MANAGEMENT OF PATIENTS WITH ONCOLOGIC CARCINOGENS

DISORDERS  Agents that initiate or promote malignant

transformation.
CANCER  A complete carcinogen is an agent that both
 A large group of disorders with different causes, initiates and promotes the development of cancer
manifestations, treatments, and prognoses. (e.g., cigarette smoking, asbestos).
 Because cancer can involve any organ system and
treatment approaches have the potential for
multisystem effects, cancer nursing practice overlaps 1. INITIATION
with numerous nursing specialties  Carcinogens (substances that can cause cancer),
PATHOPHYSIOLOGY OF THE MALIGNANT PROCESS such as chemicals, physical factors, or biologic
Cancer - a disease process that begins when a cell is agents, cause mutations in the cellular DNA.
transformed by genetic mutations of the cellular  Normally, these alterations are reversed by DNA
deoxyribonucleic acid (DNA). repair mechanisms or the changes initiate apoptosis
 Genetic mutations may be inherited or acquired, (programmed cellular death) or cell senescence.
leading to abnormal cell behavior  Cells can escape these protective mechanisms with
 The initial genetically altered cell forms a clone
permanent cellular mutations occurring, but these
↓ mutations usually are not significant to cells until the
Begins to proliferate abnormally second step of carcinogenesis.
↓
Evading normal intracellular and extracellular growth- 2. PROMOTION
regulating processes or signals as well as the  Repeated exposure to promoting agents (co-
immune system defense mechanisms of the body. carcinogens) causes the proliferation and expansion
 Genetic mutations  abnormalities in cell signaling of initiated cells with increased expression or
transduction processes (signals from outside and
manifestations of abnormal genetic information, even
within cells that turn cell activities either on or off) 
after long latency periods.
cancer development.
 Ultimately cells acquire a variety of capabilities that  Promoting agents are not mutagenic and do not need
allow them to invade surrounding tissues or gain to interact with the DNA.
access to lymph and blood vessels, which carry the  It is reversible if the promoting substance is removed
cells to other areas of the body resulting in (a key focus in the prevention of cancer)
Metastasis or the spread of the cancer  Latency periods for the promotion of cellular
BENIGN AND MALIGNANT CELLS mutations vary with the type of agent, the dosage of
(See Table 12-1) the promoter, and the innate characteristics and
 Benign genetic stability of the target cell.
 Noncancerous
 Malignant 3. PROGRESSION
 Cancerous  The altered cells exhibit increasingly malignant
REMEMBER: behavior.
 Both differ in many cellular growth characteristics,
 These cells acquire the ability to stimulate
including:
angiogenesis (growth of new blood vessels that
1. The method and rate of growth
2. Ability to metastasize or spread allow cancer cells to grow), to invade adjacent
3. Destruction of tissue, and tissues, and to metastasize.
4. Ability to cause death  Cellular oncogenes are responsible for vital cell
functions, including proliferation and differentiation.
Anaplasia  Cellular proto-oncogenes, such as those for the
 A pattern of growth in which cells lack normal epidermal growth factor receptor (EGFR),
characteristics and differ in shape and transcription factors such as c-Myc, or cell signaling
organization with respect to their cells of origin proteins such as Kirsten ras (KRAS), act as “on
 The degree of anaplasia is associated with switches” for cellular growth.
increased malignant potential. Proto-oncogenes
1. EGFR (Epidermal Growth Factor Receptor)
CARCINOGENESIS  It is a protein found on the surface of cells
Molecular Process that helps them grow and divide.
 Malignant transformation, or carcinogenesis, is  EGFR acts like a signal receiver; when
thought to be at least a three-step cellular process, certain molecules (like growth factors) bind to
involving: it, EGFR sends a message inside the cell,
telling it to grow or divide
1. Initiation  But if EGFR becomes overactive due to
2. Promotion mutations, it can lead to uncontrolled cell
3. Progression growth, which is often linked to cancer.
2. c-Myc
  is a gene that codes for a protein called Myc EXAMPLES: (viruses that are known to cause cancer)
 It’s like a switch that helps cells grow and  Human Papillomavirus (HPV)
multiply by increasing the production of o (cervical and head and neck cancers)
important proteins.  Hepatitis B virus (HBV)
3. KRAS (Kirsten ras) o (Liver cancer)
 Is a gene that makes a protein called K-Ras,  Epstein–Barr virus (EBV)
which plays a key role in cell signaling o (Burkitt lymphoma and nasopharyngeal
pathways cancer).
 K-Ras acts like a molecular switch: it turns
 BACTERIA
on in response to certain signals (like growth
 While there is little evidence to support a direct link
factors) and helps control normal cell growth.
between most bacteria and cancer, secondary
 However, when the KRAS gene is mutated, responses to certain bacterial infections, such as the
K-Ras can become permanently "switched production of carcinogenic metabolites and
on," even when it's not supposed to be. inflammatory reactions, are suspected mechanisms
 This leads to uncontrolled cell growth, which of cancer development.
can result in the formation of tumors and EXAMPLES: (Bacteria that are associated with an
contribute to cancer development. increased risk of cancer)
 Amplification of proto-oncogenes or overexpression  Helicobacter pylori
of growth factors, such as epidermal growth factor o (stomach cancer)
(EGF), can lead to uncontrolled cell proliferation  Salmonella enteritidis
(production) o (colon cancer)
 Mutations that increase the activity of oncogenes  Chlamydia trachomatis
also deregulate (leave be let alone or not interfere) o (ovarian and cervical cancers).
cell production. PHYSICAL AGENTS
 Genetic alterations in the gene for KRAS have been  Physical factors associated with carcinogenesis
associated with: include:
o Pancreatic Exposure to sunlight
Radiation
o Lung
Chronic irritation or inflammation
o Colorectal cancers Tobacco carcinogens
 Just as proto-oncogenes “turn on” cellular growth, Industrial chemicals
cancer suppressor genes “turn off,” or regulate, Asbestos
unneeded cellular proliferation.  Excessive exposure to the ultraviolet rays of the sun
 When suppressor genes are mutated  loss of is associated with skin cancers in all individuals,
function or expression  the cells begin to produce although those with fair skin are at highest risk.
mutant cell populations that are different from their  Factors such as clothing styles (sleeveless shirts or
original cellular ancestors. shorts), the use of sunscreens, occupation,
recreational habits, and environmental variables,
PROLIFERATIVE PATTERNS including humidity, altitude, and latitude, all play a
 During the lifespan, various body tissues normally role in the amount of exposure to ultraviolet light.
undergo periods of rapid or proliferative growth that  Exposure to ionizing radiation from repeated
must be distinguished from malignant growth activity. diagnostic x-ray procedures or with radiation therapy
 Several patterns of cellular adaptation include used to treat disease can cause cancer
atrophy, hypertrophy, hyperplasia, metaplasia, and CHEMICAL AGENTS
dysplasia  Most cancers are thought to be related to
 Cancerous cells, described as malignant, environmental factors
demonstrate neoplasia, or uncontrolled cell growth  Most hazardous chemicals produce their toxic effects
that follows no physiologic demand. by altering DNA structure.
ETIOLOGY  Tobacco use is thought to be the single most lethal
 Factors implicated or known to induce chemical carcinogen
carcinogenesis include:  Cigarette smoking is strongly associated with 12
 Viruses and bacteria different cancer types including:
 Physical agents 1. Cancers of the oral cavity and pharynx
 Chemicals 2. Larynx
 Genetic or Familial factors 3. Lung
 Lifestyle factors 4. Esophagus
 Hormones 5. Pancreas
VIRUSES AND BACTERIA 6. Uterine cervix
7. Kidney
 VIRUS
8. Bladder
 After infecting individuals, DNA viruses insert a part
9. Stomach
of their own DNA near the infected cell genes
10. Colorectal
causing cell division
11. Liver
 The newly formed cells that now carry viral DNA lack
12. Myeloid leukemia.
normal controls on growth.
 Environmental tobacco smoke (ETS), otherwise be passed to offspring.
known as secondhand smoke, has been linked to  This type of mutation is present in every cell
lung cancer of an individual’s body because it originates
 There is also some evidence that ETS may be linked from the sperm or egg that formed the
with cancers of the: embryo.
Larynx  Unlike mutations that occur later in life
Pharynx (somatic mutations), germline mutations
Nasal sinuses affect not just a single organ or tissue, but
Brain the entire organism.
Bladder  The hallmarks of families with a hereditary
Rectum cancer syndrome include:
Stomach 1. Cancer in two or more first-degree
Breast relatives (the parent, sibling, or child of an
 Electronic Nicotine Delivery Systems (ENDS) individual)
including e-cigarettes, e-pens, e-pipes, e-hookah,  The genetic predisposition to cancer can
and e-cigars have gained increased popularity as an be passed directly from parent to child,
alternative to tobacco. increasing the likelihood that close family
 ENDS do not contain tobacco but most contain members will also develop cancer
nicotine, which is highly addictive, and other 2. Onset of cancer in family members
potentially harmful substances, such as younger than 50 years
 Volatile organic compounds  Cancers often develop at an earlier age
 Formaldehyde compared to those in the general
 Flavoring chemicals population.
 Smokeless tobacco products (chewing tobacco,  If cancer appears in family members
snuff, and snus) used most often by young adults before the age of 50, it suggests a higher
aged 18 to 25 years, are associated with an likelihood that the cancer is caused by a
increased risk of oral, pancreatic, and esophageal genetic mutation that runs in the family.
cancer 3. The same type of cancer in several family
 Many chemical substances found in the workplace members
are carcinogens or co-carcinogens.  If multiple members of the same family
o The extensive list of suspected chemical are diagnosed with the same type of
substances continues to grow and includes: cancer (for example, breast cancer or
Aromatic amines and aniline dyes colon cancer), this can indicate an
Pesticides and formaldehyde inherited predisposition.
Arsenic, soot, and tars  Hereditary cancers are often linked to
Asbestos specific genes that increase the risk for
Benzene particular types of cancer.
Cadmium 4. Individual family members with more than
Chromium compounds one type of cancer
Nickel and zinc ores  In some cases, a person with a
Wood dust hereditary cancer syndrome may
Beryllium compounds develop more than one type of cancer
Polyvinyl chloride during their lifetime (for example, breast
GENETICS AND FAMILIAL FACTORS and ovarian cancer).
 Almost every cancer type has been shown to run in  This suggests that the underlying genetic
families. mutation may predispose them to
o This may be due to a combination of genetic, multiple cancer types.
environmental, and lifestyle factors. 5. A rare cancer in one or more family
 Genetic factors play a fundamental role in cancer members.
cell development.  If a family member is diagnosed with a
 Cancer has been associated with: cancer that is unusual or rare, it may
A. Extra chromosomes point to an inherited genetic mutation
B. Too few chromosomes that increases the risk of developing that
C. Translocated chromosomes particular cancer.
 Hereditary cancer syndromes represent a cluster
of cancers identified by a specific genetic alteration EXAMPLES OF HEREDITARY CANCER SYNDROMES:
that is inherited across generations.
o In these families, the associated genetic 1. Hereditary Breast and Ovarian Cancer Syndrome
mutation is found in all cells in the body (BRCA1 and BRCA2):
(germline mutation) and represents an o These two genes, BRCA1 and BRCA2, are
inherited susceptibility to cancer for all family well-known for their link to hereditary breast
members who carry the mutation. and ovarian cancer. Mutations in these
NOTE: genes greatly increase a person's risk of
Germline Mutation developing these cancers.
 A genetic alteration that occurs in the 2. Multiple Endocrine Neoplasia Syndrome (MEN1
reproductive cells (sperm or egg) and can and MEN2)
 o These genetic conditions affect the lower genital tract
endocrine glands (like the thyroid or adrenal o A rare but serious type of cancer that
glands). People with MEN1 or MEN2 are at affects the cells lining the vagina and
higher risk for developing tumors in these cervix, which are part of the female
glands. reproductive system.
 Other cancers associated with familial inheritance
syndromes include:  Adenocarcinoma
A. Nephroblastoma (kidney tumors, especially in o Refers to a type of cancer that starts in
children) also known as Wilms Tumor glandular cells, which are cells that
B. Pheochromocytomas (tumors of the adrenal secrete substances such as mucus.
gland)  Clear cell
C. Cancers of the colon, stomach, thyroid, o Refers to the appearance of the cancer
kidney, prostate, and lungs. cells under a microscope. These cells
LIFESTYLE FACTORS often look clear or empty because of the
Examples: way they store substances inside them.
 Obesity
 Alcohol intake REMEMBER:
 Poor diet  Prenatal exposure to diethylstilbestrol (DES)
 Physical inactivity o Refers to when a developing fetus is
exposed to a synthetic form of estrogen
 These lifestyle factors were second only to cigarette (DES) while still in the womb.
smoking as a major modifiable risk factor associated o This occurred when pregnant women were
with both cancer development and cancer mortality. prescribed DES to prevent miscarriages and
 The risk of cancer increases with long-term ingestion other pregnancy complications.
of carcinogens or co-carcinogens or the absence of Risk of Breast Cancer
protective substances in the diet.  Early onset of menses before age 12 and
o Dietary substances that appear to delayed onset of menopause after age 55.
increase the risk of cancer include:  Null parity (never giving birth)
A. Fats  Delayed childbirth after age 30
B. Alcohol NOTE:
C. Salt-cured or smoked meats Increased numbers of pregnancies 
D. Nitrate- and nitrite-containing foods ↓ incidence of breast, endometrial, and ovarian
E. Red and processed meats
cancers.
o Heavy alcohol use increases the risk of
1. Breast Cancer
cancers of the mouth, pharynx, larynx,
esophagus, liver, colon, rectum, and breast. o This is because, during pregnancy, breast
 Obesity has been linked to the development of tissue undergoes changes that make it less
cancers of the breast (in postmenopausal women), susceptible to cancerous transformations.
colon and rectum, endometrium, esophagus, kidney, 2. Endometrial (Uterine) Cancer
and pancreas. o This is because, during pregnancy, the
o It may also be associated with an increased
production of progesterone is high.
risk for cancers of the gallbladder, liver,
ovary, and cervix, and for multiple myeloma, o This hormone helps prevent the endometrial
Hodgkin lymphoma, and aggressive forms of lining from thickening excessively, which can
prostate cancer. otherwise increase the risk of cancer.
 Etiology Of Cancer In The Context Of Obesity 3. Ovarian Cancer
1. Excess fat may cause chronic inflammation o Each time a woman ovulates, there is a slight
resulting in DNA damage
trauma to the surface of the ovary, which can
2. Increased levels of certain hormones
o (e.g., estrogen, insulin, adipokines) increase the risk of cancer over time.
3. Disruptions in levels of cell growth regulators o Since pregnancy suppresses (defeats)
o (e.g., mammalian target of rapamycin and ovulation, having more pregnancies leads to
AMP-activated protein kinase) fewer ovulatory cycles, reducing the risk of
HORMONAL AGENTS ovarian cancer.
 Tumor growth may be promoted by disturbances in
hormonal balance, either by the body’s own Taking estrogen after menopause  ↓ risk of
(endogenous) hormone production or by
breast cancer, but an ↑ risk of developing
administration of exogenous hormones
 Cancers of the breast, prostate, ovaries, and endometrial cancers
endometrium are thought to depend on endogenous o Estrogen replacement alone (without
hormonal levels for growth. progesterone) may reduce the risk of breast
 Prenatal exposure to diethylstilbestrol (a synthetic cancer but increase the risk of endometrial
form of the female hormone estrogen)  risk for cancer (cancer of the lining of the uterus).
clear cell adenocarcinoma of the lower genital tract
o This is because estrogen can cause the
 Clear cell adenocarcinoma (CCA) of the
lining of the uterus to thicken, potentially
 leading to cancer if not balanced by
progesterone.

Thus, estrogen replacement alone is not used in

women who have not had a hysterectomy
o Hysterectomy - surgery to remove the
uterus
o Estrogen alone is not recommended for
women who still have a uterus (i.e.,
women who have not had a hysterectomy),
as they are at higher risk for endometrial
cancer.

Combination estrogen and progesterone therapy

is linked to a higher risk of breast cancer
o Estrogen and progesterone combination
therapy is often prescribed for women who
still have a uterus.
o Progesterone helps prevent the thickening of
the uterine lining, reducing the risk of
endometrial cancer.
o However, combination therapy has been
linked to a higher risk of breast cancer,
particularly with long-term use.
o The longer a woman uses this combined
hormone therapy, the higher her risk of
developing breast cancer becomes.
o But the increased risk of breast cancer
related to hormone therapy drops
significantly once the therapy is stopped.
ROLE OF THE IMMUNE SYSTEM
 In humans, transformed cells arise on a regular
basis, but are recognized by surveillance cells of the
immune system that destroy them before cell growth
becomes uncontrolled (immune surveillance)
 When the immune system fails to identify and stop
the growth of transformed cells, a tumor can develop
and progress.

Patients who are at risk of cancers are:

1. Immunocompromised
2. Transplant recipients who receive
immunosuppressive therapy to prevent
rejection of the transplanted organ
3. Patients with acquired immune deficiency
syndrome (AIDS)
4. Patients who were previously treated for one
cancer are at increased risk for secondary
cancers