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CSF > Block 5 > Flashcards

Block 5 Flashcards

1
Q

RTK

A

Receptors with inherent kinase activity that bind peptide hormones such as EGF; monomeric in the plasma membrane but dimerize when bound which allows them to phosphorylate target molecules

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2
Q

What is the RTK signaling pathway?

A

EFG -> binds/dimerizes RTK -> phosphorylates SH2/PTB -> recruits Grb2 -> binds Sos on its SH3 domain -> activates Ras -> Raf -> MEK -> MAP kinase

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3
Q

Grb2

A

Recruited by dimerized form of SH2, has an SH3 domain that binds the GEF SOS

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4
Q

Sos

A

GEF for Ras G protein

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5
Q

Ras

A

G protein that is inactive and membrane bound when bound to GDP but is activated by GEFs that exchange GTP for GDP; activate the Mitogen Activated Protein (MAP) kinase pathway once activated

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6
Q

MAP kinase pathway

A

Common signaling pathway to activate transcription factors; Active Ras -> activates Raf -> phosphorylates MEK -> phosphorylates MAP kinase -> MAP kinase dimerizes and translocates to nucleus -> atcivates transcription factors for cell proliferatoin (such as c-fos which activates cyclin D)

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7
Q

Cyclin D

A

Gene involved in the first step of cell division

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8
Q

How is the RTK signal terminated

A

Usually by downregulation of the receptor via phosphatases

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9
Q

Why are mutated versions of RTK clinically significant?

A

Mutated RTK can result in a constitutively active receptor that activates the Ras-MAP kinase pathway which is associated with tumor growth

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10
Q

Why are mutated Ras proteins clinically significant?

A

Mutated Ras can bind but not hydrolyze GTP causing them to be trapped in the active state

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11
Q

Her2 receptor

A

Commonly mutated in breast CA- single amino acid mutation leads to dimerization of the receptor w/o a ligand which activates downstream target proteins

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12
Q

TGF-beta signaling pathway

A

Activates many cellular processes including modulating the immune response, inhibiting cell proliferation, and promoting cell differentiation by phosphorylating proteins that are able to translocate to the nucleus and regulate transcription

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13
Q

What are the TGF-beta isoforms and what do they do?

A

TGF-beta has 3 isoforms; R2 and R3 bind TGF-beta and recruit R1, R1 is activated by R2 and then phosphorylates Smad proteins

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14
Q

What are the steps in the TGF-beta signaling pathway?

A

TGF-beta binds to R2 and R3 isoforms -> recruits R1 -> R2 phosphorylates R1 -> active R1 phosphorylates Smad3 -> dimerizes and translocates to nucleus and binds DNA

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15
Q

What are the 2 ways that the TGF-beta signaling pathway terminated?

A
  1. Sno and Ski proteins bind Smad3 and recruit HDACs to downregulate trasncription
  2. Negative feedback- TGF-beta activates inhibitory Smads which block Smad from translocating to the nucleus
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16
Q

How do cytokines transmit signals?

A

Ctokines do not have inherent kinase activity so they have to bind to other kinases; they use the JAK-STAT pathway

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17
Q

What is the JAK-STAT pathway?

A

Cytokines binds to receptor -> JAKs dimerize and activate -> creates binding site for STAT -> STAT dimerizes via SH2 domains -> translocates to nucleus and bind DNA

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18
Q

How is the cytokine signal terminated?

A

SHP1 phosphatase or SOCS proteins

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19
Q

How does SHP1 phosphatase terminate cytokine signaling?

A

Removes phosphate from JAK; w/o phosphate, JAK has very weak kinase activity and can’t phosphorylate STAT proteins

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20
Q

How do SOCS proteins terminate cytokine signaling?

A

Competitive inhibition w/ JAK or STAT bc they have SH2 domains, can also recruit ubiquitin ligase to ubiquinate JAKs

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21
Q

Xeljanz

A

RA tx that inhibits JAK

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22
Q

What cellular processes use cytokine signaling?

A

Hematopoiesis and the immune response

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23
Q

Frizzled receptor

A

Receptor for Wnt that regulates the levels of beta-catenin protein; consists of 7 transmembrane domains that associates w/ co-receptor LRP

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24
Q

What happens when Wnt is not bound to Frizzled?

A

W/o ligand, beta-catenin is recruited to a destruction complex (includes APC and Axin), phosphorylated, and ubiquinated

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25
Q

Familial Adenomatous Polyposis

A

Familial form of colon CA caused by mutated APC gene

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26
Q

What are the steps in the Wnt signaling pathway?

A

Wnt -> binds frizzled -> recruits Axin away from destruction complex -> beta-catenin is not degraded and translocates to nucleus -> associates with TCF -> activates genes for cell growth

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27
Q

How is Wnt clinically significant?

A

Wnt is critical for embryonic development and for regulating growth of colon/mammary epithelial cells

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28
Q

APC mutation

A

Common in colon CA; APC is mutated an unable to form a destruction complex which leads to overexpression of beta-catenin

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29
Q

Receptor cross talk

A

The input a cell receives from different receptors are integrated to trigger a particular pattern of changes in enzyme activity or gene expression

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30
Q

Beta-arrestin complex

A

While it normally shuts down GPCRs, it can recruit Src to activate MAP kinase which explains why cardiac hypertrophy is a feature of prolonged epi exposure

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31
Q

Cross talk between GPCRs an MAP kinase pathway

A

Prolonged epi exposure can lead to cardiac hypertrophy because beta arrestin complex recruits Src, which then activates the MAP kinase pathway

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32
Q

Mitogen

A

Any molecules that stimulates cell proliferation

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33
Q

What is the cell cycle?

A

The process that controls cell division

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34
Q

What are the 5 phases of the cell cycle?

A 
G0- quiescent
G1- initial commitment point for cell division
S- DNA replication
G2- preparation for mitosis
M- mitosis
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35
Q

Which cells go through the cell cycle?

A

All cells go through the cell cycle but at varying rates, eg cells of the GI tract are continually dividing while liver cells only divide if exposed to a specific stimulus and neurons only divide under unusual circumstances

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36
Q

Mitosis promoting factor (MPF)

A

Cyclin B-CDK1 complex that stimulates mitosis/mieosis; stimulated by progesterone

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37
Q

Cyclins

A

Proteins that are synthesized and degraded w/ the cell cycle to activate specific cyclin-dependent kinases (CDKs)

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38
Q

CDKs

A

Proteins that regulate the cell cycle by allowing for ordered recruitment and expression of genes during cell cycle progression

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39
Q

Cyclin D-CDK4,6

A

Activated by GFs during G1 to initiate the process of cell division to inhibit Rb ie induce EF2

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40
Q

Cyclin E-CDK2

A

Expressed later in G1 after the cell passes the restriction point; increases phosphorylation of Rb so that EF2 is fully activated and assemble to pre-replication complex proteins ORC, mcm helicase, CDC6, and CDT1

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41
Q

How do cyclins activate CDKs?

A

Cyclin binding causes a conformational change that facilitates ATP binding and exposes a phosphorylation site on the T-loop of the CDK; phosphorylation of the T-loop is what activates the CDK

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42
Q

At what point is the cell committed to divide?

A

Once it passes the restriction point in the G1 phase

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43
Q

What is the restriction point?

A

Once a cell has accumulated enough cyclin E

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44
Q

Rb

A

Tumor suppressor that inhibits the EF2 transcription factor; inactivated by cyclin D-CDK4,6

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45
Q

EF2

A

Transcription factor that induces DNA replication enzymes, cyclin D, cyclin E, and cyclin A which are required for cell to proceed to the next stage of the cell cycle

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46
Q

ORC

A

Origin replication complex

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47
Q

What happens during the S phase?

A

Cyclin E is degraded so CDK2 can associate with cycin A which triggers recruitment of DNA polymerase and activates mcm helicase

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48
Q

Why can DNA only be replicated once?

A

Origins that have fired once cannot be relicensed until they pass through the following mitosis; CDC6 is degraded or exported

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49
Q

What happens during the G2 phase?

A

Cyclin A and B accumulate and form complexes with CDK1

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50
Q

What determines whether the cell progresses from G2 to mitosis?

A

Cell size (ie whether it has sufficient cell components) and some external features or DNA repair pathways

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51
Q

What do cdc25 and Wee1 do?

A

Control progression from G2 to mitosis

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52
Q

cdc25

A

Phosphatase that activates the Cyclin B-CDK1 (MPF) complex so that the cell can continue to mitosis

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53
Q

Wee1

A

Kinase that adds an inhibitory phosphate to tyrosine 15 on the Cyclin b-CDK1 complex so that the cell is unable to progress to mitosis

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54
Q

How do mitotic cyclins (MPF) trigger mitosis?

A

Phosphorylate several proteins to induce mitosis including lamins, condensins, microtubule associated proteins, and Anaphase Promoting Complex/Cyclosom (APC/C)

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55
Q

What happens when MPF phosphorylates lamins?

A

Lamin network is disrupted and the nuclear envelope disassembles

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56
Q

What happens when MPF phosphorylates condensins?

A

Chromosomes condense

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57
Q

What happens when MPF phosphorylates microtubule associated proteins?

A

Mitotic spindle can form

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58
Q

What happens when MPF phosphorylates the APC/C?

A

Chromosomes are able to separate

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59
Q

APC/C

A

Ubiquitin ligase that degrades the anaphase inhibitor securin and later degrades MPF which causes degradation of cyclin B so that the cell can re-enter G1

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60
Q

cdc20

A

Binds to APC/C and triggers it to ubiquinate securin

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61
Q

cdh1

A

Binds to APC/C and triggers it to ubiquinate cyclin B

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62
Q

Which 2 proteins regulate the APC/C?

A

cdc20 and cdh1

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63
Q

What is the separase enzyme?

A

Cleaves the links holding sister chromatids together; inhibited by securin

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64
Q

Securin

A

Enzyme that inhibits anaphase by inhibiting the separase enzyme

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65
Q

Interphase

A

Encompasses G0, G1, S, and G2 phases

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66
Q

Prophase

A

Chromosomes condense and spindle begins to assemble

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67
Q

Prometaphase

A

Nuclear envelope disassembles, spindle assembly is completed, chromosomes begin to align b/w the two spindle poles

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68
Q

Metaphase

A

Chromosomes completely align to trigger anaphase

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69
Q

Anaphase

A

Chromosomes physically separate, sister chromatids move to opposite spindle poles and poles then move apart

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70
Q

Telophase

A

Nuclear envelope reforms and cytokinesis occurs

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71
Q

What % of the human genome accounts for individual differences?

A

0.1%

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72
Q

Endogenous (spontaneous) mutagenesis

A

DNA replication errors caused by normal cellular processes

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73
Q

Genetic defects

A

Defects in the endogenous DNA repair and detox machineries that increase risk of developing certain types of CAs

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74
Q

Exogenous mutagenesis

A

Mutations resulting from exposure to carcinogenic agents

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75
Q

What are the 5 types of DNA damage caused by endogenous mutagenesis?

A
  1. oxidation of bases
  2. alkylation of bases
  3. hydrolysis of bases ie deamination, depurination, etc
  4. bulky adduct formation
  5. mismatch of bases
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76
Q

Oxidation of bases

A

ROS oxidize bases and interrupt the DNA

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77
Q

Alkylation of bases

A

Addition of alkyl groups

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78
Q

Deamination

A

Loss of amino group from C, methyl C, G, or A (deamination of A or G is more rare)

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79
Q

What happens when C is deaminated?

A

Deaminated C produces U and causes a C to T point mutation

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80
Q

What happens when A is deaminated?

A

Deaminated A produces hypoxanthine (HX) and causes an A to G point mutation

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81
Q

What happens when methyl C is deaminated?

A

Deaminated methyl C is the same as T and the cell cannot differentiate between the mutated T and normal T so this causes an irreversible G-C to A-T mutation

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82
Q

Nitrous acid, HNO2

A

Potent mutagen formed from nitrates (NO3) or nitrites (NO2) that stimulates deamination

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83
Q

Vitamin C

A

Inhibits nitrosamine formation in the stomach

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84
Q

How do BRCA1 & 2 contribute to risk of breast CA?

A

These are DNA repair machinery that increase risk of breast CA when they are mutated

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85
Q

HPV

A

Causes cervical CA

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86
Q

HBV

A

Causes liver CA

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87
Q

Epstein-Barr virus

A

Causes lymphoma

88
Q

H. pylori

A

Causes gastric CA

89
Q

UVB light

A

Directly damages DNA by creating pyridine dimers by cross-linking adjacent C and T bases

90
Q

UVA light

A

Indirectly damages DNA by producing free radicals

91
Q

Ionizing radiation

A

Causes breaks in DNA strand

92
Q

Thermal disruption at elevated temperature

A

Increases the rate of depurination and single strand breaks in DNA

93
Q

How does ionizing radiation produce single or double stranded breaks in DNA?

A

ROS formation which interact with C4 and create unstable intermediates

94
Q

UV irradiation

A

Causes formation of pyridine-pyridine dimers (ie T-T, C-C, or T-C) which are difficult to repair

95
Q

Intercalating agents

A

Chemicals that slide b/w stacked bases of the DNA duplex and disrupt replication and transcription

96
Q

What are naturally occurring intercalating agents excreted by organisms

A

Actinomysin D, aflatoxin, and echinomysin

97
Q

Aflotoxin B1

A

Toxic metabolite produced by mold that can lead to liver CA if not detoxified

98
Q

Alkylating agents

A

DNA cross-linking agents containing reactive alkyl groups that prevent DNA synthesis and separation, inhibit transcription, and induct mutagenesis

99
Q

MNNG and nitrogen mustard

A

Alkylating agents

100
Q

What are the 3 main types of chemo?

A

Alkylating agents, anti-metabolites, and organic drugs/natural products

101
Q

Cyclophosphamide, cisplatin, and carboplatin

A

Alkylating chemo drug that cross-links DNA and forms adducts

102
Q

Methotrexate

A

Anti-metabolite chemo drug that mimics tetrahydrofolate and inhibits DNA synthesis

103
Q

5-flourouracil (5-FU)

A

Anti-metabolite chemo drug that inhibits DNA synthesis by competing w/ uracil

104
Q

Doxorubicin & andriamycin

A

Organic chemo drugs that inhibit topoisomerase II

105
Q

Taxol & Paclitaxel

A

Organic chemo drugs that bind beta-tubulin and stabilize microtubule assembly

106
Q

Vincristine & Vinblastine

A

Organic chemo drugs that bind to tubulin and inhibit MT assembly

107
Q

Radiation therapy

A

CA tx that produces double-stranded DNA breaks and generates massive amounts of ROS which causes the cells to commit apoptosis

108
Q

Missing base

A

Caused by acid or heat depurination

109
Q

Altered base

A

Caused by IR and alkylating agents

110
Q

Incorrect base

A

Caused by spontaneous deaminations

111
Q

Deletion-insertion

A

Caused by intercalating agents

112
Q

Dimer formation

A

Caused by UV radiation

113
Q

Double stranded DNA breaks

A

Caused by ionizing radiation and chemicals eg bleomycin

114
Q

Interstrand cross-links

A

Psoralen derivatives; Mitomycin C

115
Q

Transition mutation

A

BP substitutions from a purine to purine or pyrimidine to pyrimidine

116
Q

Transversion mutation

A

BP substitutions from a purine to a pyrimidine or vice versa

117
Q

What are the 4 types of BP mutations?

A

BP substitutions (transitions or transversions), insertions, and deletions

118
Q

What type of mutations causes SCA?

A

BP substitution

119
Q

What type of mutation causes CF?

A

BP deletion

120
Q

What type of mutation causes Fragile X mental retardation?

A

BP insertion

121
Q

What are the 3 types of DNA repair?

A

Excision repair, mismatch repair, repair DNA strand breaks

122
Q

Base excision repair (BER)

A

Pathway for repairing non-helix-distorting base lesions; glycolysases recognize and remove aberrant base, endonucleases remove the sugar phosphate, DNA polymerase beta fills in the gap, and ligase joins the strands

123
Q

Nucleotide excision repair (NER)

A

Pathway for repairing bulky-helix-distorting lesions (ie from pyridine dimers; damaged DNA is recognized, unwound, incised, and repaired

124
Q

global genomic NER and transcription-coupled NER

A

2 different methods of NER that differ in how they recognize damaged DNA

125
Q

Xeroderma pigmentosa (XP)

A

Genetic defect in genes responsible for NER pathway causing severe sensitivity to UV light and can lead to premature aging, skin CAs, and eye or neurological problems

126
Q

Mismatch Repair (MMR) System

A

Corrects mismatches of normal base-pairing and inhibits homologous recombination b/w non-identical sequences

127
Q

MSH2

A

Codes for protein that recognizes mismatched bps

128
Q

MLH1

A

Codes for enzymes that cut out the mismatched bp

129
Q

What mutations are involved in hereditary colon CA?

A

Mutations in MSH2 or MLH1 that code for proteins needed for the MMR System

130
Q

How do MMR proteins know which is the correct nucleotide?

A

In bacteria, certain A residues become methylated after a new strand is synthesized. The MMR system acts quickly and it assumes that the methylated (parent) strand is the correct bp and then it corrects the daughter strand. We aren’t sure how this process works in eukaryotes

131
Q

Hereditary nonpolyposis colon CA

A

Most involve genetic defects in the MMR system

132
Q

How are double stranded breaks (DSBs) repaired?

A

Homologous recombination (HR) or non-homologous end joining (NHEJ)

133
Q

BRCA1

A

Recruited to sites of DSBs and directs NHEJ

134
Q

BRCA2

A

Regulates HR

135
Q

DnaA

A

Prokaryotic origin binding protein

136
Q

ORC + cdt1

A

Eukaryotic origin binding protein

137
Q

SSB

A

Prokaryotic ssDNA binding protein

138
Q

RPA

A

Eukaryotic ssDNA binding protein

139
Q

DnaB

A

Prokaryotic helicase

140
Q

MCM 2-7, cdc 45, GINS (CMG)

A

Eukaryotic helicase

141
Q

DnaC

A

Prokaryotic helicase loader

142
Q

DnaG

A

Prokaryotic primase

143
Q

Polymerase primase

A

Eukaryotic primase

144
Q

Delta complex of DNA Pol III

A

Prokaryotic polymerase clamp loader

145
Q

RFC

A

Eukaryotic polymerase clamp loader

146
Q

Beta subunit of DNA Pol III

A

Prokaryotic polymerase sliding clamp

147
Q

PCNA

A

Eukaryotic polymerase sliding clamp

148
Q

DNA Pol III

A

Prokaryotic polymerase

149
Q

Pol Delta

A

Eukaryotic polymerase for lagging strand

150
Q

Pol Epsilon

A

Eukaryotic polymerase for leading strand

151
Q

Pol I and RNase H

A

Prokaryotic RNA repair and replacement

152
Q

RNase H1, FEN 1, and Pol delta

A

Eukaryotic RNA repair and replacement

153
Q

DNA ligase

A

Prokaryotic and eukaryotic gap joining protein

154
Q

Tus protein

A

Prokaryotic termination protein

155
Q

Telomerase

A

Eukaryotic termination protein

156
Q

Topisomerase and DNA gyrase

A

Prokaryotic supercoil relaxer proteins

157
Q

Topoisomerase

A

Eukaryotic supercoil relaxer proteins

158
Q

Fork protein complex

A

Link helicase and polymerase in eukaryotes

159
Q

Autophagy

A

Mildest form of cell death for organelle turnover in which the cell is engulfed from within; can be pro-life or pro-death mechanism )either via autophagy or induction of apoptosis)

160
Q

Autophagosome

A

Double membrane vacuole formed from engulfed portions of cytoplasm that will fuse with lysosomes to make an autolysosome for autophagy

161
Q

Which diseases feature autophagy?

A

Huntington’s dz, prion dx, breast CA cells tx’d w/ Tamoxifen

162
Q

Extrinsic apoptosis pathway

A

Triggered by immune response ie killer T cells or TNF-alpha –> FASR/TNFR –> oligomerizes receptor and recruits death domain containing FADD/TRADD –> recruits and activates caspase 8 –> activates effector caspases ie caspase 3 –> apoptosis

163
Q

Intrinsic apoptosis pathway

A

Activated by stress/DNA damage

164
Q

Bcl-2, bcl-xl

A

Anti-apoptotic proteins located in the mitochondrial membrane that inhibit apoptotic proteins such as Bax and Bak

165
Q

BH3-Only proteins

A

Bid and Bim; stimulate pore formation by pro-apoptotic Bcl proteins (Bax/Bak) and inhibit function of anti-apoptotic proteins (Bcl-2/bcl-xl)

166
Q

Bax, Bak

A

Pro-apoptotic Bcl proteins that dimerize and release cytochrome C through pores

167
Q

How do Bcl proteins control apoptosis

A

Bcl proteins are located in the mitochondrial membrane; they come in 3 varieties- pro and anti apoptotic and BH3-only. The ration of pro to anti apoptotic proteins determines whether the cell will commit apoptosis

168
Q

Anti-apoptotic Bcl proteins

A

Bcl-2, bcl-xl

169
Q

Pro-apoptotic Bcl proteins

A

Bax, Bak

170
Q

BH3-only Bcl proteins

A

Bid, Bim, Bad

171
Q

Apoptosome

A

Forms by binding of cytochrome c and Apaf-1 when they are released from the mitochondrial membrane in the intrinsic apoptosis pathway; binds and activates caspase 9

172
Q

Caspase 9

A

Initiator caspase in the intrinsic apoptosis pathway

173
Q

Effector caspases

A

Activated by initiator caspases and result in apoptosis

174
Q

How is the external apoptotic pathway linked to the internal pathway?

A

Caspase 8 can cleave and activate the BH3-only protein Bid, which promotes pore formation by pro-apoptotic proteins and thus apoptosis

175
Q

Anoikis

A

A specific type of apoptosis triggered by detachment from the ECM; tumor cells must learn to overcome this in order to metastasize

176
Q

Akt kinase

A

Kinase stimulated integrin-ECM binding that adds inhibitory phosphate to Bad which inhibits apoptosis

177
Q

How is anoikis activated?

A

W/o integrin-ECM binding, Akt is not activated so it can’t inhibit Bad and thus can’t inhibit apoptosis

178
Q

UPR

A

Unfolded protein response; cell death pathway activated by ER stress and unfolded proteins that leads to apoptosis via activation of caspase 12, which activates caspase 3

179
Q

BiP

A

Chaperone protein that senses ER stress

180
Q

Necrosis

A

“Extreme apoptosis” triggered by toxin exposure, ischemia, or hypoxia that causes the cell to swell and the membrane to break down, releasing intracellular contents and triggering an inflammatory response

181
Q

Repurfusion injury

A

Further injury/induction of necrosis following influx of immune cells into injury site during the inflammatory response which lead to accumulation of ROS/NGO

182
Q

What controls whether a cell will undergo necrosis vs apoptosis?

A

Extend of mitochondrial membrane permeability ie leve of energy depletion

183
Q

Beclin/Atg proteins

A

Important for forming the autophagosome

184
Q

Necroptosis

A

“Programmed necrosis”; an alternative caspase indepedent pathway from the activation of TNF-alpha receptor that involves RIP1 & 3 proteins and results in release of metabolic enzymes, increased ROS, release of cytotoxic mitochondrial proteins, and membrane damage

185
Q

Entosis

A

Cellular catabolism observed in tumor cells

186
Q

Parthanatos

A

Cell death involving Poly-ADP-ribose polymerase-1

187
Q

Proto-oncogene

A

Genes that code for protein that promotes cell proliferation or inhibits apoptosis

188
Q

Oncogene

A

Mutated proto-oncogene or one w/ altered expression that confer gain of function to the cell

189
Q

Tumor supressor gene

A

Gene coding for proteins that inhibit cell proliferation or promote apoptosis; mutation causes loss of function

190
Q

Tumorigenesis in colon CA

A

Loss of APC -> hyperplastic epithelium
DNA hypomethylation -> early adenomas
Activation of K-ras -> intermediate adenomas
Loss of 18q TSG -> late adenomas
Loss of p53 -> carcinoma -> invasion and mets

191
Q

Types of proto-oncogenes

A

Mutation (point or deletion), chromosomal translocation, amplification ie overexpression, GFs and GFRs, signaling proteins, TFs, cell cycle proteins, anti-apoptotic protiens

192
Q

How do GFs function as proto-oncogenes?

A

Trigger entry into G1

193
Q

IL-2 and IL2R

A

T cell GF that is overexpressed in T-cell leukemia

194
Q

Her2 receptor mutations

A

Feature of breast CA that causes GF receptor to autodimerize

195
Q

Trastuzumab

A

Her2 Ab used to tx breast CA pts w/ Her2 to Neu mutation

196
Q

Gefitinib

A

EGFR tyrosine kinase receptor used to tx non-small cell lung CA w/ EGFR mutations

197
Q

Erb2 oncoprotein

A

Oncogenic form of EGFR

198
Q

B-raf mutation

A

MAP kinase kinase kinase that is common in metastatic melanoma;

199
Q

Vemurafenib

A

Mutant Raf kinase inhibitor used to tx melanoma pts however pts can develop resistance

200
Q

bcr-abl

A

“philadelphia chromosome”; common chromosomal translocation seen in CLL where c-abl kinase is fused to the bcr gene which alters the specificity of the abl kinase and promotes tumorgenicity

201
Q

Gleevac

A

Abl kinase inhibitor used to tx CML and other CAs

202
Q

myc

A

TF that activates cyclin D, E2F; overexpression is seen in late-stage neuroblastomas and B-cell lymphomas

203
Q

CLL

A

Chromosomal translocation results in increased expression of anti-apoptotic protein bcl-2

204
Q

Types of tumor supressors

A

Receptors/signal transducers involved in inhibiting cel cycle, cell cycle inhibitors, check-point control proteins, pro-apoptotic proteins, DNA repair enzymes

205
Q

What is the primary anti-growth signaling pathway?

A

TGF-beta; stimulates p15 and PAI-1

206
Q

p15

A

TGF-beta responsive protein that inhibits cyclin D-CDK4

207
Q

PAI-1

A

TGF-beta responsive protein that regulates ECM proteins

208
Q

Hereditary retinoblastoma

A

Pts are heterozygous for Rb but tumor cells have lost both Rb alleles (loss of heterozygosity)

209
Q

p21-CIP family

A

Bind cyclin-CDK complexes and block activity

210
Q

INK4 family

A

CDK inhibitors specific for cyclin D-CDK4,6; includes p15 and p16

211
Q

p15 & p16

A

INK4 family CDK inhibitor that specifically inhibit cyclin D-CDK4,6

212
Q

p16 mutations

A

Seen in families genetically disposed to melanoma

213
Q

Check point control proteins

A

Regulate progression through cell cycle; include p21-CIP family and INK4 family proteins

214
Q

p53

A

Key check point control protein that is the most commonly mutated protein in CA; activates CDK inhibitors and pro-apoptotic proteins once it is stabilized by DNA damage

215
Q

BRCA1

A

Functions in DNA-damaged induced cell cycle checkpoins, and as a scaffold protein, enhances p53 phosphorylation and stabilization after DNA damage, regulates Wee1 kinase and cdc25 phosphatase

216
Q

Telomerase

A

Enzyme that extends telomeres; lacking in normal adult cells

CSF (3 decks)

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