CANCER –CH 16

Cancer
− Group of more than 200 diseases
− Characterized by uncontrolled and unregulated growth of cells
− Declining due to preventive efforts: colorectal, lung, oral, pharyngeal cancers
− Rising: non-Hodgkin’s lymphoma, skin cancer, especially MELANOMA (due to genetic
predisposition and sun exposure)
− Mostly >55 years, but ALL age groups can be affected
− Men > women
− African American > whites and other minority group
− Yet, differences in survival from cancer are attributed primarily to a combination of several
factors:
o Poverty
o Difficult access to health care
o More comorbid conditions
o Differences in tumor biology
− Nurses position – lead efforts at changing attitudes and behaviors about cancer
o Goal : implement educational interventions that will assist individuals to
 Understand, reduce, or eliminate their risk of cancer development
 Comply with cancer management regimens
 Cope with effects of cancer and related treatment

Biology of Cancer

Cancer encompasses a broad range of diseases of multiple causes that can arise in ANY CELL of the
body capable of evading regulatory controls over proliferation and differentiation.
o Two major dysfunction:
1) Defect in cellular Proliferation
2) Defective cellular differentiation

Defect in Cellular Proliferation

NORMALLY:
o Stem cell (predetermined**, undifferentiated) begins by entering cell cycle 
generation time of the cell  mature cell functions until degenerates and dies.
o Predetermined** : stem cells of a particular tissue will ultimately differentiate and become
mature, functioning cells of that tissue and ONLY that tissue.
o Generation time of the cell : time from when a cell enters the cell cycle cell divides into
two identical cells

Proliferation NORMAL CELLS CANCER CELLS

Controll
Intracellular State of equilibrium is constantly
mechanism maintained
(cellular proliferation = cell death)
o Cellular proliferation occurs only
in the presence of cellular
degeneration and death.
o Cellular proliferation also occur
when body has physiologic needs
for more cells (ex; ↑WBC when
infection)
− Don’t have state of dynamic
equilibrium.
− Proliferation of cancer cells
divide indiscriminatly
haphazardly, and
continuously. (ex; produce
more than two cells at the
time of mitosis)
− They have a pyramid effect.
124816…Time
required for a tumor mass to
double in size is known as its

Contact − Normal cells have contact inhibition:
inhibition they inhibit cellular growth through
physical contact of their neighboring
cells.
− Normal cells DO NOT invade a
territory that is not their own by
respecting boundaries and territory of
the cells surrounding them.
Rate of normal Rate of proliferation differs in each body
cellular tissue
proliferation (time Rapid cellular proliferation rate: bone
of cell birth to time marrow, hair follicles, epithelial lining of
of cell death) GI tract etc
NO or slow proliferation rate:
myocardium and cartilage
doubling time.
− Cancer cells lack contact
inhibition: they have NO
REGARD for cellular
boundaries, (ex; they grow
on top of one another, also on
top of or between normal
cells)
− Cancer cells usually proliferate
at the same rate as normal
cells

STEM CELL THEORY

Cancer cells originate from the mutation of stem cell. They loss intracellular control of
proliferation resulting from a mutation of the stem cells.
DNA of stem cell is substituted or rearranged  stem cell mutation  one of three things
can occur
cell can die either from
Damage resulting from mutation, OR
By apoptosis: initiating a programmed cellular suicide
self repair: cell can recognize the damage and repair itself
Survive : mutated cell survives and passes along the damage to its daughter cells
Potential to become malignant (cells with invasive and metastatic potential)

Defect in Cellular Differentiation

NORMALLY
− Cellular differentiation is an orderly process
o Progresses from a state of immaturity to maturity
o All cells have the potential to perform all body functions b/c body cells are derived from the
fertilized ova.
o differentiated cell is stable and WILL NOT dedifferentiate(will not revert to a previous
undifferentiated state)
o exact mechanism is not completely understood.
− two types of normal genes: protooncogenes and tumor suppressor genes
 can be affected by mutation: function as oncogenes (tumor-inducing genes)
protooncogenes
Normal cellular genes: Oncogenes:
− “genetic lock” - Important − “unlocked” through exposure to carcinogens
regulators of normal cellular (agents that cause cancer), or oncogenic viruses 
processes genetic alteration  mutation occurs  function as
− Promote growth oncogenes
− Genetic lock that keeps the cell in − Cancer cells regains fetal appearance and function
its mature functioning state by producing proteins or hormones that characterize
embryonic and fetal periods of life
o some cancer cells produce new proteins located on
the cell membrane includes:
 Carcinoembryonic antigen (CEA) -
monitor lab for treatment
effectiveness,,should ↓

tumor suppressor genes
− Regulate cell growth by
suppressing growth
− Examples of tumor suppressor
gene:
 BRCA- 1 and BRCA -2
 APC gene
 P53
 α-fetoprotein(FP)
osmall cell carcinoma of lung produce hormones
(ordinarily produced by embryonic cells as tumor
cells)
Mutation:
− Inactivate genes, resulting in a loss of their tumor-
suppressing action
− Alteration in BRCA-1 or BRCA-2 : ↑ risk for breast and
ovarian cancer
− Alteration in APC gene : ↑risk for familial adenomatous
polyposis (precursor for colorectal cancer)
− Alteration in P53 : found in bladder, breast, colorectal,
esophageal, liver, lung and ovarian cancer

benign VS. malignant neoplasms

Benign neoplasms Malignant neoplasms

− Usually encapsulated − Rarely encapsulated
− Normally well differentiated − Poorly differentiated
− No metastasis − YES metastasis (MAJOR DIFFERENCES)
− Recurrence is rare − Recurrence is possible
− Slight vascularity − Moderate to marked vascularity
− Mode of growth is expansive, but not − Infiltrate and expansive growth
infiltrates
− Cell characteristics: Fairly normal; similar to − Cells abnormal, become more unlike parent
parent cells cells
** the degree of anaplasia (lack of differentiation) determines the malignant potential.

Development of Cancer
− Likely to be multifactorial
− Common belief: development of cancer is rapid, haphazard event
− Natural history of cancer: Occurs over a period of time by an orderly process comprising
several stages.
− Stages include: initiation  promotion  progression
1st Stage : Initiation Stage (Irreversible)
− Mutation in the cell’s genetic structure  potential for developing into a clone of neoplastic
cells (NOT ALL go on to establish a tumor b/c many undergo apoptosis)
o Caused by inherited mutation (an error that occurs during DNA replication, OR
o Exposure to a chemical, radiation, or viral agent.
− Does not have the ability to self-replicate and grow therefore, NOT A TUMOR CELL YET
o May remain undetected throughout lifetime unless further events stimulate the tumor to
develop
Carcinogens : cancer-causing agents capable of producing cellular alterations
− Many are detoxified by protective enzymes and harmlessly excreted
 But, if protective mechanism fails  carcinogens enter cell’s nucleus and alter DNA
− Some cells die or repair itself
 But if not before cell division  cell replicates into daughter cells, each with same genetic
alteration
− Characteristics : irreversible and additive
Chemical Certain chemicals (identified as cancer causing agents in later eighteenth century by
Carcinoge Percival Pott) Ex; soot scrotum cancer
ns o Later on..evidence indicated that people who are exposed to certain chemicals
over time had a higher incidence of getting cancer than others.
 Certain drugs
o that interacts with the DNA are identified as carcinogens. Ex; Pts w/ HL or NHL
or Multiple myeloma  treated with alkylating agents either alone or
w/radiation therapy (cyclophosphamide[cytoxan] and nitrogen mustard) &
immunosuppressive agents  increased incidence of acute myelogenous
leukemia (Secondary leukemia)
Secondary Leukemia
o Relatively refractory to induction of remission with combination chemotherapy
o Also been observed in those who had transplant surgery and taking
immunosuppressive drugs.
Radiation − Ionizing radiation can cause cancer in almost any human body tissue.
− When cells are exposed, one or both strands of DNA are damaged.
− Certain malignancies correlates w/radiation as a carcinogenic agent:
o Hiroshima and Nagasaki atomic bomb explosions  ↑leukemia, lymphoma,
thyroid cancer, and other cancers.
o Certain occupations such as radiologists, radiation chemists, and uranium
miners  ↑incidence of bone cancer
o Those who received radiation to head and neck area for treatment such as
acne, tonsillitis, sore throat, or enlarged thyroid gland  ↑ incidence in thyroid
cancer
o Children exposed to radiation during fetal life  ↑ incidence of childhood
cancers
o UV radiation  melanoma and squamous and basal cell carcinoma of the skin
(skin cancer is poorly responsive to systemic treatment)
Viral − Certain DNA and RNA viruses (called oncogenic)
Carcinoge  transforms cells that they infect
ns  induce malignant transformation.
o Epstein-Barr virus (EBV) in vitro Burkitt’s lymphoma and infectious
mononucleosis
− why an infectious dz in some persons and lymphoma in others is not
known
o AIDS  ↑ incidence of Kaposi sarcoma
o Hepatitis B virus  hepatocellular carcinoma
o human papillomavirus  ↑lesions that progress to squamous cell
carcinomas, such as cervical cancers
Genetic − Cancer-related genes  ↑ individual’s susceptibility to development of certain
susceptibil cancers
ity − Ex; those who carries genes BRCA1 or BRCA 2 has a 40% to 80% risk of
developing breast cancer in her lifetime. But, in reality, 95% of wome who develop
breast cancer do not have these genes.
− it is believed that ONLY 10% of cancers have a strong genetic link

2nd stage: Promotion (Reversible)

• Characterized by reversible proliferation of the altered cells (an important distinction
between initiation and promotion is the activity of promoters is reversible) key concept in
cancer prevention
o With the presence of promoting factors, the odds of cancer development are increased. Factors
include:
 Dietary fat
 Obesity
 Cigarette smoking
 Alcohol consumption
o Several promoting agents exert activity against specific types of tissues or organs.
− ex; smoking is a promoting agent in bronchogenic carcinoma.
 − Ex; smoking w/ alcohol  promotes esophageal and bladder cancers)
o Complete carcinogens are capable of both INITIATING and PROMOTING the development of
cancer.
− ex; cigarette smoking is a complete carcinogen
o latent period: a period of time ranging from 1 to 40 yrs elapses between the initial genetic
alteration and the actual clinical evidence of cancer.
− Latent period is associated w/ the mitotic rate of the tissue of origin and environmental
factors
o cell must reach a critical mass to become clinically evident (Most cancers develops in years or
even decades in lengths)
 1 cm tumor – usually detected by palpation
 0.5 cm tumor – the smallest that can be detected by MRI

Final stage: Progression

o Characterized by
1) increased growth rate of the tumor,
2) increased invasiveness, and
3) spread of the cancer to a distant site (metastasis)
− certain cancers have an affinity for particular tissue or organ as a site of metastasis (ex;
colon cancer spreads to liver)
− others are unpredictable (ex; melanoma)
− most frequent sites of metastasis : lungs, brain, bone, liver, and adrenal glands
o Metastasis is a multistep process
− Begins with rapid growth of primary tumor
− Develops tumor angiogenesis: process of the formation of blood vessels within the tumor
itself. Tumor angiogenesis is facilitated by tumor angiogenesis factors produced by the
cancer cells.
− As tumor grows, it grows into areas of least resistance by mechanically invading surrounding
tissues.
o Subpopulations (segments) of tumor cells are able to detach from primary tumor invade
the tissue surrounding the tumor  penetrate the walls of lymph or vascular vessels metastasis
to a distant site
− Facilitating factors:
1. Rapid proliferation causing mechanical pressure  leading to penetration of surrounding
tissues
2. Certain malignant cells have decreased cell-to-cell adhesion in comparison with normal
cells
o Some produce metalloproteinase enzymes: an enzyme that are capable of destroying the
basement membrane of tumor itself, lymph and blood vessels, muscles, nerves, and most
epithelial boundaries.
• Metastatic tumor cells travels to distant organs via lymphatic and hematogenous routes!
o Hematogenous metastasis involves several steps
− Begins w/ penetration of blood vessels by primary tumor cells via release of metalloproteinase
enzymes  cells enter the circulation  travel through the body  adhere to small blood
vessels of distant organs  cells penetrate the blood vessels of distant organs by releasing
again metalloproteinase enzymes.
− Most tumor cells are destroyed by mechanical mechanisms (ex; turbulence of blood flow) and
cells of the immune system. However, formation of a combination of tumor cells, platelets,
and fibrin deposits may protect some tumor cells.
o Tumor cells may be “trapped” in the first lymph node OR
o Skip metastasis: may bypass regional lymph node and travel more distantly.
− Ex; esophageal cancers
− Tumor cells that do survive must create vascularization and evade cells of the immune
system for their growth and development (like primary tumor site)
 • Vascularization is critical to the supply of nutrients to the metastatic tumor and to the
removal of waste products

Role of the Immune System

o Recognition and destruction of tumor cells
− Immune system has the potential to distinguish cells that are normal(self) from
abnormal(nonself) cells (ex; transplanted organs are recognized by immune system as
‘nonself’ and elicit an immune response may result in organ rejection
− Cancer cells can be perceived as ‘nonself’ and elicit an immune response  resulting
rejection and destruction.
o However, immune response that is mounted against cancer cells may be inadequate
to effectively eradicate them.
o May be inadequate b/c cancer cells arise from normal human cells
o immunologic surveillance: response of the immune system to antigens of malignant cells such
as TAAs.
− Cancer cells may display tumor-associated antigens (TAAs) on cell surface as a result of
malignant transformation.
− Malignant transformation occurs continuously. Immune response destroys the malignant cells
 Ex; lymphocytes detect and destroy abnormal cells or altered antigenic determinants.
− Immune surveillance will prevent transformed cells from developing into tumors.

Immune response against TAAs

Cytotoxic T 1. Dominant role in resisting tumor growth
cells 2. Capable of killing tumor cells
3. Important in the production of cytokines (ex; IL-2 and y-interferon) which
stimulate t cells, natural killer cells, B cells, and macrophages
Natural killer 1. Directly lyse tumor cells spontaneously w/out any prior sensitization
(NK) cells 2. Increased cytotoxic activity by the stimulation of Y-interferon and IL-2
Macrophages o Important roles in tumor immunity
and monocytes • Macrophages become nonspecifically lytic for tumor cells (activated by y-
interferon)
1. Phagocytosis
2. Processing of target cells
3. Macrophages also secrete cytokines
− Interleukin-I (IL-1) : coupled w/ processed antigen stimulates T
lymphocyte activation and production
− a-interferon : augments killing ability of NK cells
− tumor necrosis factor (TNF) : causes hemorrhagic necrosis of
tumors and exerts cytocidal or cytostatic actions against tumor cells
− colony-stimulating factors: regulate production of various blood
cells in the bone marrow and stimulate function of various WBCs
B 1. produce specific antibodies that bind and kill tumor cells by complement
lymphocytes fixation and lysis
− antibodies often detectable in serum and saliva of patient
− antibodies that are specific for a person’s own tumor and a similar tumor in
other person have been found in some patients.

Escaping from immunologic surveillance

o Immunologic escape: process by which cancer cells evade the immune system
o THEORY: cancer cells escape mechanisms from Immunologic Surveilance.
1) Suppression of factors that stimulate T cells to react to cancer cells (ex; stress2ndary
cancer)
2) Weak surface antigens allowing cancer cells to “sneak through” immunologic
surveillance
3) The development of tolerance of the immune system to some tumor antigens
 4) Suppression of the immune response by products secreted by cancer cells
5) The induction of suppressor T cells by the tumor
6) Blocking antibodies that bind TAAs, thus preventing their recognition by T cells.

Oncofetal Antigens
o Oncofetal Antigens: type of tumor antigen
− Found on both the surfaces and inside of cancer cells, found on fetal cells as well.
− Expression of the shift of cancerous cells to a more IMMATURE METABOLIC PATHWAY
(expression usually associated with embryonic or fetal periods of life)
− Reappearance of fetal cells is not well understood. However, it is believed to occur for the cell
regaining its embryonic capability to differentiate into many different types of cells.
− Examples:
Carcinoembryonic antigen (CEA)
o Found on normal fetal cells in gut, liver, and pancreas
o normally disappears during the last 3 months of fetal life.
o Malignant conditions: Also found on surface of cancer cells derived from GI tract (originally
isolated from colorectal cancer cells)
o Nonmalignant conditions: ↑CEA have been found in cirrhosis of liver, ulcerative colitis, and heavy
smoking
• PRESENTLY, major value of CEA is NOW used as an INDICATOR OF THE SUCCESS OF CANCER
TREATMENT – so MONITOR
− Ex; persistence of elevated preoperated CEA titers post surgery  tumor is not completely
removed
− Ex; rise in CEA post chemo or radiation therapy  recurrence or spread of the cancer.
a-fetoprotein (AFP)
o Produced by fetal liver cells
o Malignant conditions: Also produced by malignant liver cells
− Has diagnostic value in primary cancer of the liver (hepatocellular cancer)
− Also produced when metastatic liver growth occurs.
o Nonmalignant conditions: testicular carcinoma, viral hepatitis, and nonmalignant liver disorders
• Detection of AFT is of value in tumor detection & determination of tumor progression
Oncofetal antigens curreintly being studied
o CA-125: found in ovarian carcinoma
o CA-19-9: found in pancreatic and gallbladder cancer
o Prostate-specific antigen(PSA): found in prostate cancer

Classification of Cancer
Classified according to
1. Anatomic site
2. Histology (grading)
3. Extent of disease (staging)
Tumor classification provide a standardized way to
1. Communicate the status of the cancer to members of health care team
2. Assist in determining the most effective treatment plan
3. Evaluate the treatment plan
4. Factor in determining the prognosis
5. Compare like groups for statistical purposes

Anatomic Site Classification

 Identified by
o tissue of origin
o anatomic site
 o behavior of the tumor (benign or malignant)
o Carcinomas:
− Originate from embryonal ectoderm – skin and glands
− Originate from embryonal endoderm – mucous membrane linings of the respiratory
tract, gastrointestinal tract, and genitourinary [GU] tract
o Sarcomas:
− originate from embryonal mesoderm – connective tissue, muscle, bone and fat
o Lymphomas and leukemias originate from hematopoietic system

Histologic Classification
 Pathologically evaluating the APPEARANCE of cells and the degree of DIFFERENTIATION.
 4 grades used to evaluate abnormal cells based on the degree to which they resemble the tissue
of origin.
• Grade I: Cells differ slightly from normal cells (mild dysplasia) and are well differentiated.
• Grade II: Cells are more abnormal (moderate dysplasia) and moderately differentiated
• Grade III: Cells are very abnormal (severe dysplasia) and poorly differentiated.
• Grade IV: Cells are immature and primitive (anaplasia) and undifferentiated; cell of
origin is difficult to determine.  NOT GOOD NEWS!
• REMEMBER: tumors that poorly differentiated (undifferentiated) have a worse
prognosis than those that are closer in appearance to the normal tissue of origin.

Extent of Disease Classification

 Staging: classifying the extent and spread of disease. Based on description of the extent of
the disease(NOT appearance)
Ex; colon cancer; look at how much PENETRATION it went through rather than appearance
o Clinical Staging (based on American Joint Committee on Cancer (AJCC) tumor site-specific
rules)
− Determines the anatomic extent of the malignant disease process
 Stage 0: cancer in situ (envelope – inside has not infiltrated)
 Stage I: tumor limited to the tissue of origin; localized tumor growth
 Stage II: limited local spread
 Stage III: extensive local and regional spread
 Stage IV: metastasis
− Used as a basis for staging a variety of tumor types (ex; cervix cancer, hodgkin’s
lymphoma. BUT NOT FOR Leukemia)
• Clinical staging is done after diagnostic workup,,, but before treatment begins.

o TNM Classification System (Represents the AJCC modification of clinical staging (originally
developed by the International Union Against Cancer (UICC))
− Made to achieve consistency w/American medical practice
− Used to determine anatomic extent of disease involvement according to three
parameters:
Primary Tumor (T) : Tumor size and invasiveness
T0 No evidence of primary tumor
Tis Carcinoma in situ (has all the histologic characteristics of cancer except invasion – primary feature of
T1-4 TNM)
Tx Ascending degrees of increase in tumor size and involvement
Tumor cannot be measure or found
Regional Lymph Nodes (N) : presence or absence of regional spread to the lymph nodes
N0 No evidence of disease in lymph nodes
N1-4 Ascending degrees of nodal involvement
Nx Regional lymph nodes unable to be assessed clinically
Distant Metastases (M) : metastasis to distant organ sites
 M0 No evidence of distant metastases
M1-4 Ascending degrees of metastatic involvement of the host, including distant nodes
Mx Cannot be determined
• TNM cannot be applied to all malignancies (ex; NO for leukemia since not a solid tumor)

o Karnofsky Functional Performance Scale describes patient performance in terms of

functionality on a percentage basis.

Staging can be performed initially and at several evaluation points.

o Clinical diagnostic staging done at the completion of diagnostic workup to determine most
effective treatment plan
Diagnostic tests:
 Radiologic studies such as bone and liver scans
 Ultrasonography
 Computed tomography (CT)
 MRI
o Surgical Staging determined by surgical excision, exploration, and/or lymph node sampling
− Ex; staging hodgkin’s lymphomia: laparotony and splenectomy
o During laprotomy, lymph node biopsies may be done and margins may be
marked w/ metal clips that are used when radiotherapy is used as treatment
modality.
− Exploration surgical staging is less used b/c noninvasive diagnostic technology are
becoming increasingly sophisticated.

• The stage classification is NOT changed after the extent of dz is determined

• Original description remains part of the original record.
o If additional treatment is needed, or if treatment fails  retreatment staging is done.
o “restaging” classification (rTNM) is differentiated from stage at diagnosis as clinical
significance may be quite different.

Prevention and Detection of Cancer

PUBLIC EDUCATION
GOAL of public education: motivate learners to change their negative health behavior patterns to
achieve and maintain an optimal state of health.
− Care should be taken to minimize fear and anxiety
− Reinforce w/ large-type prints including graphics and key concepts  increases success of
educational efforts for elderly who may have visual and hearing deficits or difficulty
processing info, or those who has English is a second language.
TEACH – Nursing Implementation
1. Reduce or avoid exposure to carcinogens and cancer-promoting agents (ex; cigarette smoke &
sun exposure)
2. Eat balanced diet including vegetables, freshfruits, whole grains, adequate amounts
of fiber. Reduce amount of fat, preservatives, including smoked and salt-cured meats
containing high nitrite concentrations.
3. Participate in regular exercise regimen (ex; ≥ 30minutes moderate physical activity 5
times weekly)
4. Obtain adequate, consistent periods of rest (at least 6 to 8 hrs /night)
5. Have health examination on a regular basis including health history, physical examination,
specific diagnostic tests for common cancers in accordance with the guidelines published by the
American Cancer Society
6. Eliminate, reduce, or change perceptions of stressors and enhance the ability to effectively cope
w/stressors
7. Know seven warning signs of cancer (actually detect fairly advanced disease)
7 WARNINGS SIGN OF CANCER
 − Change in bowel or bladder habits
− A sore that doesn’t heal
− Unusual bleeding/discharge from an orifice
− Thicking or lump in beast or elsewhere
− Indigestion or difficulty swallowing
− Obvious chage in wart or mole
− Nagging cough or hoarseness
8. Learn & practice recommended cancer screenings on a timely basis (ex; colonoscopy in average-
risk people beginning at age 50 and every 10yrs thereafter)
9. Learn & practice self-examination (ex; DO testicular self-exam & SBE starting from EARLY
20’s)
10. Seek immediate medical care if notice any change in what is normal for you and if cancer is
suspected.
• Remember! Early detection of cancer has positive impact on prognosis!

DIAGNOSIS OF CANCER
− When pt has a possible diagnosis of cancer,,,
o Stressful time for pt and family
o Fear of the unknown.
Nursing Implementation
− Be available to actively listen to concerns and skilled in techniques that will engage the in
discussion about their cancer-related fear.
− Recognize that their anxiety may arise from myths and misconceptions about cancer (ex;
cancer is a “death sentence”, cancer treatment is worse than the illness)  correcting
misconceptions will ↓anxiety
− Nurses should learn to recognize their own discomfort when discussing about cancer.
o AVOID closed communication patterns that may shut off further communication
o AVOID false reassurance that everything will be all right (ex; it’s probably nothing)
o AVOID redirecting the discussion (let’s discuss that later)
o AVOID generalizing (everyone feels this way)
− Pt may need repeated explanations of diagnostic workup due to HIGH ANXIETY &
FEAR. Clear and repeated/reinforced explanations may be necessary. (written info is
helpful for reinforcement)
− Diagnositic plan for those cancer is suspected : includes health hx, identifying risk factors,
physical exam, specific diagnostic studies
o Health history: emphasis on risk factors such as
 family or personal history of cancer
 Exposure to or use of known carcinogens (exl cigarette smoking, exposure to
occupational pollutants or chemicals)
 Disease characterized by chronic inflammation (exl ulcerative colitis)
 Drug ingestion (ex; hormone therapy, previous anticancer therapies)
 Dietary habits, ingestion of alcohol
 Lifestyle
 patterns and degree of coping w/ perceived stressors
o Physical examination
 Should be thorough
 Particular attention should be given to
• respiratory system GI system (including colon, rectum and liver),
• lymphatic system (including spleen),
• breasts,
• skin,
• reproductive system (testes and prostate gland in men; cervix, uterus,
and ovaries in women), and
 • musculoskeletal and neurologic system
o Diagnostic studies
 Studies to be performed on will depend on the suspected primary or metastatic
site(s) of the cancer
 Examples of studies or procedures:
• Cytology studies (ex; Papanicolaou[Pap] test, bronchial washings)
• Tissue biopsy
• Chest x-ray
• CBC, chemistry profile
• Sigmoidoscopy or colonoscopy exam (include guaiac test for occult blood)
• LFT (ex; aspartate aminotransferase[AST])
• Radiologic studies (ex; mammography, ultrasound)
• Radioisotope scans (ex; bone, lung, liver, brain)
• CT scan (ex; spiral)
• Positron emission tomography (PET) scan
• Presence of tumor markers (ex; CEA, AFP, PSA, CA-125) or genetic
markers (ex; BRCA-1, BRCA-2)
• Bone marrow examination (if hematolymphoid malignancy is suspected or
to document metastatic dz)
Biopsy
o The only definitive means of diagnosing cancer
o Essential in planning a treatment plan
o Involves surgical acquisition of tissue from suspicious area for histologic examination by a
pathologist
 Will determine whether tissue is benign or malignant
 The anatomic tissue from which tumor arises
 Degree of cellular differentiation
o Needle or aspiration biopsy: used to obtain cells and tissue fragments through a large-bore
needle that is guided into tissue in question (ex; bone marrow aspiration; core biopsy of
prostate gland, breast, liver, and kidney tissues)
− To determine the presence of tumor,, cytologic analysis is performed
o Incisional biopsy: performed w/ scalpel or dermal punch
− Common technique for obtaining a tissue sample for making a diagnosis of cancer
o Excisional biopsy: involves removal of entire tumor
− Used for small tumors (smaller than 2 cm), skin lesions, intestinal polyps, and breast
masses
− Considered therapeutic as well as diagnostic
− If not easily accessible major surgical procedure such as laparotomy, thoracotomy,
craniotomy, is necessary to obtain a piece of tumor tissue.
o Endoscopic procedures: biopsy specimens of GI, respiratory, and GU systems

Collaborative Care
Goals and Modalities
• GOAL of cancer treatment : CURE, CONTROL, or PALLIATION
o Factors that determine therapeutic approach are:
 Tumor cell type
 Location
 Size
 And systemic extent of dz.
o Other important considerations
 Pt’s physiologic status (ex; presence of comorbid illness)
  Psychologic status
 Personal desires (ex; active treatment versus palliation of symptoms)
o American Society of Clinical Oncologists (ASCO) and the National Comprehensive Cancer Network
(NCCN)
 Developed evidence-based cancer treatment guidelines to guide the formulation of
appropriate treatment recommendations for individual patients.

CURE is •
Treatment is expected to have the greatest chance of disease eradication.
the GOAL Treatment may involve:
o
 Local therapies (surgery or radiation) alone or in combination
 With or without periods of adjunctive systemic therapy (ex; chemotherapy)
− Ex; basal cell carcinoma of skin  cured by surgical removal OR by several
weeks of radiation therapy
− Ex; Acute promyelocytic leukemia in adults  administration of several
chemotherapy over 6 months to several years in sequential phases known as
remission induction, remission consolidation, and maintenance therapy
− Head and neck cancers  cured with combination of surgery and pre-or
postoperative radiation, with or without chemotherapy
o In general, it appears that risk for recurrent disease is HIGHEST following
treatment completion, and gradually decreases the longer the pt. remains
disease free following treatment.
− Ex; pt with rapid mitotic rate is considered cured if not detected in a 2 year time
span
− Slower mitotic rate needs 20 or more dz-free years before she can be considered
cured
CONTROL • Cannot be completely eradicated but are responsive to anticancer therapies
is the • And as with other chronic illnesses such as diabetes mellitus and heart failure, can
GOAL be maintained for long periods of time with therapy.
− Ex; multiple myeloma, certain lung cancers, and chronic lymphocytic leukemia
1. Pts undergo initial treatment,
2. followed by maintance therapy for as long as the dz is responding OR until
adverse drug effects warrant discontinuation. (pts are often treated with variety
of regimens in a sequential pattern)
3. Evidence of tumor resistance (such as dz progression)  consider to change to
alternate therapy
o Pts are followed closely for signs and symptoms of recurrence or progression and
the cumulative effects of therapy.
PALLIATI • Relief or control of symptoms and the maintenance of a satisfactory quality
ON is the of life
GOAL − Ex; pain from bone metastasis or discomforts associated with
lymphedemaradiation therapy or chemotherapy are given to reduce tumor size
and relieve pain
− May be in effect for months to years
o 4 treatment modalities for cancer
 Surgery
 Radiation therapy
 Chemotherapy
 Biologic and targeted therapy
• For many cancers, “multimodality therapy” or “combined modality therapy” are used to
achieve the goal of cure or control for long period of time
• More effective but often increased toxicity.

Surgical Therapy
o Oldest form of local cancer treatment
o Was the only effective method of cancer diagnosis and treatment in the early days
o For many years, removing the cancer w/ surrounding tissue as much as possible was treatment of
choice
o This approach did not consider the ability of malignant cells traveling to other locations
o Made surgical cure possible only when tumor was localized and relatively small
o TODAY, surgery is employed to meet a variety of goals b/c
 Surgical techniques improved
 Expanded knowledge of tumor metastasis patterns
 Availability of alternate therapies

Prevention
− Prophylactic removal of nonvital organs - used to eliminate or reduce risk of cancer
development who have underlying conditions that ↑risk of developing cancer. (Must weigh risk
vs. benefits)
o Ex; total colostomy to those who have adenomatous familial polyposis  to prevent
colorectal cancer
o Ex; prophylactic mastectomy to those who have genetic mutations of BRCA-1 or BRCA-2
and a strong family hx of early-onset breast cancer prevent breast cancer

Cure and Control

− Objective is to remove all or as much resectable tumor as possible while sparing normal
tissue.
− Good prognostic indicatiors
o Small tumor size
o Clean tissue margins (free of dz surrounding the site of resection)
o Absence of node involvement
o Absence of abnormal tumor marker values
− Several principles applicable when surgery is used to cure or control cancer
1. Only as much tissue as necessary is removed
2. When appropriate, adjuvant (additional) therapy is used to treat unresectable gross
tumor or eliminate residual undetectable micrometastases. Risk for metastaic dz is
tumor dependent. The decision regarding adjuvant therapy is customized to pt’s
tumor type, stage, level of risk for residual or metastatic dz, comorbidities, and pt
preferences.
3. Preventive measures used to reduce surgical seeding of cancer cells
4. Usual sites of regional spread may be surgically removed to evaluate presence of
microscopic dz or to minimize the risk of recurrence.

Supportive and Palliative Care

− When cure or control is no longer possible focus shifts to preservation of quality of life at
the highest possible level for the longest period of time.
− GOAL – supportive care and palliation of SYMPTOMS
− Surgical procedures for supportive care that maximizes bodily function or facilitates cancer
treatment. Examples; (to ↑ function)
1. Gastric feeding tube insertion to maintain nutrition during head and neck cancer treatment
2. Creation of colostomy to allow healing of rectal abscess
3. Suprapubic cystostomy for pt with advanced prostatic cancer
4. Placement of venous access devices to deliver chemotherapy, pain med, parenteral
nutrition, blood products, and other supplements.
− Surgical procedures for palliation of symptoms associated w/ cancer include: (to ↓pain)
1. Debulking of tumor or radiation therapy to relieve pain or pressure
 2. Colostomy for the relief of a bowel obstruction
3. Laminectomy for the relief of a spinal cord compression

Rehabilitative Care
− Cancer surgery can produce a change in body image and function. Conjunction with the
diagnosis itself may be difficult for the pt to cope with these changes.
− Patient must be able to accept and cope with their altered body image and functional
deficit on a daily basis in order to maintain its quality of life.
− The emphasis of rehabilitative role of surgery is greatly increasing to increase the quality of
life.
1. Creation of a bladder reservoir at the time of cystectomy
2. Breast reconstruction after mastectomy
3. Spinal or joint stabilizing rods insertion to facilitate function
4. Create ostomies to facilitate function

Chemotherapy

Def: the use of chemicals as a systemic therapy for cancer

MAINSTAY for treatment of most solid tumors & hematologic malignancies. (ex; leukemia,
lymphoma, myeloma, and myelodysplastic syndromes).
 Chemotherapy is a therapeutic option that can offer
o cure for certain cancers,
o control other cancers for long periods,
o and offer palliative relief of symptoms when cure or control is no longer possible
GOAL – is to eliminate or reduce number of malignant cells present in the primary tumor and
metastatic tumor sites.
Several factors determine response:
1. Mitotic rate of tissue of origin
− Rapid mitotic rate, better response (ex; acute leukemia and small cell lung cancer)
2. Size of tumor
− Smaller tumor, the greater response
3. Age of tumor
− Younger the tumor, greater response. Rationale: newly developing tumors tend to have a
greater percentage of proliferating cells
4. Location of tumor
− Certain anatomic sites provide protected environment from chemotherapy effects.
 MOST DOES NOT CROSS BLOOD BRAIN BARRIER
− Only few drugs that cross the BBB are (ex; nitrosoureas, bleomyci,
temozolomide)
 New agents and techniques are being developed to cross this barrier
 OR maybe given intrathecally in the spine
5. Presence of resistant tumor cells
− Resistant malignant cells pass resistance to daughter cells, which continue to proliferate and
remain resistant.

Effect on Cells
 Chemotherapy effects is at the cellular level : relationship to the cell cycle.
 2 major categories of chemotherapeutic drugs: (often administered in combo to maximize
effectiveness)
1) Cell cycle phase-nonspecific chemotherapeutic drugs: effect on the cells during all
phases of cell cycle
− (include cellular replication & proliferation & those in resting phase(G0)
 2) Cell cycle phase-specific chemotherapeutic drugs: most significant effects during
specific phases of cell cycle
− (process of cellular replication or proliferation during G1, S1, G2, or M)
 When cancer first develops, most cells are actively dividing  most chemoagents are most
effective against dividing cells.
 As tumor increases, more cells become inactive and convert to resting state (G0)  during
chemo, cells can escape death by staying in the G0 phase. Therefore, a major problem is the
presence of drug-resistant resting and noncycling cells.

Classification of Chemotherapeutic Drugs

 Classified in general groups according to
 Molecular structure
 Mechanisms of action
 Particular class has many similarities. Yet, there are major differences in how drugs work, and
unique side effects within each class

Preparation and Administration of Chemotherapy

• ONLY those who are SPECIFICALLY TRAINED IN CHEMOTHERAPY HANDLING
TECHNIQUES SHOULD BE INVOLVED WITH THE PREPARATION AND ADMINISTRATION OF
ANTINEOPLASTIC AGENTS.
− Specific guidelines for administration of chemotherapeutic drugs b/c may pose an
occupational hazard.
− Drugs may be absorbed when preparing, transporting, or administering chemotherapy
o skin if there is droplet exposure,
 body fluids and excretions of persons receiving chemo
o Inhalation when reconstituting a powder in an open ampule

Methods of Administration
Intravenous (IV) routes - most common
IV Peripherally Nursing implementation
o Major concerns w/ IV administration o MONITOR for extravasation
 Venous access difficulties o Promptly recognize symptoms
 Device-or catheter-related infection  swelling
 Extravasation (infiltration of drugs into tissues  redness
surrounding the infusion site) causing local tissue  presence of vesicles on the skin,
damage & PAIN  w/out pain
o immediately turn OFF infusion
o IRRITANTS – damage the intima of the vein, causing o protocols for drug-specific
phlebitis and sclerosis and limiting future peripheral extravasation to minimize further
venous access tissue damange
- BUT WILL NOT CAUSE TISSUE DAMAGE IF
INFILTRATED IV push
Fresh IV run w/ open saline bag
o VESICANTS – if extravasation or infiltrated into skin Aspirate q few seconds and see flashback
(W/OUT PAIN) may cause severe local tissue of blood..If seen, it is okay
breakdown, ulceration & necrosis (or third But if not seen blood or if pain  stop
degree burn)  potential to progress to a deep, Give Antidote intradermally
wide crater that warrants closure with skin
grafts
Central vascular access device (CVAD)
o Advantages: (can give over 4 hrs)
 To minimize associated physical discomforts, emotional distress and risks of infection and
infiltration. (still IV)
 Using large blood vessels and permit frequent, continuous, or intermittent administration of
chemotherapy
  Can also be used to administer additional fluids, and electrolytes, blood products, parenteral
nutrition, other meds (antiemetics) and for venous sampling
 Avoiding multiple venipunctures for vascular access
 ↓risk for extravasation injury – but still can occur if displacement or damage to particular
device used for central venous access
 Facilitation of supportive therapies

o Disadvantages:
 Risk of systemic infection (if pt becomes immunosuppressed during therapy)
− Write down what site looks like, or any signs of infection

o Used for:
 Those with limited vascular access
 Intensive chemotherapy
 Repetitive or continous infusion of vesicant agents
 Projected long-term need for vascular access
Tunneled Catheter
 Single-, double-, or triple lumen o MUST VERIFY accurate placement
 Approximately 90 cm in length using CHEST-X-RAY before using
catheter
 Ranging from 1 to 2 mm in internal diameters
o care requirements
− Inserted with local or general anesthesia through  Cap chage
a central vein  Cleansing
− Tip rests in distal end of superior vena cava OR right  Heparin flush
atrium of the heart  Dressing change
− Other end is tunneled through subcu tissue and exits o complications - MONITOR
through incision on chest or abdominal wall  Occlusion
 Sepsis
o DACRON cuff : serves to stabilize catheter and may  Bleeding
↓incidence of infection by impeding bacteria
 Venous thrombosis
migration along the catheter beyond the cuff
o Groshong catheter : special tube of tunneled cath  Technical problems
− Closed ended with a slit valve(pressure activated  Local infection at exit site
valve) on the side of the distal end
− Therefore, this valves opens w/infusion, flushing,
or aspirating blood. When not used, valve closes,
preventing backflow of blood or entry of air
− Does not need heparin flushing or clamping
 Peripherally inserted Central Venous Catheters o Complications - MONITOR
(PICCs)  Catheter occlusion – thrombolytic
-only MD or specially trained nurse can place agent can be used to lyse
these obstructions
 Single-, or double-lumen  Phlebitis – usually appears within 7
 Up to 60 cm in length to 10 days following insertion
 Ranging from 24 to 16 guages • Signs
 Nontunneled − Redness
 Polymer catheters − Edema
− Tenderness along track
− Inserted at or just above the antecubital fossa of catheter line
− Tip ending in the distal 1/3 of superior vena cava • If sign present
− Use guide wire or forceps to advance the line. − Remove catheter
− Primarily used in cancer care for immediate central − Must culture tip of
venous access OR for infusion therapy that is beyond catheter
the capacity of pt’s existing, long-term venous
access device. • Arm in which PICC is in place should
NOT BE USED FOR BP or blood
o Used for drawings
− short term IV therapy – can be in place for up to 6
mons
− frequent administration of blood products
− frequent blood drawing
− intermittent or continuous drug infusions
Implanted Infusion Ports
− Consists of central venous catheter connected to an o Care requirements
implanted, single or double subcu injection port  Regular flushing
− Placed into desired vein and other end is connected o Complications
to a port that is sutured to the chest wall muscle  Clotting
− Surgically implanted in a subcu pocket on the chest  Catheter migration
wall  Infection
 Bleeding
− Port consists of metal sheat w/ self-sealing silicon
septum
 Thrombosis
− Accessed via septum w/special Huber Point Needle
 Air embolism
that has a deflected tip to prevent coring of the  Infection at the exit site or in the
septum pocket
− Available w/ 90degree tips for longer invusions  Formation of “sludge” –
accumulation of clotted blood and
drug precipitate may also occur
within port septum
Infusion Pumps
− Used primarily for continous infusion of o Flow rate can be affected by
chemotherapy by IV, subcutaneous, intraarterial,  Drug concentration
and epidural rountes  Length and diameter of Silastic
− Pumps worn externally or implanted surgically Catheter
 Implanted pumps are used primarily for  Pt’s body temp; dose alterations
intraarterial administrations – continous infusion may be required if pt has change
directly to the tumor while ↓systemic effects of in temperature or travels to higher
the drug altitutdes
 2nd septum can be used for bolus medication
administration o Complications
− Most commun use:  Infection
 Hepatic artery infusion for liver metastasis  Thrombosis
usually from primary colorectal cancer  Clotting of catheter
  Pump malfunction
− Catheter is attached to a pump apparatus consisting
two chambers
 Inner chamber: serves as the drug reservoir
 Outer chamber: contains vapor pressure
providing source of power for the pump
− Pump is implanted surgically in a subcutaneous
pocket
− Access to pump via a silicone septum with a Huber-
point needle

Regional chemotherapy administration

 Involves delivery of drug DIRECTLY TO TUMOR SITE
 Advantage: Higher concentrations of drug can be delivered to the tumor with ↓systemic
toxicity

Intraarterial Chemotherapy
o Delivers drug to the tumor via arterial vessel supplying the tumor
o Method: surgical placement of a catheter connected to an external infusion pump or an implanted
infusion pump
o Treatment used for
 osteogenic sarcoma
 Cancers of head and neck,Bladder,Brain,Cervix
 Melanoma
 Primary liver cancer
 Metastatic liver disease
o reduced systemic toxicity
 type of toxicity experienced by pt depends on the site of tumor being treated
Intraperitoneal Chemotherapy – PERITONEAL METASTASES
o Delivery of drug to peritoneal cavity.
− Generally infused into peritoneum in 1 to 2 L of fluid and allowed to “dwell” in the
peritoneum for a period of 1 to 4 hrs. Following the “dwell time,” the fluid is drained from
the peritoneum.
o Method: temporary Silastic catheters (Tenckhoff, Hickman, and Groshong) are percutaneously or
surgically placed into peritoneal cavity for short-term administration.
Alternate method: implanted port can be used to administer chemotherapy intraperitoneally
o Treatment used for
 Peritoneal metastases from primary colorectal and ovarian cancers
 Malignant ascites
o Complications
 Abdominal pain
 catheter occlusion, dislodgement, and migration
 infection
Intrathecal or Intraventricular Chemotherapy - CNS
o Cancers that metastasize to CNS are difficult to treat b/c of BBB often prevents distribution of
chemotherapy to this area (ex; common in breast, lung, GI tumors, leukemia, and lymphoma)
o Method used to treat metastasis to the CNS
 Intrathecal chemotherapy:
− involves lumbar puncture and injection of chemotherapy into subarachnoid space.
− However, results in incomplete distribution of the drug in CNS, particularly to the
cisternal and ventricular areas
 Intraventricular Chemotherapy:
− Ommaya reservoir, Silastic, dome-shaped disk with an extension catheter that is
surgically implanted through the cranium into a lateral ventricle, is inserted to ensure
 more uniform distribution of chemotherapy to the cisternal and ventricular areas
− Also precludes the use of repeated, painful lumbar punctures
o Complications of both
 HA, N/V, fever, nuchal regidity
Intravesical Bladder Chemotherapy - BLADDER
o Instillation of chemotherapy into bladder via urinary catheter and retained for 1 to 3 hrs.
− Promotes destruction of cancer cells and reduces incidence of recurrent disease
− Reduces urinary and sexual dysfunction
o Complications
 Dysuria
 Urinary frequency
 Hematuria
 Bladder spasms

Effects of Chemotherapy on Normal Tissues

o Chemotherapeutic agents cannot distinguish between normal and cancer cells.
o Chemotherapy induced side effects
− result of normal cells destruction – especially those that rapidly proliferates such as bone
marrow, lining of GI system, integumentary system (skin, hair, and nails)
− Caused by general cytotoxicity and organ-specific drug toxicities
o Body’s response to products of cellular destruction:
 Fatigue
 Anorexia
 Taste alterations
o General and drug-specific adverse effects
Acute Occurs during and immediately after drug administration
toxicity  Anaphylactic
 Hypersensitivy reactions
 Extravasation or a flare reaction
 Anticipatory nausea and vomiting
 Cardiac dysrhythmias
Delayed  Delayed nausea and vomiting
effects  Mucositis
 Alopecia
 Skin rashes
 Bone marrow suppression
 Altered bowel function (diarrhea or constipation)
 A variety of cumulative neurotoxicities depending on the affected component
of the nervous system (ex; central or peripheral nervous system or cranial
nerves)
Chronic Damage to organs such as the heart, liver, kidneys, and lungs
toxicities

Treatment Plan
o Single-drug can be and sometimes prescribed
− Combining agents– proved to be more effective in managing most cancers.
o Choosing agents with different MOA and Varying toxicity profiles
− Avoids tumor cell resistance and minimizes s/e
o Drug regimens are selected based on evidence used in specific cancers, and are sometimes
customized for individual pts
o Chemotherapy is most effective when
 Tumor burden is Low
 Therapy is not interrupted
  Pt receives the intended dose
• REMEMBER~! Each drug is carefully calculated according to pt’s body surface area (ex; based
on body weight & height) – FOLFOX treatment