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Pharmacology - Winter > 7 - Anticancer > Flashcards

7 - Anticancer Flashcards

1
Q

What is cancer?

A
  • Malignant tumour or malignant neoplasm
  • Group of diseases involving abnormal cell growth w/ potential to invade or spread to other parts of the body
  • Cell division in overdrive
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2
Q

What is the path to cancer?

A
  • Clonal proliferation
  • Starts from single cell
  • Expansion in steps
  • Pre-malignant states (polyp, MDS, MGUS)
  • Serial accumulation of mutations
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3
Q

What are the hallmarks of cancer?

A
  • Aneuploidy (abnormal # of chromosomes)
  • Self-sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Evading apoptosis
  • Limitless reproductive potential
  • Tissue invasion and metastases
  • Genomic instability
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4
Q

Cancer arises from accumulation of _____

A 
Genetic changes (somatic mutations)
-- Most cancer incurs a minimum of 5 (often 6-9) different gene mutations
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5
Q

Is cancer hereditary?

A

No, but can inherit dispositions to cancer (BRCA 1/2 mutations)

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6
Q

What do the genes that are mutated in cancer code for?

A

Proteins that are involved in regulating the cell cycle

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7
Q

What are tumour initiators? Give examples

A
  • Mutagens

- Ex: X rays, UV light, DNA alkylating agents

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8
Q

What are tumour promoters? Give examples

A
  • Proliferation inducers

- Ex: phorbol esters, inflammation, alcohol, estrogens, androgens, and Epstein-Barr virus

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9
Q

What happens to the cell cycle in cancer?

A

Becomes dysregulated (cells divide when they’re not supposed to or in a place they’re not supposed to)

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10
Q

What are the phases of the cell cycle? What occurs in each phase?

A

1) G1/gap phase - cell grows and prepares to synthesize DNA
2) S/synthesis phase - cell synthesizes DNA
3) G2/second gap phase - cell prepares to divide
4) M/mitosis phase - cell division occurs
5) G0/arrest phase - cell is in resting state

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11
Q

What proteins are present during the cell cycle? How do their amounts vary?

A
  • Cyclins and cyclin dependent kinases

- Cyclin dependent kinase levels stay stable, but cyclin levels change throughout the cell cycle

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12
Q

What is the relationship between cyclin dependent kinases and cyclins?

A
  • Cdks must bind the correct cyclin in order to function
  • Cause cascade of kinases adding phosphates to other proteins to activate them, that eventually leads to transcription of genes
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13
Q

What is an oncogene?

A

Gene that when mutated, gains a function or is expressed at abnormally high levels and/or high activity (often kinases, transcription factors, or growth factors/receptors)

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14
Q

What is a tumour suppressor gene?

A
  • Encodes for a protein that is involved in suppressing cell division
  • When mutated is no longer functional (can lead to cancer)
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15
Q

What is the normal function of oncogenes? What happens to them for cancer to occur?

A
  • Normal function = cell growth and gene transcription

- Activated for cancer to occur

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16
Q

What is the normal function of tumour suppressor genes? What happens to them for cancer to occur?

A
  • Normal function = DNA repair, cell cycle control, and cell death (maintain genomic integrity)
  • Inactivated for cancer to occur
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17
Q

Chemotherapy is most effective when growth fraction is ____

A

High

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18
Q

Is a polyp benign or malignant?

A

Benign

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19
Q

What are the types of malignant cancers?

A
  • Epithelial (carcinoma)
  • Mesenchyme (sarcoma)
  • Hematopoietic (leukemia, lymphoma, myeloma)
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20
Q

Define hyperplasia

A

Increased # of cells

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21
Q

Define hypertrophy

A

Increased size of cells

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22
Q

Define dysplasia

A

Disorderly proliferation

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23
Q

Define neoplasia

A

Abnormal new growth

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24
Q

Define anaplasia

A

Lack of differentiation

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25
Q

Define tumour

A

Originally meant any type of swelling, but now equated w/ neoplasia

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26
Q

Define metastasis

A

Growth at distant site

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27
Q

What will a benign tumour end in?

A

-oma (ex: adenoma, fibroma, lipoma)

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28
Q

What will a malignant cancer end in?

A

Carcinoma or sarcoma; leukemia and lymphoma

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29
Q

What are the stages of tumour progression?

A
  • Hyperplasia
  • Dysplasia
  • Carcinoma in situ (not cross the basal lamina)
  • Cancer (malignant tumours)
  • Metastasis
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30
Q

What are characteristics of benign neoplasms?

A
  • Non-invasive
  • Well-defined borders
  • Well differentiated
  • Regular nuclei
  • Rare mitoses
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31
Q

What are characteristics of malignant neoplasms?

A
  • Invasive/metastatic
  • Irregular borders
  • Poorly differentiated
  • Irregular, larger nuclei
  • More frequent and/or abnormal mitoses
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32
Q

What are some predictors of the behaviour of a tumour?

A
  • Grade (how bad do the cells look)
  • Stage (where has the cancer spread)
  • TNM
  • Tumour
  • Nodes (lymph)
  • Metastases
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33
Q

What are the various grades of cancer?

A
  • Grade 1 = well differentiated
  • Grade 2 = moderately differentiated
  • Grade 3 = poorly differentiated
  • Grade 4 = anaplastic
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34
Q

What are the stages of colon cancer?

A

Duke’s A, B, C, or D (A has highest chance of survival after 5 years; D has lowest chance)

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35
Q

What are some possible therapeutic routes?

A
  • Surgery
  • Radiotherapy
  • Chemotherapy (hormonal therapy, specific inhibitors)
  • Immunotherapy
  • Biologic therapy (vaccines, gene therapy)
  • Combination of the above
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36
Q

What can be done to detect cancer?

A
  • Blood work
  • Palpation
  • Symptomatic
  • Coincidental
  • CT scan
  • PET/CT
  • SPECT/CT
  • MRI
  • Staging
  • Response
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37
Q

What determines the tx for cancer?

A
  • Type of tumour
  • Location and amount of disease
  • Health status of px
  • Tx used in combination
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38
Q

What is the objective of cancer tx?

A
  • Kill cancer cells and/or lead them to apoptosis

- Contain and/or limit cell growth

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39
Q

What are some cancer factors that affect outcome of tx?

A
  • Growth fraction (% of cells not in G0) - determines efficacy of CCS drugs
  • Doubling time - affects course scheduling
  • Type and stage - determines cure vs. palliation
  • Resistance - can limit tx and/or force a switch in medication
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40
Q

What are some patient factors that affect outcome of tx?

A
  • Overall health
  • Bone marrow capacity (determines dose and duration of tx)
  • Liver and kidney function (determine drug selection and/or dosage)
  • Age
  • Compliance
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41
Q

What is the major dose-limiting toxicity for most drugs?

A

Bone marrow suppression

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42
Q

Which cells are affected by cytotoxicity?

A
  • Cancer cells
  • Bone marrow
  • GI mucosa (common SE = N/V)
  • Hair follicles
  • Taste buds
  • Fetus
  • Radiation recall reaction
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43
Q

What is the radiation recall reaction? Which drugs cause it?

A
  • Erythema and desquamation of the skin at sites of prior (or simultaneous) radiation therapy (rash and skin peeling)
  • Most commonly associated w/ anthracycline antibiotics, but can occur w/ any cytotoxic drug
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44
Q

What is radiation?

A

Ionization and excitation of atoms that kill cells

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45
Q

What are side effects of radiation?

A

N/V, fatigue, somnolence

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46
Q

What is used in external beam radiation?

A

Gamma photons or neutron beams

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47
Q

What are the purposes of chemo?

A
  • Primary = shrink or eliminate tumour
  • Neoadjuvant = make tumour more amenable to other therapies
  • Adjuvant = eradicate micro metastasis
  • Palliation = symptom control
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48
Q

What are the various response to chemo?

A
  • CR = complete disappearance for at least 1 month
  • PR = 50% or more reduction in tumour size or markers and no new disease for 1 month
  • SD = no reduction or growth
  • Progression = 25% increase in tumour size
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49
Q

Do tumour cells grow faster than normal cells?

A

Not always

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50
Q

Which drugs are cell cycle specific agents?

A
  • Antimetabolites
  • Vinca alkaloids
  • Cytoskeletal inhibitors
  • Topoisomerase inhibitors
  • Hormonal therapy
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51
Q

Which drugs are cell cycle non-specific agents?

A

Doxorubicin and cisplatin

52
Q

What is involved in the most effective chemotherapy?

A
  • Multiple agent regimens
  • Optimization of PK/PD
  • Optimization to genetics of px and cancer
53
Q

Phase specific agents (CCS) are ______ dependent. What does this mean?

A
  • Schedule dependent

- More effective when given in divided doses at repeated intervals and more effective in tumours w/ high growth fraction

54
Q

Phase non-specific agents (NCCS) are ___ dependent

A

Dose or concentration dependent

55
Q

Chemotherapy follows _____ kill

A

Exponential log kill (never reaches zero)

56
Q

How are cancer chemotherapeutics normally given? What is the problem w/ this? What can be done to prevent this?

A
  • Typically given in cycles to allow normal cells time to recover from tx
  • Problem = stopping drug therapy also allows any remaining cancer cells to recover and develop resistance
  • Can employ anti-neoplastic drug therapy
57
Q

What are the key principles of anti-neoplastic drug therapy?

A
  • Use high doses (including increasing doses during tx; called dose escalation
  • Minimize recovery intervals
  • Employ sequential scheduling during combination therapy
58
Q

What are the critical factors for cancer tx?

A
  • Early start to tx
  • Tx must continue past the time when cancer cells can be detected using conventional techniques
  • Appropriate scheduling of tx courses and care to ensure that a sufficient log-kill is obtained
59
Q

What are the various mechanisms of chemotherapy?

A
  • Inhibit cell growth (growth factor proteins, ex: hormones)
  • Inhibit DNA duplication
  • Inhibit cell division
60
Q

Which part of the cell cycle can vary greatly between px?

A

Duration of G0 and G1 phases

61
Q

When will CCS drugs be least effective?

A

Cancers w/ low growth fractions (ie: most cells in G0)

62
Q

Is it common to use both NCCS and CCS drugs in cancer tx?

A

Yes, common to follow NCCS w/ a CCS drug to recruit the cancer cells into the cell cycle, where CCS drugs can be more effective

63
Q

Which phase of the cell cycle do plant alkaloids work on?

A

G2 -> M

64
Q

Which phase of the cell cycle do DNA synthesis inhibitors and anti-metabolites work on?

A

S

65
Q

Which cells do CCS drugs kill?

A

Proliferating cells

66
Q

Which phase of the cell cycle do NCCS drugs work?

A

Any phase, including G0

67
Q

Which cells do NCCS drugs kill?

A

Proliferating and non-proliferating (both high and low growth factor tumours)

68
Q

Which phase of the cell cycle do cytoskeletal inhibitors work on?

A

Mitosis

69
Q

Which phase of the cell cycle do topoisomerase inhibitors work on?

A

G2 phase

70
Q

Which phase of the cell cycle do steroid hormones work on?

A

G1 phase

71
Q

What are the functions of genotoxic agents (NCCS)?

A
  • Affect function of nucleic acids
  • Bind directly to DNA and inhibit DNA replication enzymes
  • DNA damage leads to apoptosis
72
Q

What are the most commonly used genotoxic agents?

A
  • Cisplatin
  • Carboplatin
  • Oxaliplatin
  • Doxorubicin analogs
  • Cyclophosphamide
73
Q

What are common SE of genotoxic agents?

A
  • Hematopoietic effects
  • GI
  • Hair loss
  • Renal toxicity
  • Ototoxicity w/ cisplatin
  • Heart effects w/ doxorubicin-based compounds
  • Bladder effects w/ cyclophosphamide compounds
74
Q

What are the functions of antimetabolites?

A
  • Prevent cells from carrying out vital functions, making them unable to grow and survive
  • Interfere w/ production of nucleic acids, RNA, and DNA
75
Q

What is methotrexate? What does it do?

A
  • Folate antagonist
  • Inhibits dihydrofolate reductase, an enzyme involved in formation of purine and pyrimidine nucleotides for DNA synthesis
76
Q

What are indications for methotrexate?

A
  • Acute lymphocytic leukemia
  • Large cell lymphoma
  • Head and neck cancers
  • Breast/bladder cancer
  • Rheumatoid arthritis
77
Q

What is used as an adjuvant in anti-folate therapy? Why?

A
  • Folinic acid used w/ methotrexate and anti-folates

- Reduce myelosuppression

78
Q

What do purine antagonists prevent?

A

Continued replication of DNA and therefore cell division

79
Q

What are indications for purine antagonists?

A
  • Acute lymphocytic or myelocytic leukemia
  • Lymphoblastic leukemia
  • IBD
  • Organ transplant
80
Q

What is the function fo thiopurine S-methyltransferase (TMPT)?

A

Catalyzes the S-methylation of thiopurine drugs, leading to an inactive metabolite

81
Q

What does a defect in the TMPT gene cause?

A

Decreased methylation and decreased inactivation of 6MP => enhanced bone marrow toxicity

82
Q

What are the polymorphisms of the TMPT gene?

A
  • WT (wild type)/WT normal allele = extensive metabolizer
  • WT/MUT (mutant allele) = intermediate metabolizer
  • MUT/MUT = poor metabolizer, making them intolerant to thiopurines (causes more active drug and increased toxicity)
83
Q

What do pyrimidine antagonists do?

A
  • Block synthesis of pyrimidine containing nucleotides

- Stop DNA/RNA synthesis and inhibit cell division

84
Q

Which pyrimidine antagonists are used in cancer therapy?

A
  • 5-FU (inhibits thymidylate synthase, which converts dUMP to dTMP)
  • Cytarabine
85
Q

What are indications for 5-FU?

A
  • Colorectal cancer
  • Breast cancer
  • Pancreatic cancer
  • Stomach cancer
  • Genito-urinary tract cancers
  • Esophageal cancer
  • Liver cancer
  • Skin cancer
86
Q

What do cytoskeletal inhibitors do?

A
  • Affect mechanisms of cell division

- Prevent proper microtubule formation, making cell division impossible

87
Q

What are indications for cytoskeletal inhibitors?

A
  • Breast cancer
  • Testicular
  • Hodgkin’s disease and other lymphomas
  • Childhood leukemias
  • Rhabdomyosarcoma
  • Neuroblastoma
88
Q

What are side effects of Vinca alkaloids?

A
  • Loss of white blood cells and blood platelets
  • GI problems
  • High BP
  • Excessive sweating
  • Depression
  • Muscle cramps
  • Hyponatremia
  • Constipation
  • Hair loss
89
Q

What are side effects of taxane?

A
  • N/V, loss of appetite
  • Thinned or brittle hair
  • Tingling in hands or toes
  • Bruising or bleeding
  • Fever, chills, cough, dizziness, SOB
  • Female infertility
90
Q

What are topoisomerase inhibitors do?

A
  • Interfere w/ action of topoisomerase enzymes, which control changes in DNA structure by catalyzing the breaking and rejoining of phosphodiester backbone of DNA strands during normal cell cycle
  • Block ligation step of cell cycle, generating single and double stranded breaks that harm integrity of genome => apoptosis and cell death
91
Q

What is the MOA of steroid hormones?

A
  • Enter target cells and bind to receptor, inducing conformational change
  • Hormone-receptor complex binds to DNA, inducing start of transcription
  • Many mRNA transcripts are produced, amplifying the signal
92
Q

What is the objective of hormonal therapy?

A

Starve cancer cells from hormonal signals necessary for growth

93
Q

What are the indications for hormone therapy?

A

Breast, ovarian, prostate, and endometrial cancers

94
Q

What are the types of hormonal antagonists?

A
  • SERMs (selective estrogen receptor modulators)
  • AI (aromatase inhibitors)
  • SARMs (selective androgen receptor modulators)
95
Q

Which drugs are SERMs?

A
  • Tamoxifen
  • Raloxifene
  • Toremifene
96
Q

What is the function of SERMs?

A

Occupy hormone receptor binding space, blocking estrogen from binding => prevents gene transcription and inhibits growth stimulating effects

97
Q

What is the anti-estrogen affinity of tamoxifen dependent on?

A

The primary metabolite endoxifen (tamoxifen is metabolized by CYP2D6 into endoxifen)

98
Q

What effect does a CYP2D6 polymorphism have on tamoxifen?

A

Reduces endoxifen formation, so lowers activity and drug effectiveness

99
Q

What are DDIs w/ tamoxifen?

A

Anti-depressants b/c can reduce endoxifen levels even w/ functional CYP2D6 allele

100
Q

When are SERMs and AIs indicated?

A
  • Advanced or metastatic breast cancer
  • High risk population for invasive breast cancer
  • SERM = recent use in lung tumour and GBM (brain tumours)
101
Q

Which drugs are aromatase inhibitors?

A
  • Exemestane
  • Anastrozole
  • Letrozole
102
Q

What do aromatase inhibitors do?

A

Block formation of estrogen, so prevent conversion of immature hormone into finalized active hormone

103
Q

What do SARMs do?

A

Prevent binding of testosterone to androgen receptor, so prevent gene transcription and tumour cell growth

104
Q

Which drugs are SARMs?

A
  • Flutamide

- Bicalutamine

105
Q

Which 2 anti-cancer drugs exert a synergistic effect?

A

Cisplatin and etoposide

106
Q

What are benefits to combination cancer therapy?

A
  • Synergistic effects
  • Decreased development of resistance
  • Broader cell kill in cancers w/ heterogeneous tumour cell population
107
Q

What are common side effects of chemotherapy drugs?

A
  • Bone marrow depression => anemia, bleeding, infections, secondary cancers
  • Teratogenesis
  • Carcinogenesis
  • Resistance (often px don’t die from primary tumour, they die from recurrence of resistant tumour)
108
Q

What are some cellular mechanisms for drug resistance?

A
  • Drug target alterations (up-regulation of enzyme target, enhanced drug metabolism)
  • Multi-drug resistance (drug efflux via P-glycoprotein transporters, drug conjugation by glutathione)
  • Enhanced survival (suppression of apoptosis, enhanced DNA repair systems)
109
Q

What are some non-cellular mechanisms for drug resistance?

A
  • Pharmacological sanctuaries

- Altered in vivo growth kinetics

110
Q

How can cancer cells develop resistance to methotrexate?

A

Increased concentrations of DHFR enzyme

111
Q

How can cancer cells develop resistance to tamoxifen?

A

Downregulation/mutation of estrogen receptor so tamoxifen doesn’t work, but cell is still getting growth effects

112
Q

How can cancer cells develop resistance to 5-fluorouracil?

A
  • Down-regulate thymidylate synthase, so 5-FU loses its target
  • Will still give px off-site SE, so SE doesn’t necessarily mean the drug is working in the cancer cell
113
Q

What are the mechanisms for chemotherapy resistance?

A
  • Increased expression of target proteins
  • Failure of drugs to enter cancer cells or increased rate of removal of drug from cancer cell
  • Drug fails to reach target cells
  • Target molecule altered or no longer present
    • Often more than one of these
114
Q

What is a P-glycoprotein?

A
  • Transmembrane ATP-dependent efflux pump
  • Actively transports many types of chemotherapy from cells
  • Overexpression in cancers causes drug resistance
115
Q

What is a major cause of multi-drug resistance?

A

Failure of DNA damaged cells to undergo apoptosis

116
Q

What drugs are used for monoclonal antibody therapy?

A
  • Rituximab
  • Trastuzumab
  • Cetuximab
117
Q

What does rituximab do? What are some side effects?

A
  • Binds to CD20 antigen receptor present on surface of B cells => complement-activated phagocytosis and Ab-dependent apoptosis
  • Inhibit proliferation of lymphocytes and lymphoma cells
  • SE = severe hypersensitivity reactions, anaphylactic shock
118
Q

What does trastuzumab do? What is it indicated for? What are some side effects?

A
  • Binds to human epidermal growth factor receptor protein-2 (HER2), which is overexpressed in some cancers
  • Indicated for HER2+ metastatic breast cancer and early stage HER2+ breast cancer
  • SE = allergic reaction, heart muscle damage, pulmonary toxicity
119
Q

What does cetuximab do? What is it indicated for? What are some side effects?

A
  • Acts against epidermal growth factor receptor protein (EGFR), which is overexpressed in some cancers
  • Indicated for metastatic colorectal cancer, metastatic non-small cell lung cancer, and head and neck cancer
  • SE = acne, fever, chills, hypotension, wheezing
120
Q

What is imatinib?

A

Selective tyrosine kinase inhibitor, so prevents phosphorylation of specific proteins involved in cell growth and differentiation

121
Q

What does gefitinib do?

A
  • Interrupts mutated or overactive EGFR receptor signaling
  • Used in breast and lung cancer
  • Can be used in combo w/ methotrexate
122
Q

What does erlotinib do?

A

Reversible EGFR tyrosine kinase inhibitor

123
Q

What are antibody-drug conjugates?

A

Combination of monoclonal antibodies w/ cytotoxic small molecule drugs (allows for discrimination btwn healthy and diseased tissues)

124
Q

Which drugs are antibody-drug conjugates?

A
  • Brentuximab vedotin

- Trastuzumab emtansine

125
Q

Which drug is an angiogenesis inhibitor?

A

Bevacizumab (avastin)

126
Q

What are the 2 possible approaches to gene therapy for cancer?

A
  • Injecting cancer cells w/ special genes that make tumour more receptive to effects of anti-cancer drugs
  • Introducing multi-drug resistant gene into bone marrow to make stem cells more immune to toxic SE of anti-cancer drugs

Pharmacology - Winter (18 decks)

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