C H A P T E R 1 4
Antineoplastic agents
191
function normally. They also exhibit
autonomy
, growing
without the usual homeostatic restrictions that regulate
cell growth and control. This loss of control allows the
cells to form a tumour.
Over time, these neoplastic cells grow uncontrol
lably, invading and damaging healthy tissue in the area
and even undergoing
metastasis
, or travelling from the
place of origin to develop new tumours in other areas
of the body where conditions are favourable for cell
growth (see Figure 14.2). The abnormal cells release
enzymes that generate blood vessels (
angiogenesis
) in the
area to supply both oxygen and nutrients to the cells,
thus contributing to their growth. Overall, the cancer
ous cells rob the host cells of energy and nutrients and
block normal lymph and vascular vessels as the result of
pressure and intrusion on normal cells, leading to a loss
of normal cellular function.
The body’s immune system can damage or destroy
some neoplastic cells. T cells, which recognise the
T
he use of the term chemotherapy implies cancer treat
ment to most people. However, only one branch of
chemotherapy involves drugs developed to act on and
kill or alter human cells—the
antineoplastic agents
,
which are designed to fight
neoplasms
, or cancers.
Antineoplastic drugs alter human cells in a variety
of ways. Their action is intended to target the abnormal
cells that compose the neoplasm or cancer, having a
greater impact on them than on normal cells. Unfortu
nately, normal cells also are affected by antineoplastic
agents.
This area of pharmacology, which has grown tre
mendously in recent years, now includes many drugs
that act on or are part of the immune system. These
substances fight the cancerous cells using components of
the immune system instead of destroying cells directly
(see Chapter 15). This chapter discusses the classic anti
neoplastic agents and includes those drugs that are used
in cancer chemotherapy.
CANCER
Cancer is a disease that can strike a person at any age
and is one of the leading causes of death in Australia
and New Zealand. Treatment of cancer can be pro
longed and often debilitating. The person can experience
numerous and wide-ranging complications and effects.
All cancers start with a single cell that is geneti
cally different from the other cells in the surrounding
tissue. This cell divides, passing along its abnormalities
to daughter cells, eventually producing a tumour or
neoplasm that has characteristics quite different from
those of the original tissue (see Figure 14.1). As the
abnormal cells continue to divide, they lose more and
more of their original cell characteristics. The cancerous
cells exhibit
anaplasia
—a loss of cellular differentiation
and organisation, which leads to a loss of their ability to
mitomycin
mitoxantrone
MITOTIC INHIBITORS
docetaxel
etoposide
paclitaxel
teniposide
vinblastine
vincristine
vinorelbine
HORMONES AND HORMONE
MODULATORS
abiraterone
anastrazole
bicalutamide
cabazitaxel
degarelix
exemestane
flutamide
fulvestrant
goserelin
letrozole
megestrol
nilutamide
tamoxifen
toremifene
triptorelin
CANCER CELL–SPECIFIC
AGENTS
bortezomib
erlotinib
everolimus
gefitinib
imatinib
lapatinib
nilotinib
sorafenib
sunitinib
temsirolimus
MISCELLANEOUS
ANTINEOPLASTICS
arsenic trioxide
hydroxyurea
irinotecan
topotecan
tretinoin
ANTINEOPLASTIC ADJUNCTIVE
THERAPY
amifostine
leucovorin
mesna
rasburicase
Normal
cells
Precancerous
cells
Cancer
cells
FIGURE 14.1
Malignant tumours develop from one cell, with somatic
mutations occurring during cell division as the tumour grows.
