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Chapter 11

Oncology: Nursing management in cancer care

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