This document provides information on cancer and its management. It discusses the epidemiology of cancer, mechanisms of tumor development and progression, characteristics of benign and malignant tumors, risk factors for cancer, methods for cancer prevention and screening, ways to classify cancers, and major treatment options. The key treatment options discussed are surgery, radiation therapy, chemotherapy, and hormonal therapy.

1. Alterations in Cell
Function and
Differentiation
Management of Neoplastic Disruptions

2. I. Epidemiology of cancer
 Uncontrolled and unregulated growth of cells
 Can occur in any age and ethnicity
 2nd most common cause of death in US
 1/5 deaths from cancer
 Over 50% under age 65

3. A. Cancer incidence and
prevalence by site and sex
Men Women
 Prostate  Breast
 Lung/Bronchus  Lung /Bronchus
 Colon/Rectum  Colon/Rectum
 Urinary Tract  Uterus
 Melanoma  Ovary

4. Leading
Cancer Site
Percentages

5. Estimated mortality
Men Women
 Lung/Bronchus  Lung/Bronchus
 Prostate  Breast
 Colon/rectum  Colon/rectum
 Pancreas  Pancreas
 Non-Hodgkin’s  Ovary
lymphoma

6. II. Host defense mechanisms in
control of cancer/neoplasia
A. Tumor antigens
- Tumor-associated antigens (TAAs)
result of malignant transformations
- Oncofetal antigen: found on surface & inside of
cells as well as fetal cells.
- CEA: carcinogen embryonic antigen
found in cancer cells of GI tract
- AFP: alpha-fetoprotein found in hepatocytes

7. B. Immunological defense
against CA
1. Immune surveillance mechanisms
Cytoxic T cells - kill tumor cells
Natural Killer cells - directly lyse tumor cells
Monocytes/Macrophages - important in
detection of CA cells. Secret cytokines
B cells – produce antibodies that bind to and kill
tumor cells

8. Macrophage functioning in response
to malignant target cells

9. 2. How cancerous cells evade
immune system
 Depends on ability of immune system to
recognize cancer cells as being different from
self cells
 Closely resemble cells they originate from
 Process where cancer cells evade immune
system is called immunologic escape

10. Tumor associated antigens on
surface of malignant cells

11. Blocking Antibodies Preventing T-
Cell from Destroying Malignant Cell

12. III. Normal vs. abnormal cell
growth and reproduction
A. Review of normal cell cycle
Reproduction of both healthy and malignant
cells follow cell cycle pattern
Time required for one tissue cell to divide and
reproduce into 2 identical cells

13. Phases of normal cell cycle
 G1 phase – post mitotic phase. Relatively
dormant - some RNA & protein synthesis
 S phase - DNA synthesis occurs
 G 2 phase – pre mitotic phase. Some RNA &
protein synthesis
 M Phase - cell division occurs
 G o Phase - resting phase

14. Cell Cycle

15. B. Cell proliferation
 Cells divide and reproduce
 Regulated so number of cells dividing = to
number dying or being shed
 Cell types fit into 3 large groups:
 Well differentiated neurons, skeletal and cardiac
muscle cells
 Parent or progenitor cells
 Undifferentiated stem cells

16. C. Cell differentiation
 Cells transformed into different and more
specialized cell types
 Adult cell achieves specific set of structural,
functional, and life expectancy characteristics
 Orderly process

17. Normal Cellular Differentiation

18. IV. Characteristics of Benign and
Malignant Neoplasms
A. Terminology
1. Tumor
2. Neoplasia

19. B. Benign Neoplasms
 Well differentiated cells that cluster together in
single mass
 Resemble cells of tissue of origin
 Slow, progressive rate of growth
 Expands, but unable to metastasize
 Usually enclosed in fibrous capsule

20. C. Malignant Neoplasms
 Less well differentiated cells
 Able to break loose, enter circulation or lymph
system, and form secondary malignant tumors
at other sites
 Grow rapidly, spread widely
 Potential to kill regardless of original location

21. Benign vs. Malignant

22. 1. Cancer cell characteristics
 Cells fail to undergo normal cell proliferation
and differentiation
 Anaplasia – term used to describe lack of cell
differentiation in cancerous tissue
 Cancer cells do not function properly and do
not die according to time frame of normal cells

24. 2. Invasion and metastasis
 Cancer spreads by:
 Direct invasion and extension
 Seeding of cancer cells in body cavities
 Metastatic spread through blood or lymph
pathways

25. Metastasis

26. Process of metastasis

27. Sites of bloodborne metastases

29. Metastasis to the brain

30. Metastasis to the bone

31. 3. Tumor growth
 Rate of tissue growth in normal and cancerous
cells depends on:
 Number of cells actively dividing or moving
through cell cycle
 Duration of cell cycle
 Number of cells being lost compared with number
of cells being produced
In blood cancers ex. leukemia, the cancer is rapidly dividing as it mimics
normal life-cycle of surrounding cells EXCEPT scheduled death.
The cancer cells persist.

32. V. Carcinogenesis and major
risk factors
A. Carcinogenesis
1. Terms important in carcinogenesis
 Two mutational routes that result in
uncontrolled cell proliferation are
characteristic of cancer:
 stimulation of gene causing hyperactivity
 inhibition of gene causing inactivity

33. a. Oncogene
 Cancer causing gene – altered gene
 Gene that promotes autonomous cell growth in
cancer cells
 Mutations of normal growth-regulating genes
Oncogenesis: mechanism by which normal cells mutate into cancer cells
Only one single altered gene copy can cause an overgrowth

34. b. Proto-oncogene
 Normal growth-promoting gene thought to be
active when appropriate growth-promoting
signals reach cell
 “On switch” for cellular growth
If there’s a mutation in the proto-oncogene, then the cell is released from…?

35. c. Anti-oncogene/Suppressor gene
 Gene that inhibits proliferation of cells
 Genetic signal that normally inhibits
proliferation is removed – causes unregulated
growth
 “Turns off” or regulates unneeded cellular
proliferation

36. Stages in Development of a Malignant Neoplasm

37. 2. Cancer cell transformation
a. Initiation – 1st Step
 Exposure of cells to appropriate doses of
carcinogenic agent - makes them susceptible to
malignant transformation
 Irreversible alteration in cell’s genetic structure
 Not usually significant to cells until 2 nd step of
carcinogenesis
Physical/chemical/biological agents, ex. virus, can cause cancer

38. 2. Cancer cell transformation
b. Promotion – 2nd step
Unregulated accelerated growth in already
initiated cells by various chemical and growth
factors
Characterized by reversible proliferation of
altered cell if promoter substance removed

39. 2. Cancer cell transformation
c. Progression – 3rd step
Cellular changes formed during initiation and
promotion assume increased malignant behavior
Cells divide in uncoordinated fashion, invade
and destroy neighboring tissue

40. Process of Cancer Development

41. Initiation, Promotion and Progression

42. B. Risk factors
1. Heredity
 Predisposition to approx. 50 types of cancer
has been observed in families
 10% of cancers have strong genetic link

43. 2. Hormones
 Thought to drive cell division
 Women – breast, ovary, endometrium
 Men – prostate, testis

44. 3. Immunologic mechanisms
 Cancer associated with impairment or decline
in immune system. See increase in:
 People with immunodeficiency disease
 Organ transplant pts taking immunosuppressant
drugs
 Elderly

45. 4. Chemical carcinogens
 Cigarette smoke
 Workplace carcinogens
 Air pollution
 Diet
 Alcohol

46. 5. Radiation
 Ultraviolet exposure
 Ionizing radiation exposure
 Electromagnetic field exposure

47. 6. Oncogenic viruses
 Incorporate themselves into genetic structure
of cell
 Alter future generations of cell
 Human papillomavirus (HPV)
 Epstein-Barr virus (EBV)

48. VI. Prevention and early
detection of cancer
 Primary Prevention
 Secondary Prevention
 Tertiary Prevention

49. A. Preventive measures
 Important role for RN
 Must have knowledge and skills to educate
community about:
 health-related behaviors
 risk factors
 screening and detection methods

50. 1. Patient education
 Numerous factors influence degree of
knowledge people have about CA risk factors
and health promoting behaviors:
 race
 cultural influences
 level of education
 income
 age

51. Seven Warning Signs of Cancer
 C
 A
 U
 T
 I
 O
 N – nagging cough/hoarseness
 See Lewis Table 16-8

52. B. Screening procedures for
different types of cancer sites
 SBE for breast cancer
 Rectal exams for prostate cancer
 Sigmoidoscopy/colonoscopy
 Occult blood for colon cancer

53. VII. Ways of classifying cancer
Tumors are classified on basis of:
 cell type
 tissue of origin
 benign or malignant
 degree of differentiation
 anatomic site
 function

54. A. By anatomic site
Epithelial tissue - carcinomas
Connective tissue - sarcomas
Lymphatic tissue - lymphomas
Glial cells of the CNS - gliomas
Blood forming organs (mainly bone marrow)-
leukemias

55. B. Histological Analysis
(“Grading”)
Grade I: cells differ slightly from normal cells and
are well differentiated
Grade II: cells are more abnormal and moderately
differentiated
Grade III: cells are very abnormal (severe
hyperplasia) and poorly differentiated
Grade IV: cells are immature and primitive and
undifferentiated, no resemblance to tissue of
origin

56. Mutation of a Cell Line

57. C. Extent of disease (“Staging”)
 Describes location and pattern of spread of tumor
 TNM most common:
 Tumor (primary)
 Node
 Metastasis

58. Clinical Staging
 0 - CA in situ
 I - tumor limited to tissue or organ
 II - limited local spread
 III - extensive local and regional spread
 IV - metastasis

59. VIII. Major treatment options in
cancer treatment
 Goals - Cure, Control, Palliation
 Used to be considered cured if no cancer
recurrence for 5 years after treatment
 Widespread invasions associated with poor
prognosis
 Choice of Rx depends on staging - more
metastasis = more aggressive approach

60. Goals of cancer treatment

61. A. Surgery
 Approx 90% treated surgically
 Main benefit - removal of tumor with minimal
damage to other body cells
 Surgery involves risk
 Usually followed by radiation or
chemotherapy

62. Goals of surgery

63. B. Radiation
Used to interrupt cellular growth. Can:
 immediately kill cells
 delay or halt cell cycle progression
 cause damage in nucleus that causes cell death
after replication

64. Types of Radiation
1. External radiation - source placed outside the
body
“Lethal tumor dose”: will eradicate 95% of tumor while
preserving normal tissue
2. Internal radiation/Brachytherapy - source placed
close to or directly in the tumor site
Seeds, beads, needle, catheter, etc.
Brachytherapy: limits radiation to duration of treatment?
Time, Distance, Shielding

65. Linear accelerator treatment for
head and neck cancer

66.  Wet desquamation
from RT
 Dry desquamation
from RT

67. C. Chemotherapy
 Systemic administration of anticancer
chemicals
 Most agents are cytotoxic - interfere with
some aspect of cell division
 More rapidly dividing cells more susceptible
 Normal cells die too

68. Goals of chemotherapy

69. 1. Classifications
a. Cell cycle specific
 Destroys cells in specific phases of cell cycle
b. Cell cycle non-specific
 Act independently of cell cycle phases
 Often combine with cell-cycle specific to
increase number of cells killed

70. Action Sites of CCS [Antineoplastic] Drugs

71. Action Sites of Non–Cell Cycle–Specific
Antineoplastic Agents

72. 2. Examples
 See Table 16-9 “Classifications of
Chemotherapy Drugs” in Lewis

73. Chemotherapy/survival relationship

74. 3. Routes of administration
 Topical, Oral, IM, IV, SQ, Arterial,
Intercavity, Intrathecal routes
 Depends on type of drug, required dose, and
type, location, and extent of tumor
 Patients frequently have central lines placed
for chemotherapy due to the frequency of
treatment and vesicant (caustic) nature of the
medications

75. PICC Line placement

76. Tunneled Central Line

77. Huber needle access of implanted port

78. 4. Extravasations
 “Escape of fluids into the surrounding tissue”
 Such as in IV infiltration. Apply ice to slow
circulation.
 Can cause tissue necrosis and damage to
underlying tendons, nerves, and blood vessels
 Treatment - stop drug immediately and apply
ice. Notify MD

79. 5. Toxicity and side effects
 Can be acute or chronic
 Cells with rapid growth rates are very
susceptible to damage
 Various body systems may be affected

80. 5. Toxicity and side effects (cont.)
GI system - N & V most common; stomatitis
Hematopoietic system - depressed bone marrow function
 anemia, thrombocytopenia, etc.
Renal system - damage by direct effects during excretion or
accumulation of end products after cell lysis
Hair loss (alopecia) - hair cells are rapidly dividing
Cardiopulmonary system - can cause cumulative cardiac
toxicities. Toxic effects on lung function.
Sometimes necessitates transplant.
Reproductive system - affects testicular & ovarian function
Some choose to bank their gametes.

81. 6. Nursing consideration for
patients on chemotherapy
 Fluid and electrolytes
 Infection and bleeding
 thrombocytopenia, leukopenia
 Skin Problems
 Hair Loss
 Nutritional Concerns
 d/t stomatitis, anorexia, N/V
 Chemotherapy administration
 Self protection

82. D. Hormonal therapy
 Used for cancers that are responsive to or
dependent on hormones for growth:
 breast
 prostate
 adrenal glands
 endometrium

83. E. Biotherapy
 Active Immunotherapy – acts as nonspecific
stimulant of immune system
 Passive Immunotherapy – transfer of cultured
immune cells into person with cancer
 Sensitized NK cell
 T lymphocytes
 Cytokines

84. Biologic Response Modifiers
 Changes person’s biologic response to cancer
 Cytokines: IFNs, ILs that bind
 Monoclonal antibodies: produced by B-cells
 Hematopoietic growth factors: epogen?

85. F. Targeted therapy
 Drugs that target processes of cancer cells
specifically
 Leave normal cells unharmed

86. G. Bone marrow and peripheral
blood stem cell transplantation
 High dose chemo and radiation therapy used to
ablate or suppress bone marrow
 Self or donor stem cells transplanted

87. Stem cell transplant