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Pharmacology B > Lecture 7 - Anticancer Meds > Flashcards

Lecture 7 - Anticancer Meds Flashcards

1
Q

Cancer

A

also known as a malignant tumor or malignant neoplasm, is a group of diseases involving abnormal cell growth with the potential to invade or to spread to other parts of the body

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2
Q

____ have a higher chance of getting cancer and a higher chance of dying earlier

A

men

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3
Q

List the 3 top cancers for men and women in Canada

A

Men:

1) Prostate
2) Colorectal
3) Lung

Women:

1) Breast
2) Lung
3) Colorectal

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4
Q

Cancer is primarily a disease of ____ age

A

old

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5
Q

Malignant

A

if tumor invades surrounding tissue (cancerous)

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6
Q

Benign

A

if tumor has no effect on surrounding tissue (non-cancerous)

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7
Q

Metastatic

A

if individual cells break away and start a new tumor elsewhere (cancerous)

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8
Q

Describe the path to cancer

A

-Clonal proliferation
-Starts from a single cell
-Expansion in steps
-Pre-malignant states
(Polyp, MDS, MGUS)
-Serial accumulation of mutations
(Clonal evolution, resistance)

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9
Q

List some hallmarks of cancer

A
  • Self sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Evading apoptosis
  • Limitless reproductive potential
  • Sustained angiogenesis
  • Tissue invasion and metastases
  • Genomic instability
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10
Q

Is cancer a genetic disease?

A

Yes

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11
Q

Cancer arises from the accumulation of _____ changes (somatic mutations)
*Genetic selection at the level of single cells

A

genetic

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12
Q

Most cancers incur a minimum of ______ different gene mutations

A

5 (6-9)

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13
Q

We don’t inherit cancer but we do inherit _______ to cancer

A

dispositions (susceptibility)

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14
Q

_______ is a hallmark of cancer cells

A

Aneuploidy

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15
Q

What is aneuploidy?

A

The presence of an abnormal number of chromosomes in a cell

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16
Q

2 components of Etiology of cancer

A

Nature:
-What we inherit

Nurture
-Environmental factor (what we do to our body) ex. smoking, UV radiation, etc.

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17
Q

You need an _____ and an elongated promoter to lead to cancer

A

initiator

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18
Q

Tumor initiators = ______

A

mutagens

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19
Q

Tumor Promoters = _____ ______

A

proliferation inducers

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20
Q

List some tumor initiators (mutagens)

A
  • X rays
  • UV light
  • DNA alkylating agents
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21
Q

List some tumor promoters (proliferation inducers)

A
  • Phorbol esters
  • Inflammation
  • Alcohol
  • Estrogens and Androgens
  • Epstein-Barr Virus
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22
Q

Cell cycle phases:

G1 (gap phase)

A

the cell grows and prepares to synthesize DNA

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23
Q

Cell cycle phases:

S (synthesis phase)

A

in which the cell synthesizes DNA

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24
Q

Cell cycle phases:

G2 (second gap phase)

A

in which the cell prepares to divide

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25
Q

Cell cycle phases:

M (mitosis phase)

A

cell division occurs

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26
Q

Cell cycle phases:

G0 (arrest/quiescent)

A

cell is in resting state

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27
Q

Cell cycle phases:

Checkpoint 1

A

G1/S checkpoint:

Cell monitors size and DNA integrity

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28
Q

Cell cycle phases:

Checkpoint 2

A

G2/M checkpoint:

Cell monitors DNA synthesis and damage

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29
Q

Cell cycle phases:

Checkpoint 3

A

M checkpoint:

Cell monitors spindle formation and attachment to kinetochores

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30
Q

What protein complexes are involved in the cell cycle?

A
  • Cyclins

- Cyclin dependent kinases (Cdks)

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31
Q

Are Cdk (cyclin dependent kinases) levels stable?

A

yes

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32
Q

Are cyclin levels stable?

A

no they change throughout the cell cycle

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33
Q

The ability to drive through the checkpoint are reliant on ??

A

cyclins and cdks (oncogenes)

*cdk = cyclin dependent kinase

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34
Q

Cdks must bind to the correct ___ in order to function

A

cyclin

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35
Q

What do kinases do?

A

enzymes that add phosphate groups to proteins to convert them from an “off” to an “on” state

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36
Q

Describe the pathogenesis of cancer:
_____ are activated

___ ______ ____ are inactivated

A

Oncogenes are activated

Tumor suppressor genes are inactivated

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37
Q

Oncogene = ?

A

gas pedal

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38
Q

Tumor suppressor genes = ?

A

brakes

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39
Q

What is p53?

A

a class tumor suppressor

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40
Q

What is Rb?

A

also a classic tumor suppressor

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41
Q

Rb binds to a protein called ____

A

E2F1

*when bound to Rb, E2F1 can’t function

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42
Q

_______ = drives cell cycle forward and bypasses checkpoints

A

Oncogenes

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43
Q

______ = an amplified oncogene

A

HER2/neu

*a growth factor receptor

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44
Q

25-30% of ____ cancers over-express HER2/neu

A

breast

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45
Q

____ is used as a treatment for breast cancers that over-express HER2/neu

A

Herceptin

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46
Q

___ = a frequently mutated oncogene

A

Ras

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47
Q

Translocations can be ? (2)

A
  • Balanced

- Reciprocal

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48
Q

Aneuploidy can be ? (4)

A
  • Pseudodiploid
  • Hyperdiploid
  • Complex
  • Random loss or gain
    • Loss of tumor suppressor function
    • Proto-oncogenic gain of function (into oncogene)
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49
Q

What is the Philadelphia chromosome?

A
  • Translocation between chromosome 22 and chromosome 9
  • Classic oncogenic rearrangement associated with a variety of leukemias
  • BCR-ABL tyrosine kinase fusion
  • Imatinib (Gleevec) is an Abl-kinase targeted tyrosine kinase inhibitor (TKi) used in the treatment of the Ph+ CML and other tumors
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50
Q

When is chemotherapy most effective?

A

when growth fraction is high

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51
Q

Describe early stages of tumour growth?

A
  • high growth fraction

- short doubling times

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52
Q

Describe late stages of tumour growth?

A
  • low growth fraction

- long doubling times

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53
Q

Benign = ?

A

non-cancerous

“polyp”

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54
Q

Malignant = ?

A

cancerous

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55
Q

Malignant epithelial = ?

A

carcinoma

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56
Q

Malignant mesenchyme = ?

A

sarcoma

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57
Q

Malignant hematopoietic = ?

A

leukemia, lymphoma, myeloma

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58
Q

Hyperplasia

A

increased number of cells

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59
Q

Hypertrophy

A

increased size of cells

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60
Q

Dysplasia

A

disorderly proliferation

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61
Q

Neoplasia

A

abnormal new growth

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62
Q

Anaplasia

A

lack of differentiation

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63
Q

Tumor

A

originally meant any swelling, but now equated with neoplasia (abnormal new growth)

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64
Q

Metastasis

A

growth at a distant site

65
Q

Bening tumor ends in “___”

A

“oma”

ex. adenoma
ex. fibroma
ex. lipoma

66
Q

Malignant cancer ends in ______ or ______

A

carcinoma or sarcoma

ex. adenocarcinoma
ex. fibrosarcoma
ex. liposarcoma
ex. leukemia and lymphoma (don’t follow the rule wtf)

67
Q

Describe the stages of tumor progression

A
  • Hyperplasia
  • Dysplasia
  • Carcinoma in situ (not cross the basal lamina)
  • Cancer (malignant tumors) - Metastasis
68
Q

_____ = non-invasive

69
Q

_____ = invasive/metastatic

70
Q

How do we classify cancers?

A

Grade - How bad do the cells look?

Stage - Where has the cancer spread?

T = Tumour
N = Nodes (Lymph)
M = Metastases
71
Q

Grade 1 Cancer

A

Well differentiated

72
Q

Grade 2 Cancer

A

Moderately differentiated

73
Q

Grade 3 Cancer

A

Poorly differentiated

74
Q

Grade 4 Cancer

A

Anaplastic (now all the cells look really different)

75
Q

As the cancer stage increases, survival rates ____

76
Q

If cancer spreads to another part of the body, it keeps it’s old _____

A

name

For ex. if kidney cancer spreads to the lungs, it is called kidney cancer which has metastasized to the lung

77
Q

List some cancer factors affecting outcome

A
  • Growth fraction
  • Doubling time
  • Type
  • Stage
  • Resistance
78
Q

List some patient factors affecting outcome

A
  • Overall health
  • Bone marrow capacity
  • Liver function
  • Kidney function
  • Age
  • Compliance
79
Q

Describe radiation

A
  • Ionization and excitation of atoms that kills cells
  • Cell killing, nausea, vomiting, fatigue, somnolence
  • Late effect; fibrosis and gliosis
  • Skin and mucosal reactions are accentuated by other modalities like chemotherapy

-Definitive, adjuvant, palliative

80
Q

Purpose of primary chemotherapy

A

shrink of eliminate tumor

81
Q

Purpose of neoadjuvant chemotherapy

A

make tumor more amenable to other therapies

82
Q

Purpose of adjuvant chemotherapy

A

eradicate micro metastasis

83
Q

Purpose of palliation chemotherapy

A

symptom control

84
Q

What does CR Response to chemotherapy mean?

A

complete disappearance for at least 1 month

85
Q

What does PR Response to chemotherapy mean?

A

50% of > reduction in tumor size or markers and no new disease for 1 month

86
Q

What does SD Response to chemotherapy mean?

A

no reduction or growth

87
Q

What does Progression Response to chemotherapy mean?

A

25% increase in tumor size

88
Q

What are some cell cycle specific agents?

A
  • antimetabolites

- vinca alkaloids

89
Q

What are some cell cycle non-specific agents?

A
  • doxorubicin

- cisplatin

90
Q

Drugs that act only on a specific portion of the cell cycle (CCS) drugs will be least effective at treating cancers who have ____ growth fractions

91
Q

It is common to follow treatment with a _____ drug with a ____ drug so that cancer cells are recruited into the cell cycle, where CCS drugs can be more effective

A

follow treatment with a NCCS drug with a CCS drug

92
Q

CCS:

Plant alkaloids target which phase?

93
Q

CCS:

DNA synthesis inhibitors target which phase?

94
Q

CCS:

They are ____ dependent (duration and timing more important than dose)

95
Q

CCS:

Only ___ cells killed

A

proliferating (high growth factor tumors preferentially eliminated)

96
Q

NCCS:

What cells are killed?

A

Both proliferating and non-proliferating cells are killed (attack both high and low growth factor tumors)

97
Q

NCCS:

They are ___ dependent (total dose is more important than schedule)

98
Q

Why are cancer chemotherapeutics typically given in cycles?

A

to allow normal cells time to recover from the treatment

99
Q

Fractional kill hypothesis:
In order to reduce the impact of the recovery/resistance problem, the key principles to antineoplastic drug therapy are:
? (3)

A
  • Use high doses (including increasing doses during treatment; called DOSE ESCALATION)
  • Minimize recovery intervals (cell kill hypothesis)
  • Employ sequential scheduling during combination therapy
100
Q

What are some critical factors to treatment?

A
  • Early start to the treatment
  • Treatment must continue past the time when cancer cells can be detected using conventional techniques
  • Appropriate scheduling of treatment courses and care to ensure sufficient log-kill is obtained are also crucial factors that enable success
101
Q

List 3 types of chemotherapy treatments

A

1) Inhibitors of cell growth (Growth Factor Proteins ex. hormones)
2) Inhibitors of DNA Duplication
3) Inhibitors of Cell Division

102
Q

Describe the wide range of drugs for chemotherapy

A

1) Non cell cycle dependent (Genotoxic agents)

2) Cell cycle dependent
- Cytoskeletal inhibitors
- Topoisomerase inhibitors
- Antimetabolites
- Hormonal therapy

3) Others

103
Q

What drugs are cell-cycle independent?

A
  • Platinating agents

- Alkylating agents

104
Q

What drugs target S phase?

A
  • Vinca alkaloids
  • 5-fluorouracil
  • Methotrexate
  • Hydroxyurea
  • Doxorubicin
  • Cytarabine
  • Gemcitabine
  • Etoposide
105
Q

What drugs target G2 phase?

A

-Bleomycin

106
Q

What drugs target M phase?

A
  • Taxanes
  • Vinca alkaloids
  • Etoposide
107
Q

look at slide 82 for a review man

A

omg if i have time man

108
Q

Genotoxic agents are ?

A

non cell-cycle specific

NCCS

109
Q

Anti-metabolites target __ phase

110
Q

Cytoskeletal inhibitors target _____ phase

111
Q

Topoisomerase inhibitors target ___ phase

112
Q

Steroid hormones target ___ phase

113
Q 
Genotoxic Agents (NCCS):
MOA
A
  • affect the function of nucleic acids
  • bind directly to DNA
  • inhibit DNA replication enzymes
  • DNA damage leads to apoptosis
  • *prevent the separation of strands
  • *Induce mispairing that renders them non-functional
114
Q 
Genotoxic Agents (NCCS): 
Include \_\_\_\_\_ and \_\_\_\_\_\_ agents
A

Include alkylating and intercalating agents

115
Q 
Genotoxic Agents (NCCS): 
List the most common genotoxic agents
A

1) Platinum based chemotherapeutic agents:
- cisplatin
- carboplatin
- xaliplatin

2) Doxorubicin analogs
3) Cyclophosphamide-pro drug, orally active, less side effects in normal cells

116
Q

Describe Antimetabolites (S phase - CCS):

A
  • Structurally similar to natural metabolites
  • Prevents cells from carrying out vital functions and they are unable to grow and survive
  • Interfere with the production of nucleic acids, RNA and DNA
  • If new DNA cannot be made, cells are unable to divide !!!
117
Q

Antimetabolites (S phase - CCS):

List some

A

1) Folate antagonists
ex. Methotrexate

2) Purine antagonists
ex. Thiopurine methyltransferase

3) Pyrimidine antagonists
ex. 5-Fluorouracil

118
Q

Antimetabolites (S phase - CCS):

Describe folate antagonists

A

Ex. Methotrexate

  • Folate antagonists inhibit dihydrofolate reductase, an enzyme involved in the formation of purine and pyrimidine nucleotides for DNA synthesis
  • Without DNA replication, cell growth is blocked
119
Q

Antimetabolites (S phase - CCS):

Describe the next generation Folate Antagonist

A

Permetrexed:

  • Inhibits DHFR
  • Inhibits thymidylate synthase (TS)
  • Inhibits glycinamide ribonucleotide formyl transferase (GRFT)

*More effectively inhibits DNA and RNA synthesis

120
Q

Antimetabolites (S phase - CCS):

Describe folinic acid

A

Folinic Acid (Leucovorin):

  • Used with methotrexate and antifolates to reduce (rescue therapy) myelosuppresion (often the most significant dose limiting adverse rx)
  • THF analog that can be used as a methyl donor
  • DHFR insensitive
121
Q

Antimetabolites (S phase - CCS):
Purine Antagonists:
MOA

A

Purine antagonists prevent continued replication of DNA, and therefore cell division:

6-Mercaptopurine (6-MP) - looks like Adenine

6-Thioguanine (6-TG) - looks like Guanine

122
Q

Antimetabolites (S phase - CCS):
Purine Antagonists:
Describe thiopurine methyltransferase (TPMT)

A
  • Metabolism of thiopurine drugs such as azathioprine, 6-Mercaptopurine and 6-Thioguanine
  • TPMT catalyzes the S-methylation of thiopurine drugs
  • Defects in the TPMT gene leads to decreased methylation and decreased inactivation of 6MP leading to enhanced bone marrow toxicity which may cause myelosuppresion, anemia, bleeding tendency, leukopenia & infection
123
Q

Antimetabolites (S phase - CCS):
Purine Antagonists:
What does TPMT polymorphism result in?

A

As TPMT is a deactivation pathway, the result is more active drug, increased toxicity (similar to an overdose situation)

124
Q

Antimetabolites (S phase - CCS):
Pyrimidine antagonists:
MOA

A

-Block synthesis of pyrimidine containing nucleotides
(dCTP and dTTP in DNA; CTP and UTP in RNA)

-Stop DNA/RNA synthesis and inhibit cell division

125
Q

Antimetabolites (S phase - CCS):
Pyrimidine antagonists:

List some pyrimidine Antagonists used in cancer therapy

A

1) 5-Fluorouracil (5-FU)

2) Cytarabine (cytosine arabinoside, ARA-C)

126
Q

Antimetabolites (S phase - CCS):
Pyrimidine antagonists:

MOA of 5-FU

A

inhibit thymidylate synthase

which prevents cell growth probs

127
Q

What is the mitotic spindle?

A

attaches to kinetochores, helps align chromosomes and then separates them

128
Q

What is MAD and BUB?

A

Part of the spindle checkpoint that halt the cell cycle until all chromosomes are aligned at the middle of the cell

129
Q 
Cytoskeletal inhibitors (Mitosis phase):
List 2 drugs affecting this category
A

Taxanes:

  • Paclitaxel
  • Docetaxel

Vinca alkaloids:

  • Vincristine
  • Vimblastin
  • Vindesine
130
Q 
Cytoskeletal inhibitors (Mitosis phase):
How do they work?
A
  • Affect the mechanics of cell division

- Without proper microtubule formation, cell division is not possible

131
Q

Cytoskeletal inhibitors (Mitosis phase):

How do Taxanes (Paclitaxel, Docetaxel) work?

A
  • affect anaphse

- affect depolymerization

132
Q

Cytoskeletal inhibitors (Mitosis phase):

How do Vinca alkaloids (Vincrinstine, Vimblastin, Vindesine) work?

A
  • affect metaphase

- affect polymerization

133
Q

Cytoskeletal inhibitors (Mitosis phase):

Main side effect of taxanes?

A

female infertility by ovarian damage

134
Q

Topoisomerase 1 inhibitors (G2 phase):

What do Topoisomerase inhibitors do?

A

Topoisomerase (Top1) inhibitors interfere with the action of topoisomerase enzymes (Top 1 and 2), which are enzymes that control the changes in DNA structure by catalyzing the breaking and rejoining of the phosphodiester backbone of DNA strands during the normal cell cycle.

Blocks the ligation step of the cell cycle, generating single and double stranded breaks that harm the integrity of the genome = apoptosis and cell death

135
Q

Topoisomerase 1 inhibitors (G2 phase):

List some

A

Topotecan

Irinotecan

136
Q

Topoisomerase 2 inhibitors (G2 phase):

List some

A

Etoposide

Teniposide

137
Q

Steroid hormones (G1 phase):

Describe the MOA

A

1) Steroid hormone enters target cell
2) Hormone binds to receptor, induces conformational change
3) Hormone-receptor complex binds to DNA, induces start of transcription
4) Many mRNA transcripts are produced, amplifying the signal
5) Each transcript is translated many times, further amplifying the signal

138
Q

Steroid hormones (G1 phase):

Hormone Therapy
Objective ?

A

starve cancer cells from hormonal signals necessary for growth

139
Q

Steroid hormones (G1 phase):

Hormone Therapy
Approach ?

A
  • hormone blocking drugs at target cells

- prevent hormone production

140
Q

Steroid hormones (G1 phase):

List some types of hormonal antagonists

A

1) Selective estrogen receptor modulators (SERMs)
2) Aromatase Inhibitors (AIs)
3) Selective androgen receptor modulators (SARMs)

141
Q

Steroid hormones (G1 phase):
SERMs:
ER = ?

A

positive breast cancer cells

142
Q 
Steroid hormones (G1 phase):
SERMs:

List some

A
  • Tamoxifen
  • Raloxifene
  • Toremifene

*If you’re ER negative, these drugs won’t work for you ?

143
Q 
Steroid hormones (G1 phase):
SERMs:

MOA

A

inhibition of estrogen’s growth stimulating effects

144
Q 
Steroid hormones (G1 phase):
SERMs:

Describe Tamoxifen Chemotherapy

A
  • Anti-estrogen affinity is dependent on primary metabolite, endoxifen (100x more active)
  • CYP2D6 enzyme is responsible for metabolism of tamoxifen
  • Can’t give endoxifen alone
  • Have to give tamoxifen and then have the other rxns in liver happen, and have tamoxifen converted into endoxifen
145
Q 
Steroid hormones (G1 phase):
SERMs:

Tamoxifen main DDI ?

A

Antidepressants

  • paroxetine
  • fluoxetine
  • bupropion
146
Q 
Steroid hormones (G1 phase):
Aromatase Inhibitors:

List some

A

Exemestane
Anastrozole
Letrozole

147
Q 
Steroid hormones (G1 phase):
Aromatase Inhibitors:

MOA

A

Prevents conversion of hormones into estrone and estradiol

148
Q

Steroid hormones (G1 phase):

Specific Androgen Receptor Modulators (SARMs):

List some

A

Flutamide
Bicalutamide

*Competitively bind AR

149
Q

Principles of drug selection for combination therapy?

A
  • active when used alone
  • different mechanisms of action (including different mechanisms for the development of resistance) and/or different chemical classes
  • NCCS vs CCS or active in different stages of cell cycle
  • different toxicities
150
Q

Combination therapy can result in?

A
  • Synergistic effects (ex. Cytarabine and 6-Thioguanine)
  • Decreased development of resistance
  • Broader cell kill in cancers that consist of a heterogenous tumour cell population
151
Q

List some adverse effects of chemotherapy drugs

A

Bone marrow depression

  • Anemia
  • Bleeding
  • Infections
  • Secondary cancers (Procarbazine)

Teratogenesis

Carcinogenesis

Resistance

152
Q

How can we tell there is resistance to Methotrexate?

A

Increased concentrations of DHRF enzyme in cancer cells (gene amplification)

153
Q

What is P-glycoprotein?

A
  • First multi drug resistance mechanism to be characterized
  • P-glycoprotein is transmembrane ATP-dependent efflux pump
  • Actively transports many types of chemotherapy from cells
  • Overexpression in cancers causes drug resistance
  • P-glycoprotein inhibitors tested in clinical trials
154
Q

List 5 forms of resistance mechanisms to chemotherapy

A

1) Increased expression of target proteins
2) Failure of the drugs to enter cancer cell or increased intracellular drug ejection rate
3) Drugs fail to reach target cells
4) The target molecule is no longer present
5) The target molecule is altered (mutation/deletion)

155
Q

List 3 drugs involved in Monoclonal Antibody Therapy?

A
  • Rituximab
  • Trastuzumab
  • Cetuximab
156
Q

Monoclonal Antibody Therapy:

Describe Rituximab

A
  • binds to CD20 antigen (receptor) present on the cell surface of B-lymphocytes
  • binding to CD20 targets the cell to complement-activated phagocytosis and antibody-dependent apoptosis
  • inhibit proliferation of lymphocytes and lymphoma cells
157
Q

Monoclonal Antibody Therapy:

Describe Trastuzumab

A

-binds to human epidermal growth factor receptor protein-2 (HER2)

158
Q

Monoclonal Antibody Therapy:

Describe Cetuximab

A

-chimeric (mouse/human) monoclonal antibody against epidermal growth factor receptor protein (EGFR)

159
Q

List 2 antibody-drug conjugates

A

Brentuximab vedotin

Trastuzumab emtansine

Pharmacology B (21 decks)

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