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Exam 4 (Baines + Bowles) Flashcards

1
Q

What is the Warburg Effect?

A

tumor cell has HUGE increase in glucose uptake to meet metabolic demand

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2
Q

Tumor cells need (less/more) glucose to get same ATP as normal cells because they undergo ____.

A

More
anaerobic glycolysis

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3
Q

Warburg Proposal for Cancer

A

cancer caused by damage to ETC
cancer cells use anaerobic glycolysis to compensate for lack of oxygen (sually produced by ETC)

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4
Q

How does PET scan detect cancer?

A

fluorine added to glucose (FDG)
taken up in part of body where glucose taken up
prominent fluorine = potentially cancerous

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5
Q

Why use PET + CT scan?

A

better anatomical location for exact location of cancer

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6
Q

Tumor cells produce ___ so normal cells near them cannot survive.

A

lactate = acidic environment

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7
Q

List 2 environmental advantages of tumor cells

A
  1. lack of oxygen
  2. acidosis
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8
Q

Cancer cells need _____, so they activate ______ to make cell membranes for new cells / cell proliferation.

A

lipids
lipid synthesis

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9
Q

What are the two major metabolites relied on for a proliferating cell?

A

Glucose
Glutamine

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10
Q

What pathways is associated with glutamine (used by proliferating cells)?

A

Ras/Raf/MEK/ERK pathway

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11
Q

Ras/Raf/MEK/ERK pathway mechanism

A

glutamine activates KGA
KGA converts glutamine –> glutamate
glutamate converts to TCA + ATP
= cell growth / proliferation

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12
Q

Proliferating cells have a high demand for ____ due to their need for lipid synthesis & protein synthesis

A

NADPH

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13
Q

How is skeletal muscle associated with metabolism in cancer?

A

glutamine + amino acids come from skeletal muscle mass of cancer patients

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14
Q

How is adipose tissue associated with metabolism in cancer?

A

uses lipids from adipose to make cell membrane for proliferating tumor cells

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15
Q

How is the liver associated with metabolism in cancer?

A

Cori Cycle- gluconeogenesis –> new glucose from lactate

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16
Q

A mutated nuclei put in a normal cell (converts/doesn’t not convert) it into a tumor cell

A

does NOT convert

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17
Q

A normal nuclei put in a tumor cell (converts/doesn’t convert) it back into a normal cell

A

doesn’t convert

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18
Q

What is the metabolic cause for cancer?

A

mitochondria

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19
Q

What is different about the mitochondria in the cancer cell?

A

NO cristae so ETC cannot occur

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20
Q

What are two dietary cancer therapies focused on metabolism?

A
  1. Ketogenic diet (“starve” cancer cells of glucose)
  2. Restrict overall food intake
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21
Q

What are 3 pathways that are metabolic targets for cancer treatment?

A
  1. Inhibit PFK-B
  2. Inhibit Acetyl-CoA carboxylase
  3. Inhibit Glutamine Metabolism
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22
Q

Mechanism for inhibiting PFK-B for cancer cell treatment

A

cancer cells express PFK-B (not in normal cells) that regulates glycolysis
drug inhibits PFK-B –> starve tumor cells

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23
Q

Mechanism for inhibiting Acetyl-CoA carboxylase

A

drug inhibits ACC = reduced cancer cells
disadvantage- also blocks normal cell fat synthesis

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24
Q

Mechanism for inhibiting glutamine metabolism

A

drug inhibits glutaminase
= longer lifespan, small disadvantage to normal cells

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25
What is P53
tumor suppressor protein that regulates cell division
26
What occurs with P53 that occurs in many cancers?
amplified / mutated P53 regions
27
What are the 4 main phases of the cell cycle?
G1 (1st growth phase) S (synthesis) G2 (2nd growth phase) M (mitosis)
28
What occurs in G0 phase?
cell no longer proliferates, only functional purpose
29
What 3 kinds of cells are in the G0 phase?
RBC cardiac myocytes neurons
30
What occurs in the S phase?
synthesis DNA replication occurs
31
What occurs in the G2 phase?
cell prepares for mitosis by making machinery necessary for division
32
What occurs in the M phase?
mitosis cell division
33
What is the primary regulatory of G1 phase?
Cyclin D
34
How does cyclin D regulate G1?
Cyclin binds to CDKs
35
What are the 4 things that regulate the cell cycle
regulatory proteins cyclins kinases CDKs
36
CDKs are only active when ____ is expressed.
cyclin
37
Which phase of cell cycle can activation of growth factors only influence? Example?
G1 GFs upregulation of cyclin D1 in G1 phase
38
R point
checkpoint within cell cycle where cell cannnot be influenced by GFs
39
Which two protein families inhibit the cell cycle (suppress cycle)?
INK & CIP
40
What are cell cycle checkpoints? how often do they occur?
checkpoints to stop cell cycle if there are problems occur during each phase
41
What mediates cell cycle checkpoints?
tumor suppressors
42
What are two examples of tumor suppressors that mediate cell cycle?
P53 & PRb
43
G2/M checkpoint
check DNA replicated, not damaged before dividing in mitosis
44
M checkpoint
Mitotic Checkpoint Complex (check alignment before division)
45
G1/S Checkpoint
PRb (retinoblastoma protein) tumor suppressor present
46
What tumor suppressor is activated in response to failure of the 3 critical checkpoints?
P53
47
P53 is normally kept at (low/high) levels in the cell
low
48
What targets p53 for degradation?
MDM2
49
____ leads to upregulation of p53 since MDM2 cannot degrade it.
DNA damage
50
What happens if p53 cannot fix the DNA damage?
apoptotic genes kill cell
51
What happens to p53 in cancer?
misfolded/unfolded so cannot upregulate to stop damaged cells --> cancer
52
What two processes is cell death important for?
physiological & pathological
53
Why is cell death important for physiological processes?
maintain homeostasis normal development
54
What are the 3 forms of death?
apoptosis autophagy necrosis
55
Apoptosis
cell "implosion"
56
In apoptosis, the cell (swells/shrinks), chromatin (opens/condenses) and the membrane blebs.
Shrinks Condenses
57
Autophagy
cell "eating" vacuolize around cell compartments
58
In autophagy, chromatin (condenses/does not condense)
does not condense
59
Necrosis
cell "explosion"
60
Necrosis causes cell (shrinking/swelling) and membrane ____.
swelling rupture
61
Apoptosis is a form of (physiological/pathological) death
physiological
62
Apoptosis is energy (dependent/independent)
dependent
63
(T/F): Apoptosis causes an inflammatory response
False- vacuoles enclosed so no inflamm
64
During apoptosis, the cell is broken down in vesicles called _____.
Apoptotic bodies
65
Extrinsic Apoptotic Pathway
TNFa (inflammatory cytokines) bind Caspase-8 --> Caspase-3 = apoptosis
66
What inhibits the extrinsic apoptotic pathway?
IAPs (protein inhibitors of activated proteases) inhibit caspase so apoptosis doesn't occur
67
Intrinsic Apoptotic Pathway
UV/Ischemia/Hypoxia stim. cell membrane Bax creates mitochondrial hole Cytochrome C released --> Caspase = apoptosis
68
What inhibits the intrinsic apoptotic pathway?
BCL2 (which inhibits Bax) = no apoptosis
69
PRRSV
virus affecting pigs virus activates apoptotic proteins affects pulmonary macrophages
70
What is the primary form of pathological cell death?
Necrosis
71
Necrosis is energy (dependent/independent)
independent
72
Necrosis (causes inflammatory/does not cause inflammation).
causes inflammation
73
Extrinsic Necrotic Pathway
TNFR --> RIPK --> RIPK3 --> MLKL MLKL forms hole in cell membrane water floods in = necrosis
74
Intrinsic Necrotic Pathway
Stress affects mitochondrial pore Pore opens --> inhibit ATP synthesis Electrochemical gradient lost (no ATP) mito swell + free radicals produced = necrosis
75
Necrotizing Pancreatitis
pain/fatal disease caused by viral infections/toxins
76
What protocol is used for lymphoma treatment?
CHOP protocol
77
What is the CHOP protocol
rotate weeks of drug as cancer treatment
78
What are two main types of vinca alkaloids?
vincristine vinblastine
79
What is the function of vinca alklaloids?
destabilize microtubules
80
What are 2 mechanisms vinca alkaloids use to destabilize microtubules?
1. bind to tubulin with high affinity (tubulin can't add, microtubule not lengthening) 2. bind to (+) end of microtubule --> shortening from treadmill effect
81
MDR1
P-glycoprotein in cell membrane
82
Function of MDR1
"kick-out" drug once in cell so it can't be used
83
Mechanism of MDR1
drug in cell --> MDR1 takes up drug --> ATP binds --> MDR1 changes conformation --> drug is "spit out"
84
3 main drugs that are substrates for MDR1
vincristine vinblastine doxorubicin
85
Two drugs which inhibit MDR1
verapamil chloroquine
86
How do verapamil/chloroquine inhibit MDR1?
L-type calcium channel blocker "outcompete" vinca alkaloids against MDR cancer so they are "spit out" instead of chemotherapeutic drug (vincristine)
87
3 ways to inhibit MDR1
1. modify drug (so not rec by MDR1) 2. co-administer with competitor 3. noncompetitive inhibitior of MDR1 (overall block)
88
What are two MDR proteins other than MDR1?
MRP1 ABCG2
89
What is doxorubicin?
A chemotherapeutic drug
90
List 3 mechanisms for cancer therapy that targets DNA
1. cross-link DNA (join strands so can't sep) 2. intercalator (protein between nucleotides pushes apart) 3. double-stranded break (cut in DNA)
91
2 mechanisms Doxorubicin uses for cancer?
1. intercalator (nuclei pushed apart) 2. trap/inihibit DNA topoisomerases
92
DNA Topoisomerases
enzymes that cut DNA to release tension and rebuild into correct structure
93
How does doxorubicin stop DNA replication via DNA topoisomerases?
doxorubicin continues warped structure of DNA so topoisomerases repeat; therefore, no DNA replication can occur
94
What are some phenotypic changes to the heart with doxorubicin?
cardiomyopathy arrythmias loss of myofibrils focal necrosis & replacement fibrosis
95
What does doxorubicin produce to kill cardiac monocytes?
free radicals
96
What does doxorubicin need to produce free radicals?
iron
97
Calpain
protease that degrades contractile elements in heart --> apoptosis
98
What activates calpain?
high calcium due to leaky ryanodine receptor from doxorubicin
99
______ burst in cardiac myocytes due to doxorubicin
Mitochondria
100
Potential therapies for doxorubucin cardiotoxicity
antioxidants iron chelators ryanodine receptor stabilizers calpain inhibitors mitochondrial pore inhibitors
101
Dystrophin function
used for myocyte anchoring

Cell Biology (6 decks)

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