McKenna's Pharmacology for Nursing, 2e - page 206

C H A P T E R 1 4
 Antineoplastic agents
193
used today include alkylating agents, antimetabolites,
antineoplastic antibiotics, mitotic inhibitors, hormones
and hormone modulators, cancer cell-specific agents,
protein tyrosine kinase inhibitors (which target enzymes
specific to the cancer cells) and a group of antineoplastic
agents that cannot be classified elsewhere. Other drugs
are used to combat the serious adverse effects that can
be associated with the antineoplastic drugs. These drugs
are used as adjunctive therapy. Figure 14.4 shows sites
of action of these drugs. Box 14.1 discusses use of these
drugs across the lifespan.
As discussed in Chapter 7, all cells progress through
a cell cycle. Different types of cells progress at different
rates (see Figure 7.6). Rapidly multiplying cells, or cells
that replace themselves quickly, include those lining the
gastrointestinal (GI) tract and those in hair follicles, skin
and bone marrow. These cells complete the cell cycle
every few days. Cells that proceed very slowly through
1,000,000-cell tumour
10,000-cell
tumour
1000-cell
tumour
100-cell
tumour
10-cell
tumour
1-cell
tumour
1st course of
chemotherapy
2nd course of
chemotherapy
3rd course of
chemotherapy
4th course of
chemotherapy
5th course of
chemotherapy
FIGURE 14.3 
Cell kill theory. A set percentage of cells is killed after each dose of chemotherapy. The percentage killed is dependent upon the drug
therapy. In this example, each course of chemotherapy kills 90% of cells in a cancerous tumour. After the fifth course of chemotherapy in this
example, a 1-cell tumour remains; the person’s immune system would destroy this malignant cell.
Rough
endoplasmic
reticulum
Smooth
endoplasmic reticulum
Polyribosomes
Golgi
apparatus
Cilia with
microtubules
Peroxisomes
Lysosomes
Nucleus:
Nuclear
membrane
Nuclear pore
Nucleolus
Cell membrane
Microtubules
Mitochondria
Centrioles
docetaxel
paclitaxel
cladribine
hydroxyurea
irinotecan
procarbazine
Alkylating
agents
erlontinib
gefitnib
imatinib
bortezomib
lapatinib
nilotinib
sorafenib
sunitinib
temsirolimus
Hormone
modulators
Mechanism of action unknown
tretinoin—promotes cell differentiation
FIGURE 14.4 
Sites of action of non–cell
cycle-specific antineoplastic agents.
Alkylating agents interfere with RNA,
DNA or other cellular proteins. For
example, procarbazine blocks DNA,
RNA and protein synthesis. Hormone
modulators react with specific receptor
sites to block cell growth and activity.
Mitotic inhibitors such as docetaxel
and paclitaxel inhibit microtubular
reorganisation. The antimetabolite
cladribine and miscellaneous agent
hydroxyurea block DNA synthesis.
The miscellaneous agent irinotecan
disrupts DNA strands. Cell-specific
agents such as gefitinib, erlotinib,
lapatinib, nilotinib, sorafenib,
sunitinib, temsirolimus and imatinib
inhibit protein tyrosine kinases.
Bortezomib is a proteasome inhibitor.
Mechanism of action unknown
tr tinoi —pr motes cell differentiation
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