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BIO 317 > 7 - Growth Factors, Oncogenes, and Cancer > Flashcards

7 - Growth Factors, Oncogenes, and Cancer Flashcards

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1
Q

What decisions do cells make in the cell cycle?

A

Whether to proceed to S phase, wait at G1 phase, or stop at G0 phase

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2
Q

What helps determine the decision in the cell cycle?

A

Cell signaling

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3
Q

What was used to study how cell signaling was involved in the cell cycle?

A

By studying unregulated cell signaling and cell growth (cancer)

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4
Q

What are some properties of malignant cells?

A

Not responsive to influences that normally cause cells to stop growth and division

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5
Q

What conditions will cause normal cells to stop growing?

A

Lack of growth factors, and when cells touch neighboring cells

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6
Q

What is contact inhibition?

A

Stopping of cell growth when it touches other cells

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7
Q

What do normal cells look like in a dish?

A

Thin monolayer

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8
Q

What do malignant cells look like in a dish?

A

Clumps (foci)

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9
Q

What is the phenotype of normal fibroblasts?

A

Flat, many extensions, contact inhibition

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10
Q

What is the phenotype of malignant fibroblasts?

A

Rounded, few extensions, no contact inhibition

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11
Q

What is tumorigenesis?

A

The development of a malignant tumor

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12
Q

How does cancer start?

A

Uncontrolled proliferation of a single cell

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13
Q

How does tumorigenesis occur?

A

Through a cumulative progression of genetic alterations

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14
Q

What happens to cells as they progress through tumorigenesis?

A

Cells become less responsive to growth regulation, and better able to invade normal tissues

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15
Q

What is the first step of tumorigenesis?

A

Formation of a benign tumor

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16
Q

What is a benign tumor?

A

A tumor composed of cells that proliferate uncontrollably but cannot metastasize

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17
Q

What does it mean to metastasize?

A

Leave ECM to go to the bloodstream (spread)

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18
Q

What are the genes involved in carcinogenesis responsible for?

A

Cell cycle regulation, cell adhesion, and DNA repair

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19
Q

Why is the sequence of when genes mutate important in cancer?

A

Sequence influences how the cancer develops

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20
Q

What did Peyton Rous do?

A

Isolated the first tumor-causing animal virus

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21
Q

True or false: Peyton Rous received the Nobel Prize shortly after his discovery of Rous sarcoma virus

A

False: it took nearly 50 years after his discover in 1911 to receive the Nobel Prize in 1966

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22
Q

What happened in the 1960s that helped in studying cancer?

A

Molecular biology was being used to understand how viruses contain genetic material, which could be used to infect mammalian cells

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23
Q

What led to the identification of many cancer causing genes in humans?

A

Investigations of abnormal cell growth due to viral infection

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24
Q

What did Baltimore, Dulbecco, and Temin discover about viruses?

A

They have RNA (not DNA) as genetic material, and had reverse transcriptase (RNA -> DNA)

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25
Q

What did Varmus and Bishop do?

A

Discovered the first oncogene, src

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26
Q

What is an oncogene?

A

A gene that creates oncology (cancer)

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27
Q

How was it proven that src caused tumors?

A

Adding vsrc led to a tumor, and removing vsrc stopped tumor growth

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28
Q

True or false: normal cells also contain src

A

True: c-src is a proto-oncogene

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29
Q

What is a proto-oncogene?

A

A gene that could become an oncogene when mutated

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30
Q

What is the origin of oncogenes in viruses?

A

Viruses take this DNA information from hosts

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31
Q

What did Erikson, Sefton, and Hunter do?

A

Study what src did

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32
Q

How was the function of src discovered?

A

Used radioactive ATP, and a 2D gel to find the difference between v-src lines and normal cell lines

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33
Q

What was different in the v-src 2D gel compared to the normal 2D gel?

A

Only tyrosine was phosphorylated by src

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34
Q

What was the conclusion of the 2D gels of v-src and normal cell lines?

A

Src was a tyrosine kinase

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35
Q

What is the function of src?

A

Tyrosine kinase

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36
Q

How much more active is v-src compared to c-src?

A

3x more

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37
Q

What was the significance of finding the function of src?

A

First evidence that protein kinases may play a role in cell growth

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38
Q

What cell signaling pathways are regulated by proto-oncogenes and tumor suppressor genes?

A

Apoptosis, proliferation, immortalization, and senescence

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39
Q

What is immortalization involved with?

A

The regulation of telomerase

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40
Q

What is senescence?

A

Cells are metabolically active but are non-dividing

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41
Q

What do proto-oncogenes do?

A

Promote cell survival / proliferation

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42
Q

What mutations occur with proto-oncogenes in cancer?

A

Gain of function mutations (unregulated cell growth / proliferation)

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43
Q

What do tumor suppressor genes do?

A

Inhibit cell survival or proliferation

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44
Q

What mutations occur with tumor suppressor genes in cancer?

A

Loss of function mutations (allow unregulated cell growth / proliferation)

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45
Q

What do caretaker genes do?

A

Repair or prevent DNA damage

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46
Q

What mutations occur with caretaker genes in cancer?

A

Loss of function mutations (allow mutations to accumulate)

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47
Q

Why does cancer increase as you age?

A

More time to accumulate mutations

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48
Q

What is colon cancer a good example of?

A

Cancers can have very specific sequences of mutations to develop

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49
Q

What is the structure of c-src?

A

Kinase domain (binds to ATP), C-terminal SH2 domain, and N-terminal SH3 domain

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50
Q

What does SH2/SH3 stand for?

A

src homology 2/3 domains

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51
Q

How is c-src inhibited?

A

Autoinhibition. SH3 domain binds to proline rich sequence, inhibiting kinase domain, and Phospho-Y527 binds to SH2 domain to inhibit kinase domain

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52
Q

How does SH3 inhibit c-src?

A

Binds to proline rich sequences to inhibit kinase domain

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53
Q

How does SH2 inhibit c-src?

A

Binds to Phospho-Tyr527 to inhibit kinase domain

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54
Q

What happens when Tyr527 in c-src is phosphorylated?

A

Binds to SH2 domain, inhibiting c-src

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55
Q

What happens when Tyr527 in c-src loses a phosphate?

A

Releases SH2 and SH3, activating the kinase

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56
Q

What is the difference in protein structure between c-src and v-src?

A

No Y527

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57
Q

What is the difference in genes between c-src and v-src?

A

v-src is a C-terminal truncation mutation

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58
Q

Why is v-src always active?

A

It has no Y527 to bind to SH2 to inhibit the kinase domain. Thus, it is always active

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59
Q

What question was raised by studying how viruses caused cancer?

A

If viruses use genetics to cause cancers, can human genes do the same thing?

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60
Q

How can a proto-oncogene be mutated into an oncogene?

A

Through mutation in coding sequence, gene amplification, or chromosome rearrangement

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61
Q

How does a mutation in the coding sequence affect a proto-oncogene?

A

Produces hyperactive protein in a normal amount

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62
Q

How does a gene amplification affect a proto-oncogene?

A

Normal protein is overproduced

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63
Q

How does a chromosome rearrangement affect a proto-oncogene?

A

Can be either a hyperactive protein, or overproduced

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64
Q

How can a chromosome rearrangement create a hyperactive protein from an oncogene?

A

Nearby regulatory DNA sequence

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65
Q

How can a chromosome rearrangement create overproduced proteins from an oncogene?

A

Fusion to an actively transcribed gene

66
Q

What did Robert Weinberg do?

A

Discover human cancer genes

67
Q

What techniques did Robert Weinberg use?

A

Insert human oncogene into mouse fibroblasts

68
Q

What was required to perform Weinberg’s studies?

A

1980’s technology to introduce DNA into cells

69
Q

How does DNA transfection work?

A

Add smaller and smaller fragments of cancer DNA until the gene is cloned

70
Q

What is a phage?

A

A virus that infects bacteria

71
Q

How were phages used in Weinberg’s studies?

A

Each phage had a segment of DNA to be injected into E. Coli

72
Q

How come you only get a single gene at a time with DNA transfection?

A

It is an inefficient process, so only a small proportion of cells take up the cut DNA (and the right DNA)

73
Q

How was the human DNA separated from mouse DNA in Weinberg’s studies?

A

By using an Alu probe

74
Q

What are Alu sequences?

A

Repetitive DNA sequences found in humans, and not mice

75
Q

How were Alu sequences used in Weinberg’s studies?

A

Used to probe the human oncogene from the mouse DNA

76
Q

What protein did Weinberg discover?

A

Ras

77
Q

What is ras?

A

A small monomeric G-protein

78
Q

What does ras do?

A

Activate downstream responses when bound to GTP, inactive when bound to GDP

79
Q

What is the difference between ras and other G-proteins, such as Gs?

A

Ras is monomeric, and Gs is trimeric

80
Q

What is the significance of ras in cancer?

A

Ras is mutated in many cancers

81
Q

What is needed for ras to properly function?

A

GEFs and GAPs

82
Q

What are the GEFs for trimeric G-proteins?

A

The receptors themselves

83
Q

What does an inhibitory ras mutation do?

A

Can’t bind to GEF to exchange GDP for GTP, thus staying inactive

84
Q

What does an excitatory ras mutation do?

A

Blocks ability of GAP / ras to hydrolyze GTP into GDP, thus staying active

85
Q

What are some downstream effectors of ras?

A

Raf, MEK/MAP kinases, etc.

86
Q

Generally, what does ras signal for?

A

Proliferation (stimulate cell cycle)

87
Q

What are the characteristics of ras oncoprotein?

A

Higher affinity for GTP, and lower GTPase activity (stuck in “on” position)

88
Q

True or false: growth factor is needed for oncogenic ras to function

A

False: no growth factor is needed since ras is always on

89
Q

What happens when src* is active or ras* is active?

A

Cells divide

90
Q

What happens when src* is active and ras* is inhibited?

A

Cells do not divide

91
Q

What happens when src* is inhibited and ras* is active?

A

Cells divide

92
Q

What is the simplest relationship between src* and ras*?

A

src -> ras (downstream in a common signaling pathway)

93
Q

What is the GEF for ras?

A

SOS

94
Q

What is the GAP for ras?

A

RasGAP

95
Q

What is the problem with src -> ras?

A

Normally, src is not the major upstream effector of ras

96
Q

When does src -> ras?

A

When src is mutated to be constantly active (phosphorylate things it shouldn’t)

97
Q

What does src activate (when it is mutated)?

A

SOS (GEF for ras)

98
Q

What did Stanley Cohen do?

A

Looked at growth factors to find upstream effectors of ras

99
Q

What does EGF stand for?

A

Epidermal growth factor

100
Q

What happens when EGF is added to a cell?

A

The cell will divide

101
Q

What happens when EGF and anti-ras is added to a cell?

A

The cell will not divide

102
Q

What is the conclusion of adding EGF and anti-ras to a cell?

A

EGF and ras must be in the same pathway (ras inhibition stopped growth factors)

103
Q

What does EGFR stand for?

A

Epidermal growth factor receptor

104
Q

What is EGFR?

A

A receptor tyrosine kinase that can autophosphorylate

105
Q

How many membrane passes are in EGFR?

A

One transmembrane region

106
Q

How does EGFR work?

A

Binding of a ligand causes dimerization, which activates receptors through autophosphorylation

107
Q

What happens once a tyrosine kinase receptor is activated?

A

Phospho-tyrosines act as docking sites for other proteins to continue signal

108
Q

What binds to activated EGFR?

A

SOS (and GRB2)

109
Q

What does GRB2 do?

A

Coupled SOS to phospho-tyrosines on activated EGFR

110
Q

True or false: receptor tyrosine kinases can only act in one pathway

A

False: the many phospho-tyrosines can act as docking sites for proteins in many pathways at once

111
Q

True or false: multiple receptor tyrosine kinase pathways are independent

A

False: they can also converge

112
Q

What gene encodes EGFR?

A

erb-B

113
Q

What does erb-B do?

A

Encode for EGFR

114
Q

What does v-erb-B look like?

A

Partial deletion

115
Q

What does v-EGFR look like?

A

No extracellular ligand binding site

116
Q

Why is v-EGFR always activated?

A

No extracellular domain leads to receptors being always dimerized, and thus activated

117
Q

What does EGF activate?

A

EGFR

118
Q

What are some oncogenes in the receptor tyrosine kinase / ras / MAP kinase cascade?

A

sis (PDGF, growth factor), erb-B (EGFR, receptor), ras (G-protein, and modulators), raf (MAPKKK, kinase), transcription factors (myc, fos, jun, ets)

119
Q

What do many proto-oncogenes encode for?

A

Cell surface receptors

120
Q

What mutation effects will lead to constitutive activation of receptor tyrosine kinases?

A

Ligand-independent dimerization, or overproduction

121
Q

What is Her2?

A

A receptor tyrosine kinase

122
Q

What is the difference in structure between c-Her2 and v-Her2?

A

c-Her2 has a val, while v-Her2 has a gln

123
Q

What is the significance of the val-gln mutation in Her2?

A

Keeps receptors dimerized, and thus keeps signal on

124
Q

What can be used to treat oncogenic receptors?

A

Monoclonal antibodies

125
Q

What can receptor tyrosine kinases signal for?

A

Cell growth, cytoskeleton, anchorage-dependent growth, contact inhibition, metabolism, etc.

126
Q

What is the first step of cancer?

A

Initiation (a mutation gives one cell an advantage)

127
Q

What is the second step of cancer?

A

Promotion (a second mutation increases the advantage)

128
Q

What is the third step of cancer?

A

Progression (chromosomal instability, invasive)

129
Q

What does Gleevec do?

A

Binds to oncogenic kinase through competitive inhibition

130
Q

What was the first discovered tumor suppressor gene?

A

Retinoblastoma

131
Q

What does RB stand for?

A

Retinoblastoma

132
Q

What is RB?

A

A tumor suppressor gene

133
Q

What is sporadic RB?

A

Two separate mutations leading to loss of RB

134
Q

What is familial RB?

A

One allele passed from parent, and another allele mutated, leading to loss of RB

135
Q

How can a cancerous phenotype be suppressed (for RB)?

A

By adding wild-type RB

136
Q

What strategies are being used to combat cancer?

A

Immunotherapy, targeting cancer proteins, angiogenesis

137
Q

What is passive immunotherapy?

A

Uses patient’s own antibodies to respond to tumor cells

138
Q

What is active immunotherapy?

A

Uses patient’s own immune system to target malignant cells

139
Q

How does active immunotherapy work?

A

Have cells display tumor proteins to be marked by immune system

140
Q

What is angiogenesis?

A

Formation of new blood vessels

141
Q

Why do tumors need angiogenesis?

A

Constant division is metabolically costly (needs nutrients through vasculature)

142
Q

What signal is used in angiogenesis?

A

VEGF

143
Q

How does mutating RasGAP (structurally) interact with Ras?

A

Mutated RasGAP cannot bind to ras to increase its GTPase activity, thus keeping ras GTP-bound and always on

144
Q

What do cancer drugs impact?

A

Any rapid growth

145
Q

What is meant by “collateral damage” (for cancer drugs)?

A

Many cancer drugs have side effects that need to be taken into consideration

146
Q

Why do adverse reactions arise from monoclonal antibody therapies?

A

Immune system is recruited, which can lead to many reactions

147
Q

True or false: Gleevac works for all receptors that it is meant for

A

False: there can be changes in the receptor that make it resistant to Gleevac (desensitization)

148
Q

Are oncogene mutations dominant or recessive?

A

Dominant

149
Q

Why are oncogene mutations dominant?

A

One copy is enough to keep the signal turned on (only one copy is needed to be mutated for an effect)

150
Q

Are tumor suppressor gene mutations dominant or recessive?

A

Recessive

151
Q

Why are tumor suppressor gene mutations recessive?

A

One copy is enough to keep the signal turned off (need both copies mutated for an effect)

152
Q

How can src activate SOS when overactive, and not under normal conditions?

A

Localization can be overcome with active mutations (overlapping and intersecting pathways)

153
Q

True or false: monoclonal antibody therapy is constant

A

True: you need to keep having treatment to keep the cells under control

154
Q

What environmental conditions often lead to cancer?

A

DNA damage (radiation, ultraviolet light, etc.)

155
Q

True or false: cancer treatment is unprediactable

A

True: therapies are often very personalized

156
Q

True or false: c-src is a major upstream affector of ras

A

False: it normally does not activate SOS

157
Q

True or false: v-src is a major upstream affector of ras

A

True: v-src is always on, which makes it able to activate SOS

158
Q

Why is it unlikely to reverse the mutation of c-src to v-src?

A

The truncation means that part of the gene is missing

159
Q

How do cancer cells avoid treatment?

A

Rapid division with an unstable genome leads to many mutations

160
Q

How does telomerase impact cancer cells?

A

Have just enough to maintain telomeres (not significantly longer) and maintain immortality

BIO 317 (27 decks)

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