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IHO Week 4 - WLB > Biologic Antineoplastics - Fitz > Flashcards

Biologic Antineoplastics - Fitz Flashcards

1
Q

What are the three chemical types of Drugs that Interrupt Mitosis/Antimitotics/Spindle Poisons?

A
  • Vinca alkaloids
    • vincristine, etc.
  • Taxanes
    • paclitaxel, etc.
  • Epilone
    • ixabepilone

(All CCS: M-phase)

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2
Q

What are the two groups of Plant Alkaloids?

A
  • Vinca Alkaloids
  • Taxanes
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3
Q

What are the 3 Antimitotic Vinca Alkaloid drugs that we need to know?

A
  • Vinblastine
  • Vincristine
  • Vinorelbine
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4
Q

What are the 3 Antimitotic Taxane drugs that we need to know?

A
  • Paclitaxel
  • Capazitaxel
  • Docataxel
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5
Q

What is the only Antimitotic Epilone (antibotic) drug that we need to know?

A

Ixabepilone

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6
Q

What is the MOA of Antimitotic Vinca Alkaloid antineoplastic drugs?

A

bind to tubulin at the forming end of microtubules and TERMINATE (disrupt) spindle assembly

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7
Q

What are potential forms of resistance to Antimitotic Vinca Alkaloids?

A
  • decreased accumulation via increased P-glycoprotein expression → MDR
  • changes in target proteins
    • mutations to tubulin that prevent binding
  • cross reactivity among vinca alkaloids is not absolute
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8
Q

What are the specific therapeutic uses of Antimitotic Vinca Alkaloids?

A
  • routinely used in combination therapy because of distinct mechanisms of action and toxicities
    • regimens:
      • VINCRISTINE (Oncovin):
        • MOPP for Hodgkin’s disease
        • CHOP for non-Hodgkin’s lymphoma
      • VINBLASTINE:
        • ABVD for Hodgkin’s disease
        • PVB for testicular cancer
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9
Q

As a drug class, the Antimitotic Vinca Alkaloids may cause what possible adverse side effects?

A

bone marrow suppression & neurotoxicity

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10
Q

What specific adverse side effects may be caused by Vincristine?

A
  • VINCRISTINE = CNS toxicity
    • more lipid soluble → fatal if given intrathecally
  • neurotoxicity
    • prominent because of the requirement for microtubules in axon transport
    • common symptoms:
      • motor: loss of reflexes
      • autonomic: constipation, paralytic ileus, orthostatic hypotension
      • sensory: paresthesias (“pins and needles”)
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11
Q

What particular symptom is used as an indication of sufficient dose for Vincristine? What symptoms indicate the need to decrease the dose?

A
  • depression of deep tendon reflexes occurs within 2-3 weeks in 100% of patients
    • used as an indication of sufficient dose
  • this can be followed by severe paresthesias and mild-moderate sensory loss which is an indication to decrease the dose
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12
Q

What specific adverse side effects may be caused by Vinblastine?

A
  • Vinblastine = bone marrow suppression
  • Nausea & vomiting
  • Vesicant
  • Alopecia
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13
Q

What is the MOA of Antimitotic Taxanes (Paclitaxel, etc.)?

A

bind to tubulin and ENHANCE AND STABILIZE spindle assembly

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14
Q

What is one potential form of resistance to Antimitotic Taxanes?

A

decreased accumulation via

increased P-glycoprotein expression → MDR

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15
Q

What is important to know about the metabolism (pharmacokinetics) of Antimitotic Taxanes?

A

eliminated by extensive CYP 450 metabolism- hepatobiliary excretion

(i.e. liver function is critical)

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16
Q

What are some possible toxic side effects of Antimitotic Taxanes?

A
  • bone marrow suppression
  • hypersensitivity/allergic reactions
  • peripheral neuropathy
  • nausea and vomiting
  • hypotension, arrhythmias
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17
Q

What is the MOA of the Antimitotic Epilone: Ixabepilone?

A

antibiotic that binds to tubulin and ENHANCES AND STABILIZES spindle assembly

(similar to paclitaxel)

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18
Q

What is Ixabepilone used to treat?

A

IXABEPILONE does not produce MDR, and is therefore approved for use in breast cancer patients who have failed anthracycline antibiotic and taxane treatments.

  • used in combination with CAPECITABINE for the treatment of metastatic breast cancer following treatment failure with an anthracycline antibiotic and PACLITAXEL
    • (i.e., it is a 3rd line treatment)
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19
Q

What are the potential toxic side effects of Ixabepilone?

A
  • causes bone marrow suppression
    • especially neutropenia
  • peripheral neuropathy
  • cardiac arrhythmias
  • can also produce hypersensitivity reactions
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20
Q

What are the 3 chemical classes of Immunosuppressives?

A
  1. Glucocorticoids
  2. Antibiotics
  3. Antibodies and fusion proteins
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21
Q

What is the MOA of Glucocorticoids?

A
  • interfere with the concentration, distribution and function of leukocytes
    • increases the concentration of neutrophils; decreases T & B lymphocytes, monocytes, eosinophils and basophils
    • end result is decrease in cytokine release, including decreases in IL-2 and TNF α
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22
Q

What is the naturally occurring compound associated with Glucocorticoids?

A

Cortisol

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23
Q

How are Glucocorticoids administered in chemotherapy treatments compared to their use in treating inflammatory diseases (asthma, arthritis, lupus, etc.)?

A
  • Chemotherapy:
    • given in higher doses, using a “pulse” regimen
  • Conventional Immunosuppression:
    • low dose, continuous
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24
Q

What are the four Immunosuppressive Antibiotics that we need to know?

A
  1. Cyclosporine
  2. Everolimus
  3. Tacrolimus
  4. Temsirolimus
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25
Q

What are Immunosuppressive Antibiotics used for?

A
  • prevent rejection following bone marrow transplants
    • Cyclosporine, Tacrolimus
  • angiogenesis inhibitors
    • Everolimus, Temsirolimus
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26
Q

What are the two pathways that Imunosuppressive Antibiotics are involved in?

A
  1. NFAT-mediated regulation of interleukin synthesis
  2. mTOR regulation of cell growth and angiogenesis
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27
Q

What effect does Cyclosporine and Tacrolimus have on calcineurin in Antirejection? What is the ultimate result?

A
  • bind to cytoplasmic proteins and inhibit calcineurin
    • CYCLOSPORINE binds to cyclophilin
    • TACROLIMUS binds to FK-binding protein
  • calcineurin is necessary for activation of NFAT
    • a T cell-specific transcription factor that is involved in the synthesis of interleukins by activated T cells → decreased release of IL-2 → decreased activation of IL-2 receptor → decreased cell proliferation
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28
Q

What signalling molecule do tyrosine kinases increase expression of but Everolimus and Temsirolimus inhibit in order to prevent angiogenesis/proliferation?

A
  • receptor tyrosine kinases can also increase expression of mTOR
    • intracellular signaling molecule that:
      • increases cell division
      • increases bioenergetics
      • facilitates angiogenesis in many cell types
  • therefore, EVEROLIMUS and TEMSIROLIMUS function as mTOR inhibitors
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29
Q

Antibodies have been designed to target what CD molecules?

A
  • CD20 in Non-Hodgkin’s Lymphoma
    • Rituximab
    • Ibritumomab
    • Tositumomab
  • CD52 in B-Cell Chronic Lymphoblastic Leukemia
    • Alemtuzumab
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30
Q

Antibodies have been designed to target what cell surface proteins that are overexpressed in specific cancers?

A

HER2, VEGF, EGFR

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31
Q

What is the MOA of the fusion protein, DENILEUKIN DIFTITUX, that has diphtheria toxin coupled to IL-2?

A
  • diphtheria toxin catalyzes the ADP-ribosylation of elongation factor-2 →
    • inhibits protein translation by inactivating EF2
  • goal is to kill cells expressing IL-2 receptors (activated T-lymphocytes, B lymphocytes and macrophages)
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32
Q

What is a potential form of resistance to immunosuppressive antibodies?

A

changes in target protein that prevent the antibody from recognizing its antigen

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33
Q

How are immunosuppressive antibodies administered? Half life?

A
  • IV administration
  • long half-lives - detectable at least 3-6 months after completion of treatment
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34
Q

What are the possible toxic effects of immunosuppressive antibodies and fusion proteins?

A
  • infusion reactions (77% of patients on rituximab)
  • hypersensitivity reactions: fever, muscle aches, headaches, rashes, anaphylaxis
    • mouse (MO) >> chimeric (XI) > humanized (ZU) for HAMA reaction
  • infections
    • esp reactivation of tuberculosis
  • unknown effects on immunization, carcinogenesis, mutagenesis, impairment of fertility, pregnancy, nursing infants (human IgG is secreted in milk)
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35
Q

What are possible specific toxicities of immunosuppressive anti-CD antibodies?

A
  • cardiac arrhythmias
  • tumour lysis syndrome
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36
Q

What are possible unique toxic side effects of Alemtuzumab?

A
  • cough
  • tightness in chest
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37
Q

What are the two types of Immune System Stimulants?

A
  • Cytokines
    • (biological response modifiers)
  • Hematopoietic Growth Factors
    • (supporting agents)
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38
Q

What are the three Cytokines (that we need to know) that are used as Immune System Stimulants?

A
  1. Interferon alpha
  2. Interleukin 2
  3. Tumor Necrosis Factor Alpha
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39
Q

What are 3 common characteristics that all cytokines used for cancer chemotherapy have in common?

A
  • Short half-lives
  • Not cytotoxic themselves
  • Recruit immune cells to do the actual cell killing
    • means the immune system has to recognize the tumor cells as foreign
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40
Q

What immune system response does Interleukin 2 induce?

A

induces and expands a T-cell response cytolytic for tumor cells

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41
Q

How is Interleukin 2 given as a chemotherapy?

A
  • used either alone or with IL-2-stimulated autologous lymphocytes (“lymphokine-activated-killer” or LAK cells; cytokine induced killer or CIK cells)
  • short half-life (t1/2 = 13 minutes) → either continously infused or given as multiple intermittent daily doses
42
Q

What are potential toxic side effects of high doses of Interleukin 2?

A
  • activation and expansion of lytic lymphocytes causes inflammation, vascular leak and secondary release of other cytokines (such as TNF, interferon α) = cytokine storm
  • can produce mild/moderate symptoms such as fever/chills, diarrhea and weight gain or hand-foot syndrome (palmar-plantar erythrodysesthesia)
  • serious toxicities such as thrombocytopenia, shock, respiratory distress, coma and fatal hypotension
43
Q

What are the three mechanisms of anti-tumor activity of Interferon-alpha?

A
  • decreases the production of fibroblast growth factor (FGF)
    • anti-FGF actions may be responsible for actions against leukemic stem cells in chronic myeloid leukemia
    • FGF is angiogenic
  • inhibition of cell division of both normal and tumor cells
  • increases class I MHC expression on tumor cells
    • actually restores normal MHC expression levels → increased activity of cytotoxic T lymphocytes
44
Q

What are four main potential toxic side effects of Interferon-alpha?

A
  • flu-like symptoms: fever, arthralgias, headache, fatigue
  • hypotension
  • myelosuppression
  • depression
45
Q

What are the 3 immune responses that Tumor Necrosis Factor alpha produces?

A
  • causes fibroblast proliferation
  • chemokine induction (IL-6, IL-8)
  • T and B cell activation
46
Q

How is Tumor Necrosis Factor alpha administered? Why?

A

intra-arterial administration due to extremely short half-life and toxicity

47
Q

What is the severe dose-limiting toxicity of Tumor Necrosis Factor alpha?

A

malaise and flu-like symptoms - can cause hemorrhagic necrosis

48
Q

What progenitor cells does Filgrastim activate?

A

G-CSF → neutrophils

49
Q

What progenitor cells does Sagramostim activate?

A

GM-CSF → granulocytes, eosinophils, basophils, and monocytes

50
Q

What cells does Interleukin 11 and Thrombopoietin activate?

A

Platelets

51
Q

What are tyrosine kinases important targets in cancer treatment?

A

because they are regulators of intracellular signal transduction pathways, where they are involved in development and multicellular communication

52
Q

What two things have been designed to interfere with the actions of specific tyrosine kinases?

A
  • signal transduction inhibitors
  • antibodies
53
Q

What do signal transduction inhibitors bind to?

A

bind to the ATP-binding site of tyrosine kinases (NOT the substrate binding site)

54
Q

Why do Signal Transduction Inhibitors generally have fewer side effects than conventional chemotherapies?

A

they are targeted toward the specific defect of a particular cancer (bcr-abl, EGFR, etc.)

55
Q

What are the four inhibitors of Bcr-abl?

A
  1. Bosutinib
  2. Imatinib
  3. Nilotinib
  4. Dasatanib
56
Q

What is the MOA of the three STI’s that target Bcr-abl (DASATANIB, IMATINIB (Gleevec), NILOTINIB)?

A
  • competitive antagonists of the ATP-binding site of:
    • bcr-abl, the non-receptor tyrosine kinase whose activity is deregulated by the translocation of its gene from chromosome 9 to chromosome 22 in most patients with CML
    • also target c-kit, the tyrosine kinase altered in gastrointestinal stromal tumours (GIST), and are weak antagonists of the platelet-derived growth factor (PDGF) receptor
57
Q

What cancer type is the tyrosine kinase Bcr-abl associated with?

A

Chronic Myeloid Leukemia (CML)

58
Q

How are the STI’s that target Bcr-abl (DASATINIB, IMATINIB, NILOTINIB) metabolized?

A

metabolized in the liver (CYP 3A4), and excreted in the feces (hepatobiliary excretion)

59
Q

What are potential forms of resistance to STI’s that target Bcr-abl?

A
  • change in target proteins
    • mutation of ATP-binding site that prevents drug binding in the cancer cells, often due to further mutations of bcr-abl gene (heterogeneity of tumour) - secondary resistance
  • sometimes see overexpression of bcr/abl or expression of other kinases (form of primary resistance)
    • DASATINIB and NILOTINIB were developed to target cells that have become resistant to IMATINIB
60
Q

What are the therapeutic uses of STI’s targeting Bcr-abl (DASATINIB, IMATINIB, NILOTINIB)?

A
  • can induce a complete hematological and cytological response in 85-95% of patients in the chronic phase of CML
  • can delay death in 25% of patients in blast crisis (75% of these patients initially respond)
  • also effective in gastrointestinal stromal tumours expressing c-kit
61
Q

What are the three severe potential toxic side effects of STI’s in general?

A
  • can cause congestive heart failure and/or myocardial infarction
    • incidence and severity vary widely within STIs
      • more common and more severe with DASATINIB, IMATINIB and NILOTINIB, because Abl tyrosine kinases are necessary for maintenance of normal heart function
  • teratogenic
62
Q

What are the four drugs that target EGFR?

A
  1. Cetuximab
  2. Erlotinib
  3. Gefitinib
  4. Panitumumab
63
Q

What is the MOA of Cetuximab and Panitumumab?

A

monoclonal antibodies directed against EGFR

64
Q

What is the MOA of Erlotinib and Gefitinib?

A

competitive antagonists of the ATP-binding site of EGFR

65
Q

What type of cancer is Cetuximab & Panitumumab used primarily for?

A

Metastatic Colon Cancer

66
Q

What are the potential toxic side effects of Cetuximab & Panitumumab?

A
  • infusion/hypersensitivity reactions: fever, muscle aches, headaches, rashes, anaphylaxis, infusion reactions
    • mouse (MO) >> chimeric (XI) > humanized (ZU) for HAMA reaction
  • infections
  • unknown effects on immunization, carcinogenesis, mutagenesis, impairment of fertility, pregnancy, nursing infants (human IgG is secreted in milk)
  • unique toxicities include skin (rash, photosensitivity, necrotizing fascitis) and lung (interstitial lung disease)
67
Q

What are the potential toxic side effects of Erlotinib & Gefitinib?

A
  • as with other STIs, relatively minor side effects (esp. compared to conventional therapies that work by preventing rapid cell growth): nausea, vomiting, fatigue, myalgia, diarrhea, skin rashes and acne, drug interactions
  • can cause congestive heart failure and myocardial infarction (less likely than with STIs that inhibit Bcr-Abl)
  • teratogenic
  • interstitial pneumonia (which can be fatal)
68
Q

What type of cancer is Erlotinib & Gefitinib used for?

A

approved for use in metastatic non-small cell lung cancer (NSCLC) after failure of standard chemotherapies

69
Q

What is HER2?

A

Human epithelial growth factor receptor 2

(HER2) = Neu = ErbB2 = CD340

70
Q

What type of cancer is HER2 overexpressed?

A

Aggressive breast cancers

71
Q

What are the three drugs approved to targed HER2?

A
  1. Trastuzumab
  2. Pertuzumab
  3. Ado-Trastuzumab Emtansine
72
Q

What is the MOA of Trastuzumab in targeting HER2?

A

binding of the antibody interferes with HER2 signaling, and identifies the HER2-overexpressing cells as foreign, so that they can be destroyed by the immune system

73
Q

What is the MOA of Pertuzumab in targeting HER2?

A

it prevents HER2 from dimerizing with other HER receptors

first antineoplastic DIMERIZATION INHIBITOR 
(a new class of drugs)
74
Q

What is the MOA of Ado-Trastuzumab Ematansine?

A
  • internalized and undergoes lysosomal degradation to form 2 components
    • TRASTUZUMAB
    • DM1, a small molecule inhibitor that disrupts microtubule networks by binding to tubulin
75
Q

What is the one potential form of resistance to drugs targeting HER2?

A

altering HER2 so that the antibody doesn’t recognize its target

76
Q

What three unique toxic side effects have been caused by treatment with Trastuzumab?

A
  • Birth defects/fetal loss
  • Ventricular dysfunction
  • Congestive heart failure
77
Q

How is asparagine used in normal cells?

A

the asparagine used for protein synthesis is generated from aspartate by asparagine synthase;

asparagine outside the cell is converted to aspartate by L-ASPARAGINASE before being pumped into the cell and converted back to asparagine

78
Q

What does administration of L-Asparaginase cause?

A

selective toxicity because some tumour cells lack asparagine synthase (i.e., they require an exogenous sources of L-asparagine for protein synthesis), therefore decreasing the asparagine concentration by giving L-ASPARAGINASE deprives tumour cells of asparagine

79
Q

What type of cancer is treated with L-Asparaginase?

A

childhood acute lymphocytic leukemia

80
Q

What is the main side effect of chemotherapy treatment with L-Asparaginase? Why?

A

hypersensitivity reactions (fever, chills, nausea/vomiting, skin rash and urticaria) because L-ASPARAGINASE is isolated from bacteria

81
Q

Why is L-Asparaginase usually used with other antineoplastic agents?

A

sequence of drug administration is critical, for example:

  • if METHOTREXATE is given first, you have synergistic cytotoxicity (due to synchrony)
  • if L-ASPARAGINASE is given first, the METHOTREXATE cytotoxicity is reduced as METHOTREXATE cell kill is dependent upon synthesis of the enzymes necessary for DNA synthesis (DHFR and thymidylate synthase, specifically)
82
Q

What two drugs are inhibitors of the 26S proteosome?

A
  1. Bortezomib
  2. Carfilzomib
83
Q

What does the 26S proteosome normally do? What happens when it is inhibited?

A
  • the ubiquitin-26S proteasome pathway regulates the intracellular concentration of proteins, thereby maintaining cellular homeostasis
  • inhibition of the 26S proteasome affects multiple signalling cascades, triggering apoptosis and leading to cell death
84
Q

Which drug is reversible/irreversible between Bortezomib and Carfilzomib?

A
  • Bortezomib = reversible
  • Carfilzomib = irreversible
85
Q

What are three potential toxic side effects of Bortezomib and Carfilzomib?

A
  • Thrombocytopenia, neutropenia, and/or anemia
  • Peripheral neuropathy
86
Q

What type of cancer is Bortezomib/Carfilzomib used to treat?

A

Multiple Myeloma

87
Q

What do histone deacetylases (HDACs) do in normal cells?

A
  • histone deacetylases (HDACs) work in conjunction with histone acetyltransferases to regulate gene expression
    • acetylation is associated with euchromatin (“open for transcription”)
    • deacetylation is associated with heterochromatin(“closed”)
88
Q

What do histone deacetylases (HDACs) do in cancer cells?

A
  • some cancer cells overexpress or aberrently recruit HDACs, leading to hypoacetylation of histones, condensed chromatin structure and decreased transcription
    • causes silencing of tumor suppressor genes (esp. p53)
89
Q

What is the MOA of HDAC inhibitors like ROMIDEPSIN, VORINOSTAT?

A

HDAC inhibitors increase transcription, and lead to cell cycle arrest and apoptosis

90
Q

What cancer type is Vorinostat used for?

A

approved for use in cutaneous T-cell lymphoma, and is under investigation in glioblastoma multiforme and HIV

91
Q

What are the potential toxic side effects of HDAC inhibitors like Romidepsin and Vorinostat?

A
  • Hematologic:
    • pulmonary edema
    • deep vein thrombosis
  • Drug/Drug interations:
    • severe thrombocytopenia and GI bleeding result from coadministration with valproic acid
    • PT and INR are prolonged if given with WARFARIN
92
Q

What are the three Differentiating Agents that we need to know?

A
  1. Tretinoin (ATRA, RETIN-A)
  2. Arsenic Trioxide (ATO)
  3. Bexarotene
93
Q

What is the MOA of Tretinoin?

A

in acute promyelocytic leukemia (APL), activates the differentiation program (converting promyelocytes into granulocytes) and promotes degradation of the PML-RAR fusion protein

94
Q

Why does treating cancer with Tretinoin require the addition of a cytotoxic agent?

A

doesn’t kill cells itself!

requires cytotoxic agent like ARSENIC TRIOXIDE or anthracycline antibiotic

95
Q

What are potential toxic side effects of Tretinoin?

A
  • headache, dry skin, reversible hepatic enzyme abnormalities, bone tenderness, hyperlipidemia
  • CNS toxicity: dizziness, anxiety, depression, confusion, agitation
  • DIFFERENTIATION SYNDROME (formerly called retinonic acid syndrome): fever, dyspnea, weight gain, pulmonary infiltrates
    • with or without pleural or pericardial effusions
    • with or without leucocytosis
    • can be fatal
  • birth defects (teratogenic)
96
Q

What is the MOA of Arsenic Trioxide (ATO)?

A
  • heavy metal toxin that promotes cell death through both apoptosis and necrosis
  • given in conjunction with TRETINOIN to cause death of differentiated granulocytes
97
Q

What are two potential toxic side effects of Arsenic Trioxide (ATO)?

A
  • arrhythmias (prolongation of QT interval)
  • leukocyte maturation syndrome similar to differentiation syndrome
98
Q

What is the MOA of Bexarotene?

A

rexinoid that selectively activates retinoid X receptors, which are involved in the regulation of cell growth and differentiation

99
Q

What type of cancer is treated with Bexarotene?

A

approved for use in patients with cutaneous T-cell lymphoma that is refractory to skin-directed treatment

100
Q

What are the potential toxic side effects of Bexarotene?

A
  • metabolized by CYP3A4 (potential for many drug interactions)
  • side effects include: GI symptoms, lipid abnormalities and pancreatitis (must monitor blood lipid levels)
  • TERATOGENIC

IHO Week 4 - WLB (13 decks)

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