Chapter 11
Oncology: Nursing management in cancer care
231
mechanisms and oncogenes, have enabled the appropriate
identification of families at risk for these syndromes.
Examples of these syndromes include hereditary breast and
ovarian cancer syndrome (
BRCA1
and
BRCA2
) and multiple
endocrine neoplasia syndrome (
MEN1
and
MEN2
) (for
further information on genetic considerations, see Chart 11-1
in the related ancillary file for this chapter). Cancers associ-
ated with familial inheritance syndromes include nephroblas-
tomas, pheochromocytomas, and breast, ovarian, colorectal,
stomach, thyroid, renal, prostate and lung cancers (Nussbaum,
McInnes & Willard, 2007).
Dietary factors
Dietary factors are thought to account for up to one third of
all cancers in Western countries and approximately 20% in
developing countries; diet is second only to tobacco as a pre-
ventable cause (WHO, 2009). Dietary substances can be pro-
active (protective), carcinogenic or co-carcinogenic. The risk
for cancer increases with long-term ingestion of carcinogens
or co-carcinogens or chronic absence of proactive substances
in the diet.
Dietary substances associated with an increased cancer
risk include fats, alcohol, salt-cured or smoked meats, foods
containing nitrates and nitrites, and a high kilojoule dietary
intake. Alcohol increases the risk of cancers of the mouth,
pharynx, larynx, oesophagus, liver, colorectum and breast.
Alcohol intake should be limited to no more than two drinks
per day for men and one drink per day for women. Food sub-
stances that appear to reduce cancer risk include high-fibre
foods, cruciferous vegetables (cabbage, broccoli, cauliflower,
Brussels sprouts, kohlrabi), carotenoids (carrots, tomatoes,
spinach, apricots, peaches, dark-green and deep-yellow veg-
etables), and possibly vitamins E and C, zinc and selenium.
Greater consumption of vegetables and fruits is associated with
a decreased risk of lung, oesophageal, stomach and colorectal
cancers (Kushi et al., 2006).
A high-kilojoule dietary intake is also associated with an
increased cancer risk. Obesity is clearly associated with endo-
metrial cancer, postmenopausal breast cancers, and colon,
oesophagus and kidney cancers. There is evidence that obesity
also increases the risk for cancers of the pancreas, gallbladder,
thyroid, ovary, cervix, prostate, and for multiple myeloma and
Hodgkin lymphoma (Kushi et al., 2006).
Hormonal agents
Tumour growth may be promoted by disturbances in hormonal
balance either by the body’s own (endogenous) hormone pro-
duction or by administration of exogenous hormones. Cancers
of the breast, prostate and uterus are thought to depend on
endogenous hormonal levels for growth. Diethylstilbestrol
(DES) has long been recognised as a cause of vaginal carci
nomas. Oral contraceptives and prolonged oestrogen replace-
ment therapy are associated with increased incidence of
hepatocellular, endometrial and breast cancers, whereas they
appear to decrease the risk for ovarian cancers. The com-
bination of oestrogen and progesterone appears safest in
decreasing the risk for endometrial cancers; however, some
studies recommend discontinuing hormonal therapy contain-
ing both oestrogen and progestin because of the increased risk
of breast cancer, coronary heart disease, stroke and blood clots
(Chlebowski et al., 2008).
Chemical agents
About 75% of all cancers are thought to be related to the
environment. Most hazardous chemicals produce their toxic
effects by altering DNA structure in body sites distant from
chemical exposure. The liver, lungs and kidneys are the organ
systems most often affected, presumably because of their roles
in detoxifying chemicals.
Tobacco smoke, thought to be the single most lethal
chemical carcinogen, accounts for at least 30% of cancer
deaths (WHO, 2009). Smoking is strongly associated with
cancers of the lung, head and neck, oesophagus, stomach,
pancreas, cervix, kidney and bladder, and with acute myelo-
blastic leukaemia. More than 4000 individual chemicals have
been identified in tobacco and tobacco smoke, including more
than 60 chemicals that are known carcinogens. Tobacco may
also act synergistically with other substances, such as alcohol,
asbestos, uranium and viruses, to promote cancer development.
Considerable research has also substantiated the effect of
second-hand cigarette smoke as an environmental risk factor
for both smokers and non-smokers (American Cancer Society,
2013a; 2013b; National Heart Foundation of Australia, 2008).
Many chemical substances found in the workplace have
proved to be carcinogens or co-carcinogens. The extensive
list of suspected chemical substances continues to grow and
includes aromatic amines and azo dyes; pesticides and formal
dehydes; arsenic, soot and tars; asbestos; benzene; betel nut
and lime; cadmium; chromium compounds; nickel and zinc
ores; wood dust; beryllium compounds; and polyvinyl chloride.
Genetic or familial factors
Almost every cancer type has been shown to run in families.
This pattern may be due to genetics, shared environments,
cultural or lifestyle factors, or chance alone. Genetic factors
play a role in cancer cell development. Abnormal chromo-
somal patterns and cancer have been associated with extra
chromosomes, too few chromosomes or translocated chromo-
somes. Specific cancers with underlying genetic abnormalities
include Burkitt’s lymphoma, chronic myelogenous leukae-
mia, meningiomas, acute leukaemias, retinoblastomas, Wilms’
tumour and skin cancers, including malignant melanoma.
Additionally, there are syndromes that represent a cluster of
cancers that are identified by a specific genetic alteration that
is inherited across generations of a family. In these families, the
associated genetic mutation is found in all cells and represents
an inherited susceptibility to cancer for all family members
who carry the mutation.
Approximately 5% of cancers of adulthood and childhood
display a familial predisposition. Inherited cancer syndromes,
such as premenopausal breast cancer, tend to occur at an early
age and at multiple sites in one organ or pair of organs. In
cancers with a familial predisposition, individuals may develop
multiple cancers; commonly, two or more first-degree rela-
tives share the same cancer type. There is also evidence of an
autosomal dominant inheritance pattern of cancers affecting
several generations of the family.
Since the early 1990s, there have been considerable
advances in the recognition of inherited cancer susceptibil-
ity syndromes and in the ability to isolate and identify the
inherited genetic mutation responsible for the cancer patterns.
Discoveries of mutations in genes related to critical cell
control functions, such as tumour suppression, DNA repair
