cells RAS can be

A

continuously activated by mutations induced by various factors

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23
Q

Mitated RAS cannot be inactivated by GAPS protein as in normal cells

A

this results in continuous proliferation of tumor cell

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24
Q

Growth factor signaling not only leads to cell

proliferation but also can effect

A

cell behaviors such as adhesion and motility

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25
Q

SRC

A

an intracellular tyrosine kinase coded by genes

src

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26
Q

SRC plays an important role in

A

cell adhesion, invasion and motility upon EGF activation (Metastasis)

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27
Q

Upon stimulation of EGF receptor by growth factor

A

the autophosphorylated receptor can interact with SH2

domain of SRC and activate the protein

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28
Q

One way in which SRC can be activated is

A

via EGF receptor

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29
Q

Activated SRC activates

A

wide range of target proteins such as focal adhesion proteins (FAK), adaptor proteins, motility proteins and transcription factors (Important in metastasis)

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30
Q

What pathway needs to be targeted to limit metastasis and stop FAK protein? (DESCRIBE)

A 
EGF-EGFR-> Autophosphorylation
Inactive SRC
Active SRC
FAK
Increased motility and cell invasion 
(This pathway needs to be targeted to limit metastasis and stop FAK protein)
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31
Q

Monoclonal antibodies that block the signaling pathway prevents growth factor from binding to the receptor

A

Herceptin
Erbitux
Vecitibix

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32
Q

Monoclonal antibodies that block the intracellular domain autophosphorylation stopping

A

Gilotrif
Tarceva
Tykerb

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33
Q

Monoclonal antibody that shuts down things going into the nucleus

A

Mekinist (affects MEK)

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34
Q

Monoclonal antibodies that shut down RAF signaling

A

Nexavar
Zelforab
Tafinlar

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35
Q

Herceptin (trastuzumab)

A

a monoclonal antibody that binds the extracellular domains of ErB2 receptor with high affinity

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36
Q

Herceptin functions

A

through a combination of mechanisms including enhanced receptor degradation, inhibition of angiogenesis, cell proliferation and recruitment of immune cells, resulting in antibody-dependent cellular cytotoxicity

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37
Q

Erbitux has 5 mechanisms of action

A 
Cell cycle arrest of cancer cell and inhibits proliferation, 
prevents metastasis
inhibits angiogenesis
antibody-dependent cellular cytotoxicity
inhibits DNA repair mechanisms
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38
Q

ressa and Tarceva

A

small molecule kinase inhibitors that are directed against tyrosine kinase activity of EGFR family members

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39
Q

Imatinib (Gleevec) used for

A

Chronic myelogenous leukemia

(CML) accounts for 15-20% leukemias

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40
Q

Most CML patients carry

A

Philadelphia chromosome chromosome generating BCR-ABL fusion protein

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41
Q

Gleevec

A

a tyrosine kinase inhibitor that binds to ATPbinding pocket within catalytic domain and inhibits the
action of enzyme

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42
Q

proto-oncogenes

A

Normal cellular genes that can be converted to

oncogenes

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43
Q

RAS proto-oncogene

A

normal gene produces normal protein that controls proliferation

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44
Q

Mutations in RAS proto-oncogene

A

can transform it in to RAS oncogene which can cause cancers due to uncontrolled proliferation

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45
Q

Oncogenes

A

genes whose presence can contribute to uncontrolled cell proliferation and cancer

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46
Q

Oncogenes contain which type of mutation (Dominant/recessive)

A

Dominant

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47
Q

More than ___ oncogenes have been identified and

proteins they produce fall into different categories

A

100

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48
Q

Most proteins produced by oncogenes are

A

components of signaling pathways that promote cell

proliferation and survival

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49
Q

B-RAF Function, Protein, and associated disease

A

Intracelluar signal transducers
Protein-RAS
Melanoma

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50
Q

Myc Function, Protein, and associated disease

A

c-myc (Proto-oncogene)
Transcription Factors
Myc Protein
Burkitt’s Lymphoma

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51
Q

RAS Function, Protein, and associated disease

A

Intracellular signal transducers
RAS protein
Bladder and lung cancer

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52
Q

V-erbB

A

C-erbB (Proto-oncogene)
Growth Factor Receptor
EGFR (Receptor)
Breast Cancer

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53
Q

Chromosomal translocation

A

Part of the chromosome is mixed with another part of
another chromosome, altering promoter region and
amount of protein created

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54
Q

Gene amplification

A

One gene has multiple copies and is amplified in function. Elephants have multiple p53 genes compared to humans

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55
Q

Point Mutation

A

Changes a single nucleotide in the DNA sequence, changes mRNA, changes AA sequence, and changes the protein or conformation of the protein

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56
Q

Cellular oncogenes arise due to the following

mechanisms (convert from proto to oncogene)

A 
Point mutations 
Gene amplification 
Chromosomal translocation
DNA Rearrangement
Insertional Mutations
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57
Q

Single mutation in RAS proto-oncogene results in

A

RASoncogene that produces mutated Ras protein in which single amino acid is converted from glycine to valine

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58
Q

Neuroblastoma with extensively amplified MYC gene are more likely to

A

invade and metastasize and lower survival
rates (associated with adrenal glands)
(Map Kinase applies here)

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59
Q

Philadelphia chromosome

A

abnormal version of chromosome 22 in 90% of all cases of chronic myelogenous leukemia

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60
Q

Translocation of ABL gene (tyrosine kinase) in

chromosome 9 to BCR gene (Serine/threonine kinase) on chromosome 22 and results in

A

abnormal BCR-ABL fusion gene and fusion protein

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61
Q

Viruses have special viral sequences at its end called

A

LTR’s (Long terminal repeats) which promote gene expression

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62
Q

How long does mitosis take?

A

16 hrs

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63
Q

How long does binary fission take?

A

24 mins

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64
Q

Cell Cycle Steps

A 
G1 (Growth)
S Phase (Synthesis)
G2 (Growth)
M Phase (Mitotic)
Cytokinesis (Cytoplasm split)
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65
Q

Interphase

A

G1
S
G2

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66
Q

Proteins involved in eukaryotic DNA Synthesis

A 
DNA polymerase
Helicase
Topoisomerase
SSBPS
Ligase
RNA Polymerase
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67
Q

Differentiated, living cells are also called

A

quiescent

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68
Q

G0 Phase

A

Outside the cell cycle
Cell is non-dividing and differentiated
dependent on growth signals for division

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69
Q

G1 Restirciton Point

A

Control point in cell division

If a cell crosses it’s point, it becomes irreversibly committed to go through the cell cycle without growth factors

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70
Q

Cyclins

A

proteins that have a critical role in cell cycle
coordinate and regulate the passage of
cell through different phases of cell cycle

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71
Q

Cyclins act as

A

regulatory subunits of cyclindependent kinase (cdks).

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72
Q

Upon binding of cyclin to cdk partner, cyclin undergoes

A

a conformational change in the catalytic domain, exposing an active site.

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73
Q

Concentration of cyclins during cell division is

dependent on

A

Transcription of cyclin genes

Regulated protein degredation

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74
Q

Cdk proteins are regulated by

A

binding of cyclins.

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75
Q

Does S Phase have a checkpoint?

A

NO

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76
Q

Cyclin E and CDK2 role in the cell cycle

A

Takes the cell into S Phase

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77
Q

CyclinD and CDK 4 and 6 role in the cell cycle

A

Push the cell over the restricition point, cross through the checkpoint

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78
Q

Mitogen

A

small bioactive protein or peptide that induces a cell to begin cell division, or enhances the rate of division (mitosis).

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79
Q

Mitogenesis

A

the induction (triggering) of mitosis, typically via a mitogen.

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80
Q

Mitogenesis

A

the induction (triggering) of mitosis, typically via a mitogen.

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81
Q

What phases of the cell cycle have checkpoints?

A

G1
G2
M

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82
Q

G2 Checkpoint

A

Check to make sure cell is ready for mitosis, no mutations in DNA, no breaks in chromosomes, all microtubules ready for mitosis

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83
Q

Cyclin A and CDk2 role in the cell cycle

A

Help push through the S phase

84
Q

Cyclin D

A

The first cyclin to be synthesized, and together with CDK 4/6 drives progression through the G1 Restriction point and G1 Checkpoint

85
Q

Cyclin D regulates

A

Expression of Cyclin E, which binds to CDK2 and is required for G1 to S phase transition

86
Q

CyclinA-CDK2 is important for

A

S phase progression

87
Q

Cyclin B/A-CDK1 Directs

A

G2 and G2 to M Phase Transition

88
Q

Cyclin order

A

DEABA

89
Q

CDK Order

A

4 2 1

90
Q

Why are cell cyle checkpoints important

A

Maintaining the integrity of the genome

91
Q

G1 Checkpoint

A

Arrest of the cell cycle in response to DNA Damage

92
Q

G2 Checkpoint

A

arrest of cell cycle in response to DNA damage and/or unreplicated DNA to ensure proper
completion of S phase

93
Q

M Checkpoint

A

arrest of chromosomal segregation in response to misalignment on the mitotic spindle

94
Q

Disruption of checkpoint leads to

A

Mutation and carcinogenesis

95
Q

Function of cyclin-CDK Complexes

A

They exert their effect by phosphorylating target

proteins

96
Q

Target proteins of Cyclin-CDK complexes

A

Histones
▪ Transcriptional regulators
▪ Cytoskeletal proteins
▪ Nuclear pore proteins

97
Q

Cyclin-CDK protein interaction with proteins results in

A

▪ Regulated gene expression
▪ Mitotic spindle assembly
▪ Chromosomal condensation
▪ Nuclear membrane breakdown

98
Q

CDKs

A

serine/threonine kinases that,
sequentially, regulate progression through the
phases of the cell cycle via phosphorylation

99
Q

Four Mechasnisms of CDKs

A

▪ Association with cyclins
▪ Association with cdk inhibitors
▪ Addition of phosphate groups to activate cdk activity
▪ Addition of phosphate group that inhibits cdk activity

100
Q

binding of cyclins to their partner cdk causes
a crucial conformational change in the cdk that
allows

A

the binding of protein substrates and correct

positioning of ATP

101
Q

Degradation of cyclin proteins is carried out by

A

proteasome through ubiquitin, which flags the

cyclin protein for degradation

102
Q

P16 binds with

A

cdk 4/6 and interferes with the binding of cyclin D to cdk4/6.

103
Q

P21 inhibitor binds to

A

both cyclin E and cdk 2 blocking ATP –binding site, thus disabling kinase activity.

104
Q

CDK inhibitors are regulated by

A

ubiquitin-mediated degradation.

105
Q

Addition of the phosphate group to the threonine 14 and 15 positions by wee 1 Kinase

A

inactivates the cyclin

106
Q

Removal of the phosphate groups to threonine 14 and 15 positions by CDC 25 Phosphatase

A

Activates the Cyclin

107
Q

Function transcription factors

A

Proteins that control transcription

108
Q

E2F Makes

A 
SSBP
DNA Polymerase
Primase
Helicase
Ligase
109
Q

When Rb (Retinoblastoma) protein is binded to E2F

A

Genes needed for S Phase are NOT Transcribed

110
Q

When Rb protein is phosphorylated and unbound from E2F,

A

E2F is free to promote transcription
MRNA Translation
Enzymes and other proteins required for S phase
Cell Proliferation

111
Q

Rb Protein serves as

A

a molecular link for the G1-S phase transition

112
Q

Rb binds to transcription factor E2F which is

A

crucial for the expression of genes needed for S

phase.

113
Q

Rb protein comprises the

A

A domain and B domain joined by a linker region

114
Q

Histone deacetylase (HDAC) binds to

A

domain B and E2F binds to domain A

115
Q

Function of HDAC

A

wraps the DNA tightly around the Histone, increasing positive charge of histone and it glues more to the DNA

116
Q

Hypophosphorylated Rb

A

sequesters E2F/DP and HDAC which results in complete repression of transcription.

117
Q

Partial phosphorylation of Rb protein by cyclin D/cdk4/6 causes

A

a conformation change releases HDAC but not E2F/DP. This results in relieving repression of some genes such as cyclin E but not E2F target genes

118
Q

Additional phosphorylation by cyclin E-cdk2

causes

A

an additional conformational change and releases E2F/DP, and transcription of all of E2F target genes.

119
Q

The G2 checkpoint

A

blocks entry into M phase in cells that have incurred DNA damage in previous phase or have not correctly completed S phase

120
Q

DNA damage activates

A

ATM or ATR. These kinases then phosphorylate and activate chk1 and chk2 kinases

121
Q

One target of the checkpoint kinases are the cdc25

tyrosine phosphatase

A

regulate cdk activity by removing inhibitory phosphatase

122
Q

Activation of G2 checkpoint results in

A

the inhibition of cdc25 by chk1.

123
Q

decatenation

A

the process of separating this physical linkage

124
Q

Z-TMS

A

induces cell-cycle arrest at G2/M Phase

that is accompanied by the activation of p21, downregulation of CDK1

125
Q

Cleavage Furrow

A

Contracting ring of microfilaments

126
Q

Mitotic Checkpoint is also known as the

A

spindle assembly checkpoint

127
Q

Mitotic checkpoint prevents

A

mis-segregation of chromosomes

128
Q

If any of the sister chromatids are not attached to

microtubules at their centromeres during mitosis

A

they recruit checkpoint proteins that act as inhibitors of

anaphase-promoting complex such as securin

129
Q

When securin are attached to sister chromatids without microtubules

A

they inhibit enzyme separase

130
Q

Separase

A

cleaves the link (cohesin) between sister

chromatids and helps their separation during anaphase

131
Q

Aurora Kinase

A

regulate important aspects of mitosis, such as
chromosome segregation and the spindle
checkpoint

132
Q

Mutations in cell cycle regulators can result in

A

aberrant regulation of cell cycle, uncontrolled proliferation and carcinogenesis

133
Q

Chromosomal translocations cause over-expression

of

A

CDK6 in some leukemia’s

134
Q

DNA amplification of cyclin D and E by gene

amplification result in

A

15% of breast cancers and 20% squamous cell carcinoma

135
Q

p16 inhibitor deletions have been observed

A

Pancreatic cancers

136
Q

Abnormal chromosome numbers or aneuploidy

caused by

A

defects in centrosomes, mitotic spindle,
or cytokinesis is often observed in many solid
tumors

137
Q

Over expression of Aurora kinase A gene has

been commonly reported in

A

94% of invasive ductal breast adenocarcinomas

138
Q

Flavopiridol acts as

A

competitive inhibitor of all cdks.
▪ It induces cell cycle arrest at G1/S and G2/M phase.
▪ It also regulates gene expression of cyclin D1 and D3.

139
Q

CYC-116 and AZD1152

A

Are aurora Kinase inhibitors

140
Q

Vinblastine

A

inhibits microtubule assembly resulting in activation of mitotic checkpoint

141
Q

Paclitaxel/taxol

A

Mitotic inhibitor

142
Q

Chemotherapeutic effects on the GI Tract

A

Ulcers, nausea, vomiting, diarrhea, loss

of appetite

143
Q

Chemotherapeutic effects on the Bone Marrow

A

Suppressed immune system, anemia

144
Q

Chemotherapeutic effects on the skin

A

Skin easily damaged, wounds take longer

to heal

145
Q

chemotherapeutic effects on Hair follicles

A

Hair Loss

146
Q

Necrosis

A

Cells swell, membranes become leaky, and the cells spill out their contents into the surrounding tissue and cause inflammation

147
Q

Autophagy

A

A type of cell death that is self-eating

148
Q

Autophagosomes

A

spherical structure with double layer membranes. It is the key structure in macroautophagy, the intracellular degradation system for cytoplasmic contents (e.g., abnormal intracellular proteins, excess or damaged organelles, invading microorganisms)

149
Q

Steps of autophagy

A
  • Starts with ER and formation of preautophagosome

* Matures into autophagosomes and fuses with lysosomes in cells

150
Q

Activation signals for autophagy

A

○ Triggered by starvation
○ Cellular Stress
○ Infection

151
Q

Proteins invovled in autophagy

A

LC3, Beclin-1 ULK

152
Q

Autophagy is inhibited by

A

○ Cell growth and proliferation
○ Excess cellular energy
○ MTOR and PI3K complex

153
Q

Apoptosis

A
  • Active cell death that happens in normal cells and diseased organs
  • Need ATP For this process
  • Involves a single cell
  • Programmed Cell Death (Basically from a checklist
  • Decrease in cell size
  • Cell membrane is intact
  • Does not trigger local inflammatory responses or absent
  • Involves cellular Makers CD95 protein
  • DNA Gel has a ladder pattern
154
Q

Necrosis

A

• Passive Form of Cell death that happens in injured tissue or organs
• No ATP Needed
• Involves groups of cells
• Involves Extrinsic (External) stimuli
• Increase in Cell size (Cells swell and Explode)
• Cell membrane damage is involved
• Involves local inflammatory response (Activating immune cells
• in the local environment
• No Cellular Markers (G1 Phase Cyclins, and things like that)
DNA has a smear pattern

155
Q

Apoptosis

A

Highly regulated programmed cell death

156
Q

Apoptosis plays an important role in

A

developmental morphogenesis
Control of cell numbers and tissues
Gets rid of damaged cells

157
Q

Apoptosis is a main Tumor suppressive mechanism that

A

Disposes the cell with extenisve DNA damage and mutations

158
Q

A specialized group of proteases called _________ play a main role in apoptosis

A

Caspases

159
Q

Proteases

A

enzyme that breaks down proteins

160
Q

Caspases

A

Specialized proteases involved in apoptosis

161
Q

Annexin V

A

A phospholipid binding protein

162
Q

Caspases

A

Cysteine-Rich Aspartate Proteases

163
Q

How many mammalian caspases have been identified

A

13

164
Q

Caspases are synthesized as inactive ________ which when cleaved as aspartate residues results in activation of enzymes(_______)

A

Procaspases

Caspases

165
Q

Caspases participate in a cascade of activation , activating

A

downstream caspases and amplifying the signals

166
Q

Cells may be induced to undergo apoptosis by what external factors

A

Extracellular signals
TNF (Soluble) death factor
Membrane-bound fas ligand bound to neighboring cells or certain immune cells

167
Q

Cells may be induced to undergo apoptosis by what internal factors

A

DNA Damage or oxidative Damage (Ionizinf radiation-Reactive Oxygen Species

168
Q

If CDC 25 is active or not inhibited by CHK1

A

CDC25 dephosphorylates CDK protein
CDK activates
Progression of cells into Mitosis phase

169
Q

If CDC25 is inactivatedby CHK1

A

No dephosphorylation of CDK protein

No progression of cells into M Phase

170
Q

Cell stress signals and DNA damage activate

A

ATM/ATR kinases
which activate CHK1 / Casein Kinase II
These disrupt the P53-MDM2 Complex which activates P53 Protein

171
Q

P53-MDM2 complex activates

A

P53 protein

172
Q

P 53 activates ____ Protein, which in turn activates ____ Protein

A

Bax

Bid

173
Q

Conormational change in BAX protein causes it to

A

insert into the outer mitochondrial membrane and oligomerize (6-8 molecules)

174
Q

Mitochondria release

A

Cytochrome C and Procaspase 9 into the cytoplasm

175
Q

Released cytochrome C and procaspase 9 bind with

A

apaf-1 to form the apoptosome

176
Q

caspase aggregation leads to

A

activation of procaspase 9

which in turn triggers caspase cascade activating caspase 3

177
Q

Caspase 3 cleaves

A

target proteins and causes apoptosis of the cell

178
Q

Anit-Apoptotic proteins

A

BCL-2
BCL-X
BCL-W

179
Q

Pro-Apoptotic Proteins

A

BAX
BAD
BID

180
Q

Extrinsic pathway mediated by membrane death receptors

A

TNF and FAS bind to their receptors
Binding causes conformational change and oligomerization
Adaptor proteins TRADD and FADD recognize the activated receptors and lead to the aggregation of Procaspase 8
Procaspase 8 aggregation leads to the activation of caspase 8
Caspase 8 initiates a caspase cascade, proteolysis and apoptosis

181
Q

Both intrinsic and extrinsic pathways activate

A

Caspase 3

182
Q

______ is an important mediator of apoptosis as it moves the cell into execution phase of apoptosis

A

Caspase 3

183
Q

_____ causes proteolysis of different target proteins

A

Caspase 3

184
Q

Target proteins for execution of apoptosis

A

Nuclear Lamins
Cytoskeletal proteins
Activation of DNAse

185
Q

Nuclear Lamins role in apoptosis

A

Allowing for nuclear membrane shrinkage

186
Q

Cytoskeletal proteins’ role in apoptosis

A

such as actin filaments affecting the cell structure

187
Q

Activation of DNAse role in apoptosis

A

Resulting in cleavage of DNA

188
Q

The extrinsic pathway of apoptosis is regulated by inhibitor protein

A

CFlip

189
Q

C-Flip binds to _____ and inhibits What?

A

FADD

activation of activation of procaspase 8

190
Q

Inhibitors of Apoptosis (IAPs) regulate apoptosis by

A

binding and inhibiting the activity of caspase 3 and caspase 7

191
Q

SMAC (Second Mitochondria-Derived Activator)/ DIABLO

A

Is released from mitochondria eliminates the inhibition by IAPs

192
Q

Caspase 8 is a key regulator of

A

Extrinsic pathway and also cleaves and activates BID in the intrinsic pathway

193
Q

How do intrinsic and extrinsic pathways of apoptosis converge

A

Activation of caspase 3, which causes proteolysis

194
Q

Cancer cells contain

A

activated caspases that are inhibited by upregulated IAPs

195
Q

TRAIL Receptors

A

triggers apoptosis via extrinsic pathway

196
Q

TRAIL receptor and TRAIL Ligand interactions induce

A

apoptosis in many cancer cells but not in most normal cells

197
Q

Mutations in death receptor genes such as FAS and Trail have been reported in what types of cancers

A

Melanomas and squamous cell carcinoma

198
Q

Suppression of Caspase gene expression has been demonstrated in

A

small-cell lung carcinoma

199
Q

mutation in LEU62

A

Blocks the interaction of caspase 8 with the adaptor FADD, thus stopping the signal

200
Q

Mutations in p53 genes

A

Provide the cancer cells with a survival advantage by disrupting apoptosis is common in lymphomas

201
Q

Chromosomal translocation of ___________is observed by many B-Cell lymphomas

A

anti-apoptotic protein BCL2

202
Q

Mutations in ___ and ___ genes that code for apoptotic proteins are mutated in______

A

Bax
BID
50% of colon tumors

203
Q

A successful chemotherapy will be one that

A

triggers apoptosis

204
Q

Many Chemotherapeutic agents

A

trigger DNA mutations or DNA damage, thus activating the intrinsic apoptotic pathway

205
Q

What contributes to chemotherapy resistance

A

Upregulation of anti-apoptotic members of BCL2 family and the downregulation of pro-apoptotic members

Biology of Cancer (4 decks)

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