ANTINEOPLASTIC AGENTS differentiation and organization


CELL CYCLE
AUTONOMY – growing without the
1. G0 Phase
usual homeostatic restrictions

 Resting phase, cell is stable,

 METASTASIS – neoplastic cells
dormant
grow uncontrollably damaging healthy


Cells that just functions as they
are supposed to do
 Cancer chemotherapy usually
works on active, dividing cells.
tissue in the area to develop new
tumors
 Some CA cells can be destroyed by T
cells, antibodies and interferons, TNF (tissue
necrosis factor)

 5-year cancer-free period is

usually the basic guide for
 Cause of cancer: Still unknown

considering a cancer to be cured.

2. G1 Phase
 Genetic link (breast cancer)

 The time of stimulation from the  Viral infections

resting phase until the formation of
DNA
 Constant irritation and cell

 Cell synthesizes substances for

turnover

DNA formation
 Prolonged stress
3. S Phase

 Actual synthesis of DNA, w/c is an

 Pipe smokers (carcinogenic)

energy consuming activity

 2 Types of Cancer:
 The cell remains in this phase
until the DNA doubles  Solid tumor – originate in any
4. G2 Phase body organ and further divided into:

 Cell produces all the substances

 Carcinoma

required for the manufacture of mitotic Ex: granular cell tumor of the
spindles breast, bronchial tumors,
squamous and basal tumors of
5. M Phase (Cellular division phase)
the skin

 The cell splits to form two  Sarcoma – osteogenic

identical daughter cells - mitosis tumors, which form in the
primitive cells of the bone
CHEMOTHERAPY
Ex: osteogenic tumors,
Cancer rhabdomyosarcoma

 Arise from a single cell that is  Hematological malignancies –

genetically different that divides and bone marrow & lympathics system
produce a tumor or neoplasm
Ex: leukemias, lymphomas – alter the

 CA cells - as abnormal cells continue to

body’s ability to produce and regulate
cells found in the blood
divide, they lose more and more of their
original cell characteristics.
ANTINEOPLASTIC DRUGS
 ANAPLASIA – a loss of cellular
  ALKYLATING AGENTS  Carmustine (Gliadel)

 ANTIMETABOLITES  Chlorambucil (Leukeran)

 ANTINEOPLASTIC ANTIBIOTICS  Cyclophosphamide

 MITOTIC INHIBITORS  Ifosfamide (Ifex)

 HORMONES AND HORMONE  Lomustine (CeeNU)

MODULATORS

 CANCER CELL-SPECIFIC AGENTS

 Mechlorethamine (Mustargen)

 PROTEIN TYROSINE KINASE INHIBITORS

 Melphalan (Alkeran)

Considerations:  Procarbazine (Matulane)

 Combination of antineoplastic
 Streptozocin (Zanosar)
agents targeting different phases of the cell
cycle is frequently most effective in
treating many cancers.
 Temozolomide (Temodar)

 Antineoplastic agents primarily

 Thiotepa (Thioplex)
affect human cells that are rapidly
multiplying.



Therapeutic action:
Antineoplastic drugs are
associated with many adverse effects
(unpleasant & debilitating).  react chemically with portions of RNA
and DNA to produce cytotoxic effects
 BONE MARROW SUPPRESSION –
inhibiting the blood forming components of
the body’s normal protective actions
 Indications:


against abnormal cells.
Lymphomas
 GOAL OF CHEMOTHERAPY – limit
the offending cells to the degree that the
immune system can respond without  Leukemias
causing too much toxicity to the host.

NON-CELL CYCLE SPECIFIC

 Myelomas
1. ALKYLATING AGENTS – affects cells even in


the resting phase
- for slow growing cancers Breast, Pancreatic, Ovarian and
Testicular Cancer
 Altretamine (Hexalen)
 Adverse effects:

 Bendamustine (Treanda)

 Bone marrow suppression

 Busulfan (Busulfex, Myleran) (leukopenia, thrombocytopenia,
anemia, pancytopenia)
  NAVDA  Menopause-associated effects

 Hepato/Nephrotoxicity
 Hypercalcemia

 Alopecia
 Cardiovascular diseases



Drug-to-drug interaction:
Hyperuricemia

2. HORMONE & HORMONE MODULATORS  Hormone and hormone modulators when

taken with oral anticoagulants, can increase

 Anastrazole (Arimidix)
risk of bleeding.

CELL-CYCLE SPECIFIC

 Bicalutamide (Casodex)
1. ANTINEOPLASTIC ANTIBIOTIC

 Degarelix
 Bleomycin (Blenoxane)

 Estramustine (Emcyt)
 Dactinomycin (Cosmegen)

 Exemestane (Aromasin)
 Mitomycin (Mutamycin)

 Flutamide
 Daunorubicin (DaunoXome)

 Fulvestrant (Faslodex)
 Doxorubicin (Doxil)

 Goserelin (Zoladex)
 Epirubicin (Ellence)

 Action:
 Idarubicin (Idamycin)


 Valrubicin (Valstar)
are hormone-specific or receptor-
site specific to block the stimulation of
growing cancer cells that are sensitive  Mitoxantrone (Novantrone)
to the presence of that hormone

 Indication:
 Therapeutic action:

 Breast and Prostatic Cancers

 cytotoxic and interfere with
cellular DNA synthesis by inserting
themselves between base pairs in the

 Contraindications:
DNA chain



Indication:
Pregnancy and lactation

 Hypercalcemia
 Skin – Squamous cell carcinoma,
Kaposi’s Sarcoma

 Adverse effects:  GIT

  Bone marrow (lymphomas)  Action:

 Adverse effects:  inhibit DNA production in cells

that depend on certain metabolites to

 Hematological effects:
produce DNA

Bone marrow suppression  Most effective for rapidly dividing

cells preventing cell replication

 GI effects:
 Indication:

nausea, vomiting, anorexia,

diarrhea, and mucous membrane
deterioration.
 Acute Lymphoblastic Leukemia

Hepatotoxicity and nephrotoxicity  GI basal cell cancers

Alopecia  Adverse effects:

 Toxic to heart and lungs.

 Hematological effects:
2. ANTIMETABOLITES
 Bone marrow suppression
 Capecitabine (Xeloda)

 GI effects:
 Cladribine (Leustatin)
nausea, vomiting, anorexia, diarrhea, and
 Clofarabine (Clolar)
mucous membrane deterioration.

Hepatotoxicity and nephrotoxicity

 Cytarabine (DepoCyt)
Alopecia
 Budarabine (Fludara)
Pulmonary toxicity (interstitial
pneumonitis)
 Gemcitabine (Gemzar) 3. MITOTIC INHIBITORS

 Fluxoridine (FUDR)  Docetaxel (Taxotere)

 Fluorouracil (Adrucil)  Paclitaxel (Taxol, Onxol)

 Mercaptopurine (Purinethol)  Vinblastine (Velban)

 Methotrexate (Rheumatrex)  Vincristine (Oncovin, Vincasar)

 Pemetrexed (Alimta)  Vinorelbine (Navelbine)

 Pentostatin (Nipent)  Etoposide (Toposar)

 Thioguanine (Tabloid)  Teniposide (Vumon)

  Ixabepilone (Ixempra)  Bortezomib (Velcade)

 Action:  General Adverse Effects


HEMATOLOGICAL
interfere with the ability of a cell to
divide  BM Suppression

 Block or alter DNA synthesis

GI Effects:

 Indication:
 NAVDA

 Treatment of varieties of tumors

 Mucous Membrane Deterioration

and leukemias.

OTHER ANTINEOPLASTICS  Stomatitis

CANCER CELL-SPECIFIC AGENTS CNS

1. Protein Tyrosine Kinase Inhibitors
 Headache, drowsiness, aphasia,
 Everolimus (Afinitor) fatigue, malaise and paresthesia

 Temsirolimus (Torisel)  Hepatic and Renal Toxicity

 Gefitinib (Iressa)  Alopecia

 Imatinib (Gleevec)
 Hyperuricemia

 Lapatinib (Tykerb)
 General Nursing Responsibilities



Nilotinib (Tasigna)
Arrange for blood tests (CBC)

 Sorafenib (Nexavar)
before, during and after therapy

 Sunitinib (Sutent)
 Administer medication as
scheduled and ordered

 Act on specific enzymes that are

 Ensure hydration
needed for protein building by specific
tumor cells.

 Protect from infection & limit

 Each drug that has been invasive procedures
developed inhibits a very specific protein
kinase and acts on very specific tumors.

2. Epidermal Growth Factor Inhibitor

 Provide small, frequent meals and
oral care

 Erlotinib (Tarceva)
 Anticipate the need for antiemetic

3. Proteasome Inhibitor
 Offer wearing of wig, scarf, hat at
extremes of temperature

 Use barrier contraceptives

 Frequent mouth care

 Monitor cardiac and respiratory

functions

 Avoid direct skin or eye contact

with the drug

 Monitor injection sites

 Use distal veins

 Avoid small veins

 Never use existing lines unless it

is running well

 Give antidotes if extravasation

occurs.