Basic Pharmacology

Basic Pharmacology
Lindsay Williamson
ARNP, MSN, AOCNP

Bibliography
 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 Affiliates in
Trinity, Florida as an Oncology Nurse Practitioner. Lindsay is a member of the
Advanced Practice Society for Hematology and Oncology and the Oncology Nursing
Society.

Objectives
 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

Cancer Therapy Goals
 Cure
 No evidence of disease (NED)
 Control
 Prolong length and quality of life, prevent distant and
possible unknown metastases
 Cure is not realistic
 Palliation
 Symptom management, improve comfort and quality
of life
 Appropriate when cure and control are not feasible

Cancer Therapy Overview
 Treatment types
 Manage disease and related symptoms
 Manage treatment toxicities
 Localized
• Surgery
• Radiation therapy
 Systemic
• PO, IV, IM, SQ, IT
 Neoadjvuant, Adjuvant, Induction, Maintenance, Metastatic
 Radiosensitizer

Cancer Therapy Agents
 Chemotherapy
 Hormonal Therapy
 Immunotherapy
 Therapeutic Antibodies
 Antibody-Drug Conjugates
 Kinase Inhibitors
 Other

Common Cancer Therapy
Side Effects
 Fatigue
 Myelosuppression
 Nausea/Vomiting
 Diarrhea/Constipation
 Mucositis
 Peripheral Neuropathy
 Alopecia
 Oncology Emergencies
 Tumor Lysis Syndrome, Hypercalcemia, SIADH

Tumor Response Factors
 Tumor burden
 Single agent versus combination therapy
 Receptor status
 Administration schedule
 Drug resistance

Cancer Therapy Limitations
 Toxicity of agents
 Lifetime dose
 Hypersensitivity reactions
 Drug resistance
 Secondary malignancies

Normal Cell Growth Principles
 Cell proliferation signals
 Normal cells stop dividing when a certain level
has been attained
 Cell division
 Body sends message to divide cell
 Contact Inhibition
 Cells stop dividing when they come in direct
contact with other cells

Development of Cancer Cells
 Carcinogenesis
 Process by which a normal cell converts to a tumor cell
 Initiation phase
 A biological, chemical, or physical change occurs to the cell
 Promotion phase
 Alteration of expression of cell (i.e. DNA)
 Conversion
 Act of change and continued alteration
 Progression
 Changes from pre-malignant to higher level of malignancy

Malignant Cell
 Uncontrolled proliferation
 Abnormal cell structure
 Accelerated use of nutrients
 Loss of contact inhibition
 Lack of adhesion
 Inability to differentiate fully

Benign versus Malignant
 Benign
 Regular and
consistent shape
 Small nucleus
 Well differentiated
 Orderly, controlled,
slow growth
 Rare
 No tissue destruction
 Usually encapsulated
 Malignant
 Irregular
 Nucleus larger than
normal and may have
multiple nuclei
 Undifferentiated
 Random, uncontrolled
growth
 Frequent mitosis
 Tissue destruction

Cell Cycle
 Definition
 Series of changes occurring from the time a cell is first formed until it
divides into two daughter cells
 G0
 Resting phase, non-dividing, most chemotherapy agents do not affect
cell during this phase
 G1
 RNA and protein synthesis (prepares for DNA), 8-48hours
 S phase
 DNA synthesis, cellular DNA doubles, preparing for mitosis, 10-20 hours
 G2
 DNA synthesis stops and prepares for cell division
 M phase
 Mitosis, separation of chromosomes and cell division, 1 hour

Chemotherapy
 Treatment of cancer cells with chemicals
 Cytotoxic-poisonous to cells
 Many new oral agents in last decade
 Types
 Combination therapy
• More than one drug
• More than one treatment modality either sequentially or
concurrently
 Adjuvant therapy
• Primary tumor eradiated by surgery or radiation prior to
chemotherapy
 Neo-adjuvant therapy
• Chemotherapy prior to radiation or surgery

Cell Kill Theory
 Explains the need for repeated doses
chemotherapy
 With each dose of chemotherapy, a specific
percent of cells are killed
 Belief that the same percent of cells are killed
each time chemotherapy is given
 Tumor cell kill increases as doses of
chemotherapy increase
 Theory limitation
 Cancer cells can mutate and develop resistance to
chemotherapy

Chemotherapy Classifications
 Phase cycle specific agents-only the cells
in a specific cycle are affected
 Cell cycle specific agents-effects are
mostly on the cells actively dividing
throughout cycle
 Cell cycle nonspecific agents-effects are
on cells at any phase

Chemotherapy Classifications
 Alkylating Agents
 Antimetabolites
 Antimicrotuble Agents
 Topoisomerase I Inhibitors
 Topoisomerase II Inhibitors
 Antitumor Antibiotics
 Aspariginase derivatives
 Hypomethylating Agents
 Other

Alkylating Agents
 Mechanisms of action: Interfere with DNA
replication through cross linking of DNA
strands, DNA strand breaking, and
abnormal base pairing of proteins
 Most agents are cell cycle nonspecific
 Activated by cytochrome p450
 Toxicities: Nausea/Vomiting,
Hematopoietic, Reproductive

Alkylating Agents
 Alkyl sulfonates
 Busulfan (Myleran); CML, Myelofibrosis
 Ethyleneimines
 Thiotepa (Thioplex); Breast, Ovarian
 Nitrogen mustards
 Bendamustine (Treanda, Ribomustin); CLL, NHL
 Chloambucil (Leukeran); HL, NHL, CLL
 Cyclophosphamide (Cytoxan);
• HL, NHL, MM, CML, AML, Breast
 Ifosfamide (Ifex); Testicular, Sarcoma
 Melphalan (Alkeran); MM

Alkylating Agents
 Nitrosoureas
 Most agents cross blood-brain barrier
 Carmustin (BICNU); Brain, MM, HL, NHL
 Lomustine (Gleostine)-oral agent: Brain, HL,
NHL
 Streptozotocin (Zanosar); Pancreatic

Alkylating Agents
 Platinum Analogues
 Cisplatin (Platinol)-heavy metal; Testicular,
Ovarian, Bladder, Lung
 Carboplatin (Paraplatin)-2nd generation
platinum analogue; Solid tumors
 Oxaliplatin (Eloxatin)-3rd generation platinum
analogue; Colorectal
 Triazenes
 Dacarbazine (DTIC); HL, Melanoma
 Temozolomide (Temodar); Brain

Alkylating Agents
 Other
 Procarbazine (Matulane); HL

Antimetabolites
 Mechanism of action: Inhibit DNA
synthesis by substituting metabolites or
structural analogues during DNA synthesis
 Most agents are phase cycle specific
 Toxicities: Hematopoietic and GI

Antimetabolites
 Folate Antagonists
 Methotrexate (Abitexate); Breast,
Osteosarcoma, H/N
 Pemetrexed (Alimta); Lung, Mesothelioma
 Pralatrexate (Folotyn); Peripheral T-cell
lymphoma

Antimetabolites
 Purine Antagonists
 cladribine (Leustatin); Hairy Cell Leukemia
 fludarabine phosphate (Fludara); CLL
 Pyrimidine Antagonists
 5 fluorouracil (5-FU); GI malignancies
 capecitabine (Xeloda)-oral agent; GI, Breast
 cytarabine (Cytosar); AML
 fluorouracil (Adrucil); GI, Pancreatic, Breast
 gemcitabine (Gemzar); Pancreatic, breast,
ovarian, Lung

Antimetabolites
 Other
 Hydroxyurea (Hydrea)-oral agent; P vera,
thrombocythemia, H/N

Antimicrotubule Agents
 Mechanism of action: Block cell division by
preventing microtubule function
 Plant derived
 Toxicities: Peripheral Neuropathy

Antimicrotuble Agents
 Epothilones
 Ixabepilone (Ixempra); Breast
 Halichonrin B analogue
 Eribulin mesylate (Halaven); Breast, Liposarcoma
 Taxanes
 Paclitaxel (Taxol); Breast, Ovarian, Lung, Sarcoma
 Albumin-bound paclitaxel, nab-paclitaxel (Abraxane);
Breast, Pancreatic, Lung
 Cabazitaxel (Jevtana); Prostate

Antimicrotubules
 Vinca Alkaloids
 Vinblastine (Velban, Velsar); HL, Testicular
 Vincristine (Vincasar PFS); HL, NHL, ALL,
Solid tumors
 Liposomal vincristine (Marqibo); ALL
 Vinorelbine (Navelbine); Lung, Breast

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

Topoisomerase I Inhibitors
 Camptothecin derivatives
 Irinotecan (Camptosar); Colorectal
 Topotecan (Hycamptin); Ovarian, Lung,
Cervical

Topoisomerase II Inhibitors
 Mechanism of action: Interferes with the
activity of topoisomerase in the process of
DNA replication
 Toxicities: Nausea, vomiting, diarrhea,
bone marrow suppression
 Anthracenedione
 Mitoxantrone (Novantrone); AML, Prostate

 Anthracyclines
 Daunorubicin (Cerubidine); ALL, AML
 Doxorubicin (Adriamycin)-baseline EF;
Breast, Sarcoma
 Liposomal doxorubicin (Doxil); Ovarian,
Kaposi sarcoma
 Epirubicin (Ellence); Breast
 Idarubicin (Idamycin); AML

 Epipodrophyllotoxins
 Etoposide (Toposar); Lung, Testicular

Antitumor Antibiotics
 Mechanism of action: DNA intercalation (insert
between two strands of DNA), generate highly
reactive free radicals that damage intercellular
molecules
 Toxicities: Bone marrow suppression
 Antitumor antibiotics
 Bleomycin (Blenoxane)- Pulmonary toxicities;
Lung, Testicular, NHL
 Mitomycin (Mutamycin)-Delayed bone marrow
suppression; Anal, Pancreatic, Stomach

Aspariginase Derivatives
 Mechanism of action: Catalyzes asparagine
deamidation resulting in decreased circulating
asparagine and cytotoxicity of asparagine-
dependent leukemic cells
 Toxicities: Hypersensitivity reaction,
hyperglycemia
 E. coli derived asparaginase (Elspar); ALL
 Pegaspargase (Oncaspar); ALL

Hypomethylating Agents
 Mechanism of action: Produces DNA
hypomethylation restoring normal tumor
suppressor gene function and control of
cellular differentiation and proliferation
 Toxicities: Bone marrow suppression
 Azacitidine (Vidaza); MDS
 Decitabine (Dacogen); MDS

Other Chemotherapy
 Other
 Arsenic trioxide (Trisenox); causes apoptosis-
like changes to NB4 human promyelocytic
leukemia cells in vitro; APL
 Trabectedine (Yondelis); binds and alkylates
DNA in the minor grove leading to disruption
of the cell cycle and eventual cell death;
Liposarcoma, Leiomyosarcoma
 Octreotide (Sandostatin); inhibits multiple
hormones including growth hormone,
glucagon, insulin and LH; Carcinoid tumors,

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

Side Effects of Hormonal Therapy
 Women
 Fatigue
 Hot flashes
 Mood swings
 Nausea
 Osteoporosis
 Weight gain
 Men
 Decreased sexual
desire
 Enlarged breasts
 Hot flashes
 Impotence
 Incontinence
 Osteoporosis

Examples of Hormonal Therapy
 Androgen receptor antagonists
 Aromatase Inhibitors
 Estrogen receptor antagonist
 Selective estrogen receptor modulator
(SERM)
 LH-RH (GnRh) analogues and antagonists
 Other

Androgen Receptor Antagonists
 Mechanism of action: Binds and inhibits
androgen receptors
 Bicalutamide (Casodex); Prostate
 Flutamide (Eulexin, Apimid); Prostate
 Enzalutamide (Xtandi); Prostate

Aromatase Inhibitors
 Mechanism of action: lowers the amount of
estrogen which signals hormone receptors.
Slows tumor growth by inhibiting this process.
Used in post-menopausal women with hormone
receptor positive breast cancer
 Toxicities: Arthralgia, vaginal dryness,
accelerated bone loss
 Letrozole (Femara); Breast
 Exemestane (Aromasin); Breast
 Anastrozole (Arimidex); Breast

Estrogen Receptor Antagonist
 Mechanism of action: Binds to estrogen
receptors and down regulates estrogen
receptor protein producing anti-estrogenic
effects
 Toxicities: Injection site pain, hot flashes,
arthralgia
 Fulvestrant (Faslodex); Breast

Selective Estrogen Receptor
Modulator (SERM)
 Mechanism of action: Selectively binds to
estrogen receptors producing anti-estrogenic
effects
 Toxicities: Hot flashes, vaginal dryness
 Tamoxifen (Nolvadex)-Need baseline GYN
exam; Breast, premenopausal
 Raloxifene (Evista, Keoxifene); Post
menopausal high risk for invasive breast cancer

Luteinizing Hormone-Releasing Hormone
 Agonists
 Suppress secretion of follicle-stimulating
hormone (FSH) and luteinizing hormone (LH)
from pituitary gland thus decreasing
testosterone levels
 Antagonists
 Works on the gonadotropin releasing
hormone

Luteinizing Hormone-Releasing
Hormone Agonists
 Leuprolide (Lupron)
 Gonadotropin-releasing hormone (GnRH)
agonist
 Indicated for prostate cancer
 Goserelin (Zoladex)
 Indicated for advanced breast and prostate
cancers
 Triptorelin (Trelstar)
 Indicated for ovarian and prostate cancers

Other Hormonal Agents
 abiraterone (Zytiga)-inhibits 17 alpha-
hydroxylase/C17,20-lyase to block androgen
biosynthesis leading to decreased androgen-
sensitive tumor growth; Prostate
 megestrol acetate (Megace)-agonizes
glucocorticoid receptors; Cancer related
anorexia;
 ketoconazole-inhibits fungal cell membrane
ergosterol synthesis; Prostate

Immunotherapy
 Also called Biological Response Modifier
Therapy
 Stimulate or restore immune system to
fight cancer cells
 Modify the relation between the tumor and
the host
 Includes antibodies, cytokines, and other
substances that stimulate immune function

Immunotherapy
 Types
 Interferon, interleukins, CTLA4, PD-1, cancer
vaccines
 Ipilimumab (Yervoy)-binds to CTLA-4 antigen
to block activity and augment T-cell activation
and proliferation; Melanoma
 Nivolumab (Opdivo)-binds to PD-1 receptor
on T-cells blocking PD-1 pathway mediated anti-
tumor immune response inhibition

Immunotherapy
 Pembrolizumab (Keytruda)-binds to PD-1
receptor on T-cells blocking PD-1 pathway
mediated anti-tumor immune response
inhibition; Melanoma, Lung
 Sipuleucel-T (Provenge)-Induces T-cell
mediated immune response targeted against
prostatic acid phosphate antigen; Prostate

Immunotherapy
 Taliminogene laherparepvec (Imlygic)-
Replicates within tumor and produces GM-
CSF inducing tumor cell death and
enhancing antitumor immune response;
genetically engineered oncolytic virus;
Melanoma

Interferon
 Mechanism of action: Antiviral (inhibits viral
replication), antiproliferative, and
immunomodulatory effects, activate and
increases cytotoxicity of natural killer cells,
enhances immune response
 Cytokines
 Alpha, beta, and gamma derivatives
 Interferon alfa 2b (Intron A); Hairy cell
leukemia, Melanoma, NHL, Hepatitis

Interleukins
 Mechanism of action: Stimulates T-
lymphocyte proliferation, enhances killer
T-cell activity, stimulates and enhances
natural killer cells
 Cytokines
 Produced by helper T-cells
 Aldesleukin (Proleukin); Renal cell,
Melanoma

Colony Stimulating Factors
 Red Cell
 Darbepoietin alpha (Aranesp)
 Epoetin alpha (Epogen, Procrit,
Erythropoietin)
 White Cell
 Filgrastim (Neupogen, G-CSF)
 Pegfilgrastim (Neulasta)
 Sargramostim (Leukine, GM-CSF)

Therapeutic Antibodies
 Engineered antibodies produced by a
single clone of cells that is specific for a
given antigen
 Passive immunotherapy
 Names end in “mab”

 Murine-mouse
 Humanized-human
 Human Anti-Murine Antibody (HAMA)
 Chimeric-part mouse/human
 Conjugated-a chemotherapy drug, radioactive
particle, or toxin is connected to monoclonal
antibody
 Unconjugated-monoclonal antibody without any
drug, radioactive particle, or toxin attached

Common Targets
 CD20
 CD52
 EFGR
 HER2
 PD 1
 PIGF
 VEGFA

Therapeutics Antibodies
 CD20
 Rituximab (Rituxan); NHL, RA
 Ibritumomab (Zevalin); NHL
 Ofatumumab (Arzerra); CLL

 EGFR
 Panitumumab (Vectibix); Colorectal
 Cetuximab (Erbitux); Colorectal, Squamous
H/N
 HER2
 Pertuzumab (Perjeta): HER2 positive Breast
 Trastuzumab (Herceptin); HER2 positive
Breast, HER2 positive Gastric

 PIGF
 Ziv-afibercept (Zaltrap); Colorectal
 RNAKL
 Denosumab (Xgeva); Solid tumor bone metastasis,
hypercalcemia, Giant cell tumor of bone
 VEGF
 Bevacizumab (Avastin); Colorectal, NSC Lung non
squamous, GBM, Renal cell, Cervical, Breast
 Ramucirumab (Cyramza); Gastric, NSC lung,
colorectal

Antibody-Drug Conjugates
 CD30
 Brentuximab vedotin (Adcetris); HL, Systemic
anaplatic large cell lymphoma
 HER2
 Ado trastuzumab emtansine (Kadcyla); HER2
positive breast

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

Kinase Inhibitors
 ABL
 Nilotinib (Tasigna); Ph-positive CML
 Dasatinib (Sprycel); Ph-positive CML
 Bosutinib (Bosuilf); Ph-positive CML
 ALK (anaplastic lymphoma kinase)
 Alectinib (Alecensa); ALK positive NSC Lung
 Ceritinib (Zykadia); ALK positive NSC Lung
 Crizotinib (Xalkori); ALK positive NSC Lung

Kinase Inhibitors
 BRAF
 Dabrafenib (Tafinlar); Melanoma
 Vemurafenib (Zelboraf); Melanoma
 BTK
 Ibrutinib (Imbruvica); CLL, Mantle cell
lymphoma
 CDK 4,6
 Palbociclib (Ibrance); ER/PR positive HER2
negative Breast

Kinase Inhibitors
 EGFR
 Osimertinib (Tagrisso) wild type sparing; NSC
Lung with EGFR T790M mutations
 Afatinib (Gilotrif, Tomtovok); NSC Lung with
EGFR exon 19 deletions or exon 21
 Erlotinib (Tarceva); NSC Lung with EGFR exon 19
deletions or exon 21, Pancreatic with gemcitabine
 Gefitinib (Iressa); NSC Lung with EGFR exon 19
deletions or exon 21 mutations

Kinase Inhibitors
 FLT3
 Sorafenib (Nexavar); Hepatocellular, Renal
Cell, Thyroid
 Sunitinib (Sutent); Renal Cell, GIST,
Pancreatic neuroendocrine

Kinase Inhibitors
 HER2 (ERBB2/neu)
 Afatinib (Gilotrif, Tomtovok); NCS Lung with
EGFR exon 19 deletions or exon 21
mutations
 Lapatinib (Tykerb); HER2 overexpressing
Breast
 JAK ½
 Ruxolitinib (Jakafi); Myelofibrosis,
Polycythema vera

Kinase Inhibitors
 KIT
 Axitinib (Inlyta); Renal cell
 Regorafenib (Stivarga); Colorectal, GIST
 Dasatinib (Sprycel); Ph-positive CML, Ph-
positive ALL
 Pasopanib (Votrient); Renal cell, Soft tissue
sarcoma
 Imatinib (Gleevac); Ph-positive CML
 Sunitinib (Sutent); Renal cell, GIST

Kinase Inhibitors
 MEK
 Trametinib (Mekinist); Melanoma
 mTOR
 Sirolimus (Rapamune); Kidney transplant
rejection prophylaxis
 Temsirolimus (Torisel); Renal cell
 Everolimus (Afinitor); ER/PR positive HER2
negative Breast, Pancreatic neuroendocrine,
Renal cell

Other Cancer Therapy
 PARP (poly (ADP-ribose) polymerase)
 Olaparib (Lynparza); BRCA-mutated Ovarian
 Proteasome
 Bortezomib (Velcade); Multiple Myeloma,
Mantle Cell Lymphoma
 Carfilzomib (Kyprolis); Multiple Myeloma

Other Cancer Therapy
 Other
 Pomalidomide (Pomalyst); Multiple Myeloma
 Lenalidomide (Revlimid); Multiple Myeloma,
MDS, Mantle Cell Lymphoma
 Thalidomide (Thalomid); Multiple Myeloma

Advanced Practice Considerations
 Maintain awareness of cancer agents and treatment
options
 Utilize Package Insert for drug details including dosing
and toxicity management
 Encourage supportive care to minimize toxicity
 Collaborate with respective disciplines
 Support patients physically (symptom management),
psychosocially (referrals to social work/case
management), emotionally (referrals to
psychology/support groups) and spiritually (refer to
chaplain/spiritual counselor)

Resources
 American Cancer Society
 1-800-813-HOPE (4673)
 http://www/cancer.org/
 National Cancer Institute
 1-800-4-CANCER (422-6237)
 http://www.cancer.gov/
 National Comprehensive Cancer Network
 http://www.nccn.org/
 Vanderbilt My Cancer Genome
 www.mycancergenome.org

References
 Adams, W. R., DeRemer, D., & Holdworth, M. T. (2005). Guide to
cancer chemotherapeutic regimens 2005. New York: McMahon
Publishing Group.
 American Cancer Society (2016). Retrieved February 3, 2016 from
http://www.cancer.org
 Anderson K. N. & Anderson, L. E. (1998). Mosby’s pocket dictionary
of medicine, nursing, and allied health. St. Louis: Mosby Inc.
 Baltzer Cleri, L. & Haywood, R. (2002). Oncology pocket guide to
chemotherapy 5th edition. New York: Mosby.
 Center for Disease Control (2016). Breast cancer among women.
Retrieved February 5, 2016 from http://www.cdc.gov/
 Kasper, D et all. (2005). Harrison’s Manual of Medicine 16th edition.
New York: McGraw-Hill.
 Katzung, B. (2004). Basic and Clinical Pharmacology 9th Edition.
Lange Medical Books/McGraw-Hill: New York.

References
 Kumar, R. & Yarmand-Bagheri, R. (2001). The role of HER2 in
angiogenesis. Seminars in Oncology, 28(5), 27-32
 Lynch, M. P. (2005). Essentials of oncology care. New York:
Professional Publishing Group, Ltd.
 Michalides, RJAM (1999). Cell cycle regulators: mechanisms and
their role in the etiology, prognosis, and treatment of cancer. Journal
of Clinical Pathology 52, 555-568.
 Nursing 2007 Drug Handbook 27th Edition. (2007). Philadelphia:
Lippincott Williams & Wilkins.
 Peedell, C. (2005). Concise Clinical Oncology. Philadelphia:
Elsevier.
 Vanderbilt (2016). Retrieved February 3, 2016 from
www.mycancergenome.org
 Von Roenn, J. H. (2006). Your guide to the latest cancer research
and treatments. Cancer Care Inc.
 Wilkes, G. M. & Barton-Burke, M. (2005). Oncology nursing
handbook 2005. Boston: Jones and Bartlett Publishers.

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