Pharamcology I | By: Lindsay Williamson, ARNP, MSN, AOCNP

1. PHARMACOLOGY 101
MECHANISM AND TARGETS
IN MEDICAL ONCOLOGY
Lindsay WilliamsonLindsay Williamson
ARNP, MSN, AOCNPARNP, MSN, AOCNP

2. BiographyBiography
 Lindsay Williamson is board certified as an Advanced Oncology Certified
Nurse Practitioner as well as an Adult Nurse Practitioner. She received her
BSN at West Chester University in West Chester, Pennsylvania and her
MSN at La Salle University in Philadelphia, Pennsylvania. Lindsay has been
an Oncology Nurse for 15 years with 7 of those years in the role of Nurse
Practitioner. She has worked in a variety of settings including inpatient and
outpatient as well as community based and academic based. Also, she has
worked in a variety of roles including Oncology Staff Nurse, Infusion Nurse,
ARNP in a community practice, Pharmaceutical Sales Representative and
Clinical Operations Manager of the Lab Draw and Infusion areas at Moffitt
Cancer Center. She is currently working with Florida Cancer Specialists in
New Port Richey, Florida as an Oncology Nurse Practitioner. Lindsay is a
member of the Advanced Practice Society for Hematology and Oncology
and the Oncology Nursing Society.

3. Financial DisclosureFinancial Disclosure
 No financial disclosures existNo financial disclosures exist

4. ObjectivesObjectives
 Define the purposes of cancer therapy
 Describe the differences among chemotherapy, hormonal therapy,
immunotherapy and kinase inhibitors
 Have a basic understanding of the different drug classifications of
chemotherapy, the different types of hormonal therapy and the many targets
that therapies affect
 Have a basic understanding for common toxicities for cancer treatments
 Define available resources for drug indications, dosing and adverse effects
profile

6. Benign HematologyBenign Hematology
 AnemiaAnemia
 Iron OverloadIron Overload
 Idiopathic Thrombocytopenia (ITP)Idiopathic Thrombocytopenia (ITP)
 ThalassemiaThalassemia
 Sickle Cell AnemiaSickle Cell Anemia
 HemophiliaHemophilia
 Blood ClotsBlood Clots
 Myeloproliferative diseasesMyeloproliferative diseases

7. AnemiaAnemia
 Chronic Kidney DiseaseChronic Kidney Disease

Erythropoiesis-stimulating agentErythropoiesis-stimulating agent
• Stimulates erythroid progenitor division andStimulates erythroid progenitor division and
differentiation (erythropoiesis-stimulating agent)differentiation (erythropoiesis-stimulating agent)

epoetin alpha (Procrit)epoetin alpha (Procrit)

darbepoietin alfa (Aranesp)darbepoietin alfa (Aranesp)

8. AnemiaAnemia
 Iron DeficiencyIron Deficiency

OralOral
• ferrous sulfate, ferrous fumarate, ferrous gluconateferrous sulfate, ferrous fumarate, ferrous gluconate

ParenteralParenteral
• iron dextran (INFed, DexFerrum)iron dextran (INFed, DexFerrum)
• iron sucrose (Venofer)iron sucrose (Venofer)
• sodium ferric gluconate complex (Ferrlecit)sodium ferric gluconate complex (Ferrlecit)
• Ferumoxytol (Feraheme)Ferumoxytol (Feraheme)
• Ferric carboxymaltose (Injectafer)Ferric carboxymaltose (Injectafer)

9. Iron OverloadIron Overload
 Iron chelatorsIron chelators

deferoxamine (Desferal)deferoxamine (Desferal)
• Promotes urinary iron excretionPromotes urinary iron excretion
• Given IV or IMGiven IV or IM

deferasirox (Exjade, Jadenu)deferasirox (Exjade, Jadenu)
• Promotes fecal iron excretionPromotes fecal iron excretion
• OralOral

10. Idiopathic ThrombocytopenicIdiopathic Thrombocytopenic
PurpuraPurpura
 CorticosteroidsCorticosteroids

May raise platelets by decreasing activity of immuneMay raise platelets by decreasing activity of immune
systemsystem
 IVIGIVIG
 rituximab (Rituxan)rituximab (Rituxan)

Reduces immune system response that damages plateletsReduces immune system response that damages platelets
 Thrombopoietin receptor agonistsThrombopoietin receptor agonists

Binds and activates thrombopoietin (TPO) receptors onBinds and activates thrombopoietin (TPO) receptors on
hematopoietic cells, increasing platelet productionhematopoietic cells, increasing platelet production

eltrombopag (Promacta), oral agenteltrombopag (Promacta), oral agent

romiplostim (Nplate), SQ injectionromiplostim (Nplate), SQ injection

11. AnticoagulantsAnticoagulants
 InjectableInjectable
• HeparinHeparin

Acts at multiple sites in the coagulation process,Acts at multiple sites in the coagulation process,
inactivates thrombin and other clotting factorsinactivates thrombin and other clotting factors
• Low-molecular weight heparinLow-molecular weight heparin

dalteparin (Fragmin)dalteparin (Fragmin)

enoxaparin (Lovenox)enoxaparin (Lovenox)
• fondaparinux (Arixtra)fondaparinux (Arixtra)

Selectively binds to antithrombin III, potentiatingSelectively binds to antithrombin III, potentiating
factor Xa neutralization and inhibiting thrombinfactor Xa neutralization and inhibiting thrombin
formation (synthetic selective factor Xa inhibitor)formation (synthetic selective factor Xa inhibitor)

12. AnticoagulantsAnticoagulants
 OralOral
• warfarin (Coumadin, Jantoven)warfarin (Coumadin, Jantoven)

Inhibits vitamin K-dependent coagulation factorInhibits vitamin K-dependent coagulation factor
synthesis (II, VII, IX, X, proteins C and S)synthesis (II, VII, IX, X, proteins C and S)

Regulate INRRegulate INR

Antidote is Vitamin KAntidote is Vitamin K
• Factor Xa inhibitorFactor Xa inhibitor

apixaban (Eliquis) BID dosingapixaban (Eliquis) BID dosing

rivaroxaban (Xarelto) daily dosingrivaroxaban (Xarelto) daily dosing

13. Cancer Therapy GoalsCancer Therapy Goals
 CureCure

No evidence of disease (NED)No evidence of disease (NED)
 ControlControl

Prolong length and quality of life, prevent distant andProlong length and quality of life, prevent distant and
possible unknown metastasespossible unknown metastases

Cure is not realisticCure is not realistic
 Palliation/ComfortPalliation/Comfort

Symptom management, improve comfort and qualitySymptom management, improve comfort and quality
of lifeof life

Appropriate when cure and control are not feasibleAppropriate when cure and control are not feasible

14. Cancer Therapy OverviewCancer Therapy Overview
 Treatment goalsTreatment goals

Manage disease and related symptomsManage disease and related symptoms

Manage treatment toxicitiesManage treatment toxicities
 Treatment typesTreatment types

LocalizedLocalized
• SurgerySurgery
• Radiation therapyRadiation therapy

SystemicSystemic
• PO, IV, IM, SQ, ITPO, IV, IM, SQ, IT
 Treatment considerationsTreatment considerations

Neoadjuvant, Adjuvant, Induction, Maintenance, MetastaticNeoadjuvant, Adjuvant, Induction, Maintenance, Metastatic

Radio sensitizerRadio sensitizer

15. Cancer Therapy AgentsCancer Therapy Agents
 ChemotherapyChemotherapy
 Hormonal TherapyHormonal Therapy
 ImmunotherapyImmunotherapy
 Therapeutic AntibodiesTherapeutic Antibodies
 Antibody-Drug ConjugatesAntibody-Drug Conjugates
 Kinase InhibitorsKinase Inhibitors
 OtherOther

16. Common Cancer TherapyCommon Cancer Therapy
Side EffectsSide Effects
 FatigueFatigue
 MyelosuppressionMyelosuppression
 Nausea/VomitingNausea/Vomiting
 Diarrhea/ConstipationDiarrhea/Constipation
 MucositisMucositis
 Peripheral NeuropathyPeripheral Neuropathy
 AlopeciaAlopecia
 Immune-Mediated pneumonitis, hepatitis, colitis,Immune-Mediated pneumonitis, hepatitis, colitis,
endocrinopathies and rashendocrinopathies and rash
 Oncology EmergenciesOncology Emergencies

Tumor Lysis Syndrome, Hypercalcemia, SIADHTumor Lysis Syndrome, Hypercalcemia, SIADH

17. Cancer Therapy LimitationsCancer Therapy Limitations
 Toxicity of agentsToxicity of agents
 Lifetime doseLifetime dose
 Hypersensitivity reactionsHypersensitivity reactions
 Drug resistanceDrug resistance
 Secondary malignanciesSecondary malignancies
 AdherenceAdherence
 Insurance AuthorizationInsurance Authorization
 Patient costPatient cost

18. Development of Cancer CellsDevelopment of Cancer Cells
 CarcinogenesisCarcinogenesis

Process by which a normal cell converts to a tumor cellProcess by which a normal cell converts to a tumor cell
 Initiation phaseInitiation phase

A biological, chemical, or physical change occurs to the cellA biological, chemical, or physical change occurs to the cell
 Promotion phasePromotion phase

Alteration of expression of cell (i.e. DNA)Alteration of expression of cell (i.e. DNA)
 ConversionConversion

Act of change and continued alterationAct of change and continued alteration
 ProgressionProgression

Changes from pre-malignant to higher level of malignancyChanges from pre-malignant to higher level of malignancy

19. Malignant CellMalignant Cell
 Uncontrolled proliferationUncontrolled proliferation
 Abnormal cell structureAbnormal cell structure
 Accelerated use of nutrientsAccelerated use of nutrients
 Loss of contact inhibitionLoss of contact inhibition
 Lack of adhesionLack of adhesion
 Inability to differentiate fullyInability to differentiate fully

21. ChemotherapyChemotherapy
 Treatment of cancer cells with chemicalsTreatment of cancer cells with chemicals
 Cytotoxic-poisonous to cellsCytotoxic-poisonous to cells
 TypesTypes

Combination therapyCombination therapy
• More than one drugMore than one drug
• More than one treatment modality either sequentially orMore than one treatment modality either sequentially or
concurrentlyconcurrently

Adjuvant therapyAdjuvant therapy
• Primary tumor eradiated by surgery or radiation prior toPrimary tumor eradiated by surgery or radiation prior to
chemotherapychemotherapy

Neo-adjuvant therapyNeo-adjuvant therapy
• Chemotherapy prior to radiation or surgeryChemotherapy prior to radiation or surgery

22. Chemotherapy ClassificationsChemotherapy Classifications
 Phase cycle specific agentsPhase cycle specific agents-only the cells-only the cells
in a specific cycle are affectedin a specific cycle are affected
 Cell cycle specific agentsCell cycle specific agents-effects are-effects are
mostly on the cells actively dividingmostly on the cells actively dividing
throughout cyclethroughout cycle
 Cell cycle nonspecific agentsCell cycle nonspecific agents-effects are-effects are
on cells at any phaseon cells at any phase

23. Chemotherapy ClassificationsChemotherapy Classifications
 Alkylating AgentsAlkylating Agents
 AntimetabolitesAntimetabolites
 Antimicrotuble AgentsAntimicrotuble Agents
 Topoisomerase I InhibitorsTopoisomerase I Inhibitors
 Topoisomerase II InhibitorsTopoisomerase II Inhibitors
 Antitumor AntibioticsAntitumor Antibiotics
 Aspariginase derivativesAspariginase derivatives
 Hypomethylating AgentsHypomethylating Agents
 OtherOther

24. Alkylating AgentsAlkylating Agents
 Mechanisms of action: Interfere with DNAMechanisms of action: Interfere with DNA
replication through cross linking of DNAreplication through cross linking of DNA
strands, DNA strand breaking, andstrands, DNA strand breaking, and
abnormal base pairing of proteinsabnormal base pairing of proteins
 Most agents areMost agents are cell cycle nonspecificcell cycle nonspecific
 Activated by cytochrome p450Activated by cytochrome p450
 Toxicities: Nausea/Vomiting,Toxicities: Nausea/Vomiting,
Hematopoietic, ReproductiveHematopoietic, Reproductive

25. Alkylating AgentsAlkylating Agents
 Alkyl sulfonatesAlkyl sulfonates

busulfan (Myleran); CML, Myelofibrosisbusulfan (Myleran); CML, Myelofibrosis
 EthyleneiminesEthyleneimines

thiotepa (Thioplex); Breast, Ovarianthiotepa (Thioplex); Breast, Ovarian
 Nitrogen mustardsNitrogen mustards

bendamustine (Bendeka, Treanda); Given IV; CLL,bendamustine (Bendeka, Treanda); Given IV; CLL,
NHLNHL

chlorambucil (Leukeran); HL, NHL, CLLchlorambucil (Leukeran); HL, NHL, CLL

cyclophosphamide (Cytoxan); Given IV or POcyclophosphamide (Cytoxan); Given IV or PO
• HL, NHL, MM, CML, AML, BreastHL, NHL, MM, CML, AML, Breast

ifosfamide (Ifex); Testicular, Sarcomaifosfamide (Ifex); Testicular, Sarcoma

melphalan (Alkeran); MMmelphalan (Alkeran); MM

26. Alkylating AgentsAlkylating Agents
 NitrosoureasNitrosoureas

Most agents cross blood-brain barrierMost agents cross blood-brain barrier

carmustin (BICNU); Brain, MM, HL, NHLcarmustin (BICNU); Brain, MM, HL, NHL

lomustine (Gleostine)-oral agent: Brain, HL,lomustine (Gleostine)-oral agent: Brain, HL,
NHLNHL

streptozotocin (Zanosar); Pancreaticstreptozotocin (Zanosar); Pancreatic

27. Alkylating AgentsAlkylating Agents
 Platinum AnaloguesPlatinum Analogues

cisplatin (Platinol)-heavy metal; Testicular,cisplatin (Platinol)-heavy metal; Testicular,
Ovarian, Bladder, LungOvarian, Bladder, Lung

carboplatin (Paraplatin)-2carboplatin (Paraplatin)-2ndnd
generationgeneration
platinum analogue; Solid tumorsplatinum analogue; Solid tumors

oxaliplatin (Eloxatin)-3oxaliplatin (Eloxatin)-3rdrd
generation platinumgeneration platinum
analogue; Colorectalanalogue; Colorectal
 TriazenesTriazenes

dacarbazine (DTIC); HL, Melanomadacarbazine (DTIC); HL, Melanoma

temozolomide (Temodar); Braintemozolomide (Temodar); Brain

28. Alkylating AgentsAlkylating Agents
 OtherOther

procarbazine (Matulane); HLprocarbazine (Matulane); HL

29. AntimetabolitesAntimetabolites
 Mechanism of action: Inhibit DNAMechanism of action: Inhibit DNA
synthesis by substituting metabolites orsynthesis by substituting metabolites or
structural analogues during DNA synthesisstructural analogues during DNA synthesis
 Most agents areMost agents are phase cycle specificphase cycle specific
 Toxicities: Hematopoietic and GIToxicities: Hematopoietic and GI

30. AntimetabolitesAntimetabolites
 Folate AntagonistsFolate Antagonists

methotrexate (Abitexate); Breast,methotrexate (Abitexate); Breast,
Osteosarcoma, H/NOsteosarcoma, H/N

pemetrexed (Alimta); Lung, Mesotheliomapemetrexed (Alimta); Lung, Mesothelioma

pralatrexate (Folotyn); Peripheral T-cellpralatrexate (Folotyn); Peripheral T-cell
lymphomalymphoma

31. AntimetabolitesAntimetabolites
 Purine AntagonistsPurine Antagonists

cladribine (Leustatin); Hairy Cell Leukemiacladribine (Leustatin); Hairy Cell Leukemia

fludarabine phosphate (Fludara); CLLfludarabine phosphate (Fludara); CLL
 Pyrimidine AntagonistsPyrimidine Antagonists

5 fluorouracil (5-FU); GI malignancies5 fluorouracil (5-FU); GI malignancies

capecitabine (Xeloda)-oral agent; GI, Breastcapecitabine (Xeloda)-oral agent; GI, Breast

cytarabine (Cytosar); AMLcytarabine (Cytosar); AML

fluorouracil (Adrucil); GI, Pancreatic, Breastfluorouracil (Adrucil); GI, Pancreatic, Breast

gemcitabine (Gemzar); Pancreatic, breast,gemcitabine (Gemzar); Pancreatic, breast,
ovarian, Lungovarian, Lung

32. AntimetabolitesAntimetabolites
 OtherOther

hydroxyurea (Hydrea)-oral agent; P vera,hydroxyurea (Hydrea)-oral agent; P vera,
thrombocythemia, H/Nthrombocythemia, H/N

33. Antimicrotubule AgentsAntimicrotubule Agents
 Mechanism of action: Block cell division byMechanism of action: Block cell division by
preventing microtubule functionpreventing microtubule function
 Plant derivedPlant derived
 Toxicities: Peripheral NeuropathyToxicities: Peripheral Neuropathy

34. Antimicrotuble AgentsAntimicrotuble Agents
 EpothilonesEpothilones

ixabepilone (Ixempra); Breastixabepilone (Ixempra); Breast
 Halichonrin B analogueHalichonrin B analogue

eribulin mesylate (Halaven); Breast, Liposarcomaeribulin mesylate (Halaven); Breast, Liposarcoma
 TaxanesTaxanes

paclitaxel (Taxol); Breast, Ovarian, Lung, Sarcomapaclitaxel (Taxol); Breast, Ovarian, Lung, Sarcoma

albumin-bound paclitaxel, nab-paclitaxel (Abraxane);albumin-bound paclitaxel, nab-paclitaxel (Abraxane);
Breast, Pancreatic, LungBreast, Pancreatic, Lung

cabazitaxel (Jevtana); Prostatecabazitaxel (Jevtana); Prostate

35. AntimicrotubulesAntimicrotubules
 Vinca AlkaloidsVinca Alkaloids

Vinblastine (Velban, Velsar); HL, TesticularVinblastine (Velban, Velsar); HL, Testicular

Vincristine (Vincasar PFS); HL, NHL, ALL,Vincristine (Vincasar PFS); HL, NHL, ALL,
Solid tumorsSolid tumors

Liposomal vincristine (Marqibo); ALLLiposomal vincristine (Marqibo); ALL

Vinorelbine (Navelbine); Lung, BreastVinorelbine (Navelbine); Lung, Breast

36. Topoisomerase I InhibitorsTopoisomerase I Inhibitors
 Mechanism of action:Mechanism of action: Interferes with theInterferes with the
activity of topoisomerase in the process ofactivity of topoisomerase in the process of
DNA replicationDNA replication
 Toxicities:Toxicities: Nausea, vomiting, diarrhea,Nausea, vomiting, diarrhea,
abdominal cramping.abdominal cramping.

37. Topoisomerase I InhibitorsTopoisomerase I Inhibitors
 Camptothecin derivativesCamptothecin derivatives

irinotecan (Camptosar); Colorectalirinotecan (Camptosar); Colorectal

topotecan (Hycamptin); Ovarian, Lung,topotecan (Hycamptin); Ovarian, Lung,
CervicalCervical

38. Topoisomerase II InhibitorsTopoisomerase II Inhibitors
 Mechanism of action: Interferes with theMechanism of action: Interferes with the
activity of topoisomerase in the process ofactivity of topoisomerase in the process of
DNA replicationDNA replication
 Toxicities: Nausea, vomiting, diarrhea,Toxicities: Nausea, vomiting, diarrhea,
bone marrow suppressionbone marrow suppression
 AnthracenedioneAnthracenedione

Mitoxantrone (Novantrone); AML, ProstateMitoxantrone (Novantrone); AML, Prostate

39. Topoisomerase II InhibitorsTopoisomerase II Inhibitors
 AnthracyclinesAnthracyclines

Daunorubicin (Cerubidine); ALL, AMLDaunorubicin (Cerubidine); ALL, AML

Doxorubicin (Adriamycin)-baseline EF, lifetimeDoxorubicin (Adriamycin)-baseline EF, lifetime
cumulative dose; Breast, Sarcomacumulative dose; Breast, Sarcoma

Liposomal doxorubicin (Doxil); Ovarian,Liposomal doxorubicin (Doxil); Ovarian,
Kaposi sarcomaKaposi sarcoma

Epirubicin (Ellence); BreastEpirubicin (Ellence); Breast

Idarubicin (Idamycin); AMLIdarubicin (Idamycin); AML

40. Topoisomerase II InhibitorsTopoisomerase II Inhibitors
 EpipodrophyllotoxinsEpipodrophyllotoxins

etoposide (Toposar); Lung, Testicularetoposide (Toposar); Lung, Testicular

41. Antitumor AntibioticsAntitumor Antibiotics
 Mechanism of action: DNA intercalation (insertMechanism of action: DNA intercalation (insert
between two strands of DNA), generate highlybetween two strands of DNA), generate highly
reactive free radicals that damage intercellularreactive free radicals that damage intercellular
moleculesmolecules
 Toxicities: Bone marrow suppressionToxicities: Bone marrow suppression
 Antitumor antibioticsAntitumor antibiotics

bleomycin (Blenoxane)- Pulmonary toxicities;bleomycin (Blenoxane)- Pulmonary toxicities;
Lung, Testicular, NHLLung, Testicular, NHL

mitomycin (Mutamycin)-Delayed bone marrowmitomycin (Mutamycin)-Delayed bone marrow
suppression; Anal, Pancreatic, Stomachsuppression; Anal, Pancreatic, Stomach

42. Aspariginase DerivativesAspariginase Derivatives
 Mechanism of action:Mechanism of action: Catalyzes asparagineCatalyzes asparagine
deamination resulting in decreased circulatingdeamination resulting in decreased circulating
asparagine and cytotoxicity of asparasparagine and cytotoxicity of asparagine-agine-
dependent leukemic cellsdependent leukemic cells
 Toxicities:Toxicities: Hypersensitivity reaction,Hypersensitivity reaction,
hyperglycemiahyperglycemia
 E. coli derived asparaginase (Elspar); ALLE. coli derived asparaginase (Elspar); ALL
 Pegaspargase (Oncaspar); ALLPegaspargase (Oncaspar); ALL

43. Hypomethylating AgentsHypomethylating Agents
 Mechanism of action: Produces DNAMechanism of action: Produces DNA
hypomethylation restoring normal tumorhypomethylation restoring normal tumor
suppressor gene function and control ofsuppressor gene function and control of
cellular differentiation and proliferationcellular differentiation and proliferation
 Toxicities: Bone marrow suppressionToxicities: Bone marrow suppression
 azacitidine (Vidaza); MDSazacitidine (Vidaza); MDS
 decitabine (Dacogen); MDSdecitabine (Dacogen); MDS

44. Other ChemotherapyOther Chemotherapy
 OtherOther

arsenic trioxide (Trisenox); causes apoptosis-likearsenic trioxide (Trisenox); causes apoptosis-like
changes to NB4 human promyelocytic leukemia cellschanges to NB4 human promyelocytic leukemia cells
in vitro; APLin vitro; APL

trabectedine (Yondelis); binds and alkylates DNA intrabectedine (Yondelis); binds and alkylates DNA in
the minor grove leading to disruption of the cell cyclethe minor grove leading to disruption of the cell cycle
and eventual cell death; Liposarcoma,and eventual cell death; Liposarcoma,
LeiomyosarcomaLeiomyosarcoma

octreotide (Sandostatin); inhibits multiple hormonesoctreotide (Sandostatin); inhibits multiple hormones
including growth hormone, glucagon, insulin and LH;including growth hormone, glucagon, insulin and LH;
Carcinoid tumors, diarrheaCarcinoid tumors, diarrhea

45. Hormonal TherapyHormonal Therapy
 Used in managing hormonally sensitiveUsed in managing hormonally sensitive
cancers (Breast, Prostate, Ovarian, andcancers (Breast, Prostate, Ovarian, and
Endometrial cancer)Endometrial cancer)
 Mechanism of action: The hormoneMechanism of action: The hormone
changes the hormonal environment thatchanges the hormonal environment that
alters growth factors thus the stimulus foralters growth factors thus the stimulus for
tumor growth is suppressed or removedtumor growth is suppressed or removed

46. Side Effects of Hormonal TherapySide Effects of Hormonal Therapy
 WomenWomen

FatigueFatigue

Hot flashesHot flashes

Mood swingsMood swings

NauseaNausea

OsteoporosisOsteoporosis

Weight gainWeight gain
 MenMen

Decreased sexualDecreased sexual
desiredesire

Enlarged breastsEnlarged breasts

Hot flashesHot flashes

ImpotenceImpotence

IncontinenceIncontinence

OsteoporosisOsteoporosis

47. Examples of Hormonal TherapyExamples of Hormonal Therapy
 Androgen receptor antagonistsAndrogen receptor antagonists
 Aromatase InhibitorsAromatase Inhibitors
 Estrogen receptor antagonistEstrogen receptor antagonist
 Selective estrogen receptor modulatorSelective estrogen receptor modulator
(SERM)(SERM)
 LH-RH (GnRh) analogues and antagonistsLH-RH (GnRh) analogues and antagonists
 OtherOther

48. Androgen Receptor AntagonistsAndrogen Receptor Antagonists
 Mechanism of action: Binds and inhibitsMechanism of action: Binds and inhibits
androgen receptorsandrogen receptors
 bicalutamide (Casodex); Prostatebicalutamide (Casodex); Prostate
 flutamide (Eulexin, Apimid); Prostateflutamide (Eulexin, Apimid); Prostate
 enzalutamide (Xtandi); Prostateenzalutamide (Xtandi); Prostate

49. Aromatase InhibitorsAromatase Inhibitors
 Mechanism of action: lowers the amount of estrogenMechanism of action: lowers the amount of estrogen
which signals hormone receptors.which signals hormone receptors.
 Slows tumor growth by inhibiting this process.Slows tumor growth by inhibiting this process.
 Used in post-menopausal women with hormoneUsed in post-menopausal women with hormone
receptor positive breast cancerreceptor positive breast cancer
 Toxicities: Arthralgia, vaginal dryness, acceleratedToxicities: Arthralgia, vaginal dryness, accelerated
bone lossbone loss
 letrozole (Femara); Breastletrozole (Femara); Breast
 exemestane (Aromasin); Breastexemestane (Aromasin); Breast
 anastrozole (Arimidex); Breastanastrozole (Arimidex); Breast

50. Estrogen Receptor AntagonistEstrogen Receptor Antagonist
 Mechanism of action: Binds to estrogenMechanism of action: Binds to estrogen
receptors and down regulates estrogenreceptors and down regulates estrogen
receptor protein producing anti-estrogenicreceptor protein producing anti-estrogenic
effectseffects
 Toxicities: Injection site pain, hot flashes,Toxicities: Injection site pain, hot flashes,
arthralgiaarthralgia
 Fulvestrant (Faslodex); BreastFulvestrant (Faslodex); Breast

51. Selective Estrogen ReceptorSelective Estrogen Receptor
Modulator (SERM)Modulator (SERM)
 Mechanism of action:Mechanism of action: Selectively binds toSelectively binds to
estrogen receptors producing anti-estrogenicestrogen receptors producing anti-estrogenic
effectseffects
 Toxicities:Toxicities: Hot flashes, vaginal drynessHot flashes, vaginal dryness
 Tamoxifen (Nolvadex)-Tamoxifen (Nolvadex)-Need baseline GYNNeed baseline GYN
exam; Breast, premenopausalexam; Breast, premenopausal
 Raloxifene (Evista, Keoxifene);Raloxifene (Evista, Keoxifene); PostPost
menopausal high risk for invasive breast cancermenopausal high risk for invasive breast cancer

52. Luteinizing Hormone-Releasing HormoneLuteinizing Hormone-Releasing Hormone
 AgonistsAgonists

Suppress secretion of follicle-stimulatingSuppress secretion of follicle-stimulating
hormone (FSH) and luteinizing hormone (LH)hormone (FSH) and luteinizing hormone (LH)
from pituitary gland thus decreasingfrom pituitary gland thus decreasing
testosterone levelstestosterone levels
 AntagonistsAntagonists

Works on the gonadotropin releasingWorks on the gonadotropin releasing
hormonehormone

53. Luteinizing Hormone-ReleasingLuteinizing Hormone-Releasing
Hormone AgonistsHormone Agonists
 Leuprolide (Lupron, Eligard)Leuprolide (Lupron, Eligard)

Gonadotropin-releasing hormone (GnRH)Gonadotropin-releasing hormone (GnRH)
agonistagonist

Indicated for prostate cancerIndicated for prostate cancer
 Goserelin (Zoladex)Goserelin (Zoladex)

Indicated for advanced breast and prostateIndicated for advanced breast and prostate
cancerscancers
 Triptorelin (Trelstar)Triptorelin (Trelstar)

Indicated for ovarian and prostate cancersIndicated for ovarian and prostate cancers

54. Other Hormonal AgentsOther Hormonal Agents
 Abiraterone (Zytiga)-Abiraterone (Zytiga)-inhibits 17 alpha-inhibits 17 alpha-
hydroxylase/C17,20-lyase to block androgenhydroxylase/C17,20-lyase to block androgen
biosynthesis leading to decreased androgen-biosynthesis leading to decreased androgen-
sensitive tumor growth; Prostatesensitive tumor growth; Prostate
 Megestrol acetate (Megace)-Megestrol acetate (Megace)-agonizesagonizes
glucocorticoid receptors; Cancer relatedglucocorticoid receptors; Cancer related
anorexia;anorexia;
 Ketoconazole-Ketoconazole-inhibits fungal cell membraneinhibits fungal cell membrane
ergosterol synthesis; Prostateergosterol synthesis; Prostate

56. ImmunotherapyImmunotherapy
 Also called Biological Response ModifierAlso called Biological Response Modifier
TherapyTherapy
 Stimulate or restore immune system toStimulate or restore immune system to
fight cancer cellsfight cancer cells
 Modify the relation between the tumor andModify the relation between the tumor and
the hostthe host
 Includes antibodies, cytokines, and otherIncludes antibodies, cytokines, and other
substances that stimulate immunesubstances that stimulate immune
functionfunction

57. ImmunotherapyImmunotherapy
 TypesTypes

Interferon, interleukins, anti-CTLA4, anti-PD-1, anti-Interferon, interleukins, anti-CTLA4, anti-PD-1, anti-
PDL-1, cancer vaccinesPDL-1, cancer vaccines
 Ipilimumab (Yervoy)-binds to CTLA-4 antigen to blockIpilimumab (Yervoy)-binds to CTLA-4 antigen to block
activity and augment T-cell activation and proliferation;activity and augment T-cell activation and proliferation;
MelanomaMelanoma
 Nivolumab (Opdivo)-binds to PD-1 receptor on T-cellsNivolumab (Opdivo)-binds to PD-1 receptor on T-cells
blocking PD-1 pathway mediated anti-tumor immuneblocking PD-1 pathway mediated anti-tumor immune
response inhibition; NSCLC, Metastatic Melanoma,response inhibition; NSCLC, Metastatic Melanoma,
RCC, Squamous cell H/N, Classic HL, Urothelial.RCC, Squamous cell H/N, Classic HL, Urothelial.

58. ImmunotherapyImmunotherapy
 Pembrolizumab (Keytruda)-binds to PD-1 receptorPembrolizumab (Keytruda)-binds to PD-1 receptor
on T-cells blocking PD-1 pathway mediated anti-on T-cells blocking PD-1 pathway mediated anti-
tumor immune response inhibition; Melanoma,tumor immune response inhibition; Melanoma,
NSCLC, HNSCC, Classical HL, Urothelial/BladderNSCLC, HNSCC, Classical HL, Urothelial/Bladder
 Durvalumab (Imfinzi)-blocks PD-L1 with the PD-1Durvalumab (Imfinzi)-blocks PD-L1 with the PD-1
and CD80 molecules; recombinant DNA technologyand CD80 molecules; recombinant DNA technology
in Chinese Hamster Ovary cell suspension culture;in Chinese Hamster Ovary cell suspension culture;
UrothelialUrothelial
 Atezolizumab (Tecentriq)-binds to PD-L1 and blocksAtezolizumab (Tecentriq)-binds to PD-L1 and blocks
interactions with both PD-1 and B7.1 receptors;interactions with both PD-1 and B7.1 receptors;
Urothelial.Urothelial.

59. ImmunotherapyImmunotherapy
 Elotuzumab (Empliciti)-humanizedElotuzumab (Empliciti)-humanized
monoclonal antibody targeting SLAMF7monoclonal antibody targeting SLAMF7
(Signaling Lymphocytic Activation Molecule(Signaling Lymphocytic Activation Molecule
Family member 7) protein; activates NKCFamily member 7) protein; activates NKC
through both the SLAMF7 pathway and Fcthrough both the SLAMF7 pathway and Fc
receptors; Multiple Myelomareceptors; Multiple Myeloma
 Sipuleucel-T (Provenge)-Induces T-cellSipuleucel-T (Provenge)-Induces T-cell
mediated immune response targeted againstmediated immune response targeted against
prostatic acid phosphate antigen; Prostateprostatic acid phosphate antigen; Prostate

60. ImmunotherapyImmunotherapy
 Taliminogene laherparepvec (Imlygic)-Taliminogene laherparepvec (Imlygic)-
Replicates within tumor and produces GM-Replicates within tumor and produces GM-
CSF inducing tumor cell death andCSF inducing tumor cell death and
enhancing antitumor immune response;enhancing antitumor immune response;
genetically engineered oncolytic virus;genetically engineered oncolytic virus;
Given in divided doses to the tumorGiven in divided doses to the tumor
lesions in Melanomalesions in Melanoma

61. InterferonInterferon
 Mechanism of action:Mechanism of action: Antiviral (inhibits viralAntiviral (inhibits viral
replication), antiproliferative, andreplication), antiproliferative, and
immunomodulatory effects, activate andimmunomodulatory effects, activate and
increases cytotoxicity of natural killer cells,increases cytotoxicity of natural killer cells,
enhances immune responseenhances immune response
 CytokinesCytokines
 Alpha, beta, and gamma derivativesAlpha, beta, and gamma derivatives
 interferon alfa 2b (Intron A);interferon alfa 2b (Intron A); Hairy cellHairy cell
leukemia, Melanoma, NHL, Hepatitisleukemia, Melanoma, NHL, Hepatitis

62. InterleukinsInterleukins
 Mechanism of action: Stimulates T-Mechanism of action: Stimulates T-
lymphocyte proliferation, enhances killerlymphocyte proliferation, enhances killer
T-cell activity, stimulates and enhancesT-cell activity, stimulates and enhances
natural killer cellsnatural killer cells
 CytokinesCytokines
 Produced by helper T-cellsProduced by helper T-cells
 aldesleukin (Proleukin); Renal cell,aldesleukin (Proleukin); Renal cell,
MelanomaMelanoma

63. Colony Stimulating FactorsColony Stimulating Factors
 Red CellRed Cell

Darbepoietin alpha (Aranesp)Darbepoietin alpha (Aranesp)

Epoetin alpha (Epogen, Procrit,Epoetin alpha (Epogen, Procrit,
Erythropoietin)Erythropoietin)
 White CellWhite Cell

Filgrastim (Neupogen, G-CSF)Filgrastim (Neupogen, G-CSF)

Tbo-filgrastin (Granix)Tbo-filgrastin (Granix)

Pegfilgrastim (Neulasta)Pegfilgrastim (Neulasta)

Sargramostim (Leukine, GM-CSF)Sargramostim (Leukine, GM-CSF)

65. Therapeutic AntibodiesTherapeutic Antibodies
 Engineered antibodies produced by aEngineered antibodies produced by a
single clone of cells that is specific for asingle clone of cells that is specific for a
given antigengiven antigen
 Passive immunotherapyPassive immunotherapy
 Names end in “mab”Names end in “mab”

66. Therapeutic AntibodiesTherapeutic Antibodies
 Murine-mouseMurine-mouse
 Humanized-humanHumanized-human
 Human Anti-Murine Antibody (HAMA)Human Anti-Murine Antibody (HAMA)
 Chimeric-part mouse/humanChimeric-part mouse/human
 Conjugated-a chemotherapy drug, radioactiveConjugated-a chemotherapy drug, radioactive
particle, or toxin is connected to monoclonalparticle, or toxin is connected to monoclonal
antibodyantibody
 Unconjugated-monoclonal antibody without anyUnconjugated-monoclonal antibody without any
drug, radioactive particle, or toxin attacheddrug, radioactive particle, or toxin attached

67. Therapeutic AntibodiesTherapeutic Antibodies
Common TargetsCommon Targets
 CD20CD20
 CD52CD52
 EFGREFGR
 HER2HER2
 PD 1PD 1
 PIGFPIGF
 VEGFAVEGFA

68. Therapeutics AntibodiesTherapeutics Antibodies
 CD20CD20

Rituximab (Rituxan); NHL, CD20-positiveRituximab (Rituxan); NHL, CD20-positive
CLL, RACLL, RA

Ibritumomab tiuxetan(Zevalin); NHLIbritumomab tiuxetan(Zevalin); NHL

Ofatumumab (Arzerra); CLLOfatumumab (Arzerra); CLL

69. Therapeutic AntibodiesTherapeutic Antibodies
 EGFR (EGFR (epidermal growth factor receptor)

Panitumumab (Vectibix); ColorectalPanitumumab (Vectibix); Colorectal

Cetuximab (Erbitux); Colorectal, SquamousCetuximab (Erbitux); Colorectal, Squamous
H/NH/N
 HER2HER2

Pertuzumab (Perjeta): HER2 positive BreastPertuzumab (Perjeta): HER2 positive Breast

Trastuzumab (Herceptin); HER2 positiveTrastuzumab (Herceptin); HER2 positive
Breast, HER2 positive GastricBreast, HER2 positive Gastric

70. Therapeutic AntibodiesTherapeutic Antibodies
 PIGF (PIGF (Phosphatidylinositol-glycan biosynthesis class F
protein)

Ziv-afibercept (Zaltrap); ColorectalZiv-afibercept (Zaltrap); Colorectal
 RNAKL (RNAKL (Receptor Activator of Nuclear Factor Kappa-B
Ligand)

Denosumab (Xgeva); Solid tumor bone metastasis,Denosumab (Xgeva); Solid tumor bone metastasis,
hypercalcemia, Giant cell tumor of bonehypercalcemia, Giant cell tumor of bone
 VEGF (VEGF (Vascular endothelial growth factor)

Bevacizumab (Avastin); Colorectal, NSC Lung nonBevacizumab (Avastin); Colorectal, NSC Lung non
squamous, GBM, Renal cell, Cervical, Breastsquamous, GBM, Renal cell, Cervical, Breast

Ramucirumab (Cyramza); Gastric, NSC lung, colorectalRamucirumab (Cyramza); Gastric, NSC lung, colorectal

71. Antibody-Drug ConjugatesAntibody-Drug Conjugates
 CD30CD30

Brentuximab vedotin (Adcetris); HL, SystemicBrentuximab vedotin (Adcetris); HL, Systemic
anaplatic large cell lymphomaanaplatic large cell lymphoma
 HER2HER2

Ado trastuzumab emtansine (Kadcyla); HER2Ado trastuzumab emtansine (Kadcyla); HER2
positive breastpositive breast

72. Kinase InhibitorsKinase Inhibitors
 Mechanism of action: Enzyme inhibitorMechanism of action: Enzyme inhibitor
that blocks the action of one or morethat blocks the action of one or more
protein kinase which alters biologicalprotein kinase which alters biological
processes including but no limited toprocesses including but no limited to
modulate cell function; Most names end inmodulate cell function; Most names end in
“nib”“nib”
 Toxicities: Vary based on targetToxicities: Vary based on target

74. Kinase InhibitorsKinase Inhibitors
 BCR-ABL (BCR-ABL (Abelson murine leukemia viral oncogene)

nilotinib (Tasigna); Ph-positive CMLnilotinib (Tasigna); Ph-positive CML

dasatinib (Sprycel); Ph-positive CMLdasatinib (Sprycel); Ph-positive CML

bosutinib (Bosuilf); Ph-positive CMLbosutinib (Bosuilf); Ph-positive CML
 ALK (anaplastic lymphoma kinase)ALK (anaplastic lymphoma kinase)

crizotinib (Xalkori); 1crizotinib (Xalkori); 1stst
generation ALK/ROS1 positivegeneration ALK/ROS1 positive
NSCLCNSCLC

Ceritinib (Zykadia);2Ceritinib (Zykadia);2ndnd
generation ALK positive NSCLCgeneration ALK positive NSCLC

alectinib (Alecensa); 3alectinib (Alecensa); 3rdrd
generation ALK positive NSCLCgeneration ALK positive NSCLC

brigatinib (Alunbrig); ALK positive NSC Lungbrigatinib (Alunbrig); ALK positive NSC Lung

75. Kinase InhibitorsKinase Inhibitors
 BRAFBRAF

dabrafenib (Tafinlar); Melanomadabrafenib (Tafinlar); Melanoma

vemurafenib (Zelboraf); Melanomavemurafenib (Zelboraf); Melanoma

cobimetinib (Cotellic); in combination withcobimetinib (Cotellic); in combination with
vemurafenib; Melanomavemurafenib; Melanoma
 BTK (Bruton’s Tyrosine Kinase)BTK (Bruton’s Tyrosine Kinase)

ibrutinib (Imbruvica); CLL, Mantle cell lymphomaibrutinib (Imbruvica); CLL, Mantle cell lymphoma
 CDK 4,6CDK 4,6

palbociclib (Ibrance); ER/PR positive HER2palbociclib (Ibrance); ER/PR positive HER2
negative Breastnegative Breast

76. Kinase InhibitorsKinase Inhibitors
 EGFREGFR (epidermal growth factor receptor)

osimertinib (Tagrisso) wild type sparing; NSC Lungosimertinib (Tagrisso) wild type sparing; NSC Lung
with EGFR T790M mutationswith EGFR T790M mutations

afatinib (Gilotrif); NSC Lung with EGFR exonafatinib (Gilotrif); NSC Lung with EGFR exon
19 deletions or exon 2119 deletions or exon 21

erlotinib (Tarceva); NSC Lung with EGFRerlotinib (Tarceva); NSC Lung with EGFR
exon 19 deletions or exon 21, Pancreatic withexon 19 deletions or exon 21, Pancreatic with
gemcitabinegemcitabine

gefitinib (Iressa); NSC Lung with EGFR exongefitinib (Iressa); NSC Lung with EGFR exon
19 deletions or exon 2119 deletions or exon 21 mutationsmutations

77. Kinase InhibitorsKinase Inhibitors
 FLT3 (FMS related Tyrosine Kinase 3)FLT3 (FMS related Tyrosine Kinase 3)

sorafenib (Nexavar); Hepatocellular, Renalsorafenib (Nexavar); Hepatocellular, Renal
Cell, ThyroidCell, Thyroid

sunitinib (Sutent); Renal Cell, GIST,sunitinib (Sutent); Renal Cell, GIST,
Pancreatic neuroendocrinePancreatic neuroendocrine

78. Kinase InhibitorsKinase Inhibitors
 HER2 (ERBB2/neu)HER2 (ERBB2/neu)

afatinib (Gilotrif, Tomtovok); NCS Lung withafatinib (Gilotrif, Tomtovok); NCS Lung with
EGFR exon 19 deletions or exon 21 mutationsEGFR exon 19 deletions or exon 21 mutations

lapatinib (Tykerb); HER2 overexpressinglapatinib (Tykerb); HER2 overexpressing
BreastBreast
 JAK 1/2JAK 1/2

ruxolitinib (Jakafi); Myelofibrosis, Polycythemaruxolitinib (Jakafi); Myelofibrosis, Polycythema
veravera

79. Kinase InhibitorsKinase Inhibitors
 KITKIT

axitinib (Inlyta); Renal cellaxitinib (Inlyta); Renal cell

regorafenib (Stivarga); Colorectal, GISTregorafenib (Stivarga); Colorectal, GIST

dasatinib (Sprycel); Ph-positive CML, Ph-dasatinib (Sprycel); Ph-positive CML, Ph-
positive ALLpositive ALL

pasopanib (Votrient); Renal cell, Soft tissuepasopanib (Votrient); Renal cell, Soft tissue
sarcomasarcoma

imatinib (Gleevac); Ph-positive CMLimatinib (Gleevac); Ph-positive CML

sunitinib (Sutent); Renal cell, GISTsunitinib (Sutent); Renal cell, GIST

80. Kinase InhibitorsKinase Inhibitors
 MEK (Mitogen-activated protein kinase)MEK (Mitogen-activated protein kinase)

trametinib (Mekinist); Melanomatrametinib (Mekinist); Melanoma
 mTOR (Mechanistic Target of Rapamycin)mTOR (Mechanistic Target of Rapamycin)

sirolimus (Rapamune); Kidney transplantsirolimus (Rapamune); Kidney transplant
rejection prophylaxisrejection prophylaxis

temsirolimus (Torisel); Renal celltemsirolimus (Torisel); Renal cell

everolimus (Afinitor); ER/PR positive HER2everolimus (Afinitor); ER/PR positive HER2
negative Breast, Pancreatic neuroendocrine,negative Breast, Pancreatic neuroendocrine,
Renal cellRenal cell

81. Kinase InhibitorsKinase Inhibitors
 Idelalisib (Zydelig); inhibits P13K,Idelalisib (Zydelig); inhibits P13K,
disrupting B-cell receptor and cytokinedisrupting B-cell receptor and cytokine
signaling pathways, thus inhibitingsignaling pathways, thus inhibiting
malignant B-cell proliferation; CLLmalignant B-cell proliferation; CLL

83. Other Cancer TherapyOther Cancer Therapy
 PARP (poly (ADP-ribose) polymerase)PARP (poly (ADP-ribose) polymerase)

olaparib (Lynparza); BRCA-mutated Ovarianolaparib (Lynparza); BRCA-mutated Ovarian
 ProteasomeProteasome

bortezomib (Velcade); Multiple Myeloma, Mantle Cellbortezomib (Velcade); Multiple Myeloma, Mantle Cell
LymphomaLymphoma

carfilzomib (Kyprolis); Multiple Myelomacarfilzomib (Kyprolis); Multiple Myeloma

Ixazomib (Ninlaro); Multiple MyelomaIxazomib (Ninlaro); Multiple Myeloma
 Omacetaxine mepesuccinate (Synribo)-inhibits proteinOmacetaxine mepesuccinate (Synribo)-inhibits protein
synthesis; CMLsynthesis; CML
 Venetoclax (Venclexta);BCL2 inhibitor, restoresVenetoclax (Venclexta);BCL2 inhibitor, restores
apoptosisapoptosis

84. Other Cancer TherapyOther Cancer Therapy
 OtherOther

pomalidomide (Pomalyst); Multiple Myelomapomalidomide (Pomalyst); Multiple Myeloma

lenalidomide (Revlimid); Multiple Myeloma,lenalidomide (Revlimid); Multiple Myeloma,
MDS, Mantle Cell LymphomaMDS, Mantle Cell Lymphoma

thalidomide (Thalomid); Multiple Myelomathalidomide (Thalomid); Multiple Myeloma

85. Supportive Care MedicationsSupportive Care Medications
 IV hydrationIV hydration
 Electrolyte replacementElectrolyte replacement
 Antiemetic'sAntiemetic's
 AntidiarrhealAntidiarrheal
 Stool softeners/laxativesStool softeners/laxatives
 Nutritional supportNutritional support
 Appetite stimulantsAppetite stimulants
 Antidepressants/AntianxietyAntidepressants/Antianxiety

87. Advanced Practice ConsiderationsAdvanced Practice Considerations
 Maintain awareness of cancer agents and treatmentMaintain awareness of cancer agents and treatment
optionsoptions
 Utilize Package Insert for drug details including dosingUtilize Package Insert for drug details including dosing
and toxicity managementand toxicity management
 Encourage supportive care to minimize toxicityEncourage supportive care to minimize toxicity
 Collaborate with respective disciplinesCollaborate with respective disciplines
 Support patients physically (symptom management),Support patients physically (symptom management),
psychosocially (referrals to social work/casepsychosocially (referrals to social work/case
management), emotionally (referrals tomanagement), emotionally (referrals to
psychology/support groups) and spiritually (refer topsychology/support groups) and spiritually (refer to
chaplain/spiritual counselor)chaplain/spiritual counselor)
 Spend time with other team membersSpend time with other team members

89. Patient Focused CarePatient Focused Care
 You treat a disease, you win, you lose. You treat a person, I guarantee You treat a disease, you win, you lose. You treat a person, I guarantee
you, you’ll win, no matter what the outcome.you, you’ll win, no matter what the outcome.
 Our job is improving the quality of life, not just delaying death.
•-Patch Adams-Patch Adams

90. ResourcesResources
 chemocare.comchemocare.com
 uptodate.comuptodate.com
 American Cancer SocietyAmerican Cancer Society

1-800-813-HOPE (4673)1-800-813-HOPE (4673)

http://www/cancer.org/http://www/cancer.org/
 National Cancer InstituteNational Cancer Institute

1-800-4-CANCER (422-6237)1-800-4-CANCER (422-6237)

http://www.cancer.gov/http://www.cancer.gov/
 National Comprehensive Cancer NetworkNational Comprehensive Cancer Network

http://www.nccn.org/http://www.nccn.org/
 Vanderbilt My Cancer GenomeVanderbilt My Cancer Genome

www.mycancergenome.orgwww.mycancergenome.org

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