1. WHAT’S UNDER YOUR SKIN?
Skin Care of Breast Cancer Patients Undergoing Standard External Beam Radiation
Donna M. Braunreiter RN BSN OCN
MSN Student
Alverno College
Spring 2009, MSN 621
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2. Objectives Explain effects of external beam radiation therapy.
Briefly describe genetic mechanisms involved in radiation.
Summarize the acute physiologic mechanisms of inflammation.
Describe the structure and function of skin.
Identify breast skin changes after radiation treatment.
Review nursing care for breast cancer patients undergoing radiation therapy.

3. Directions
To move to the next slide, click this To move to the previous slide, click this To return to the beginning, click this To return to the topics section, click this

4. SKIN STRUCTURE AND FUNCTION
RADIATION
SKIN STRUCTURE AND FUNCTION
GENETICS
BREAST SKIN CHANGES
INFLAMMATION
NURSING CARE AND PATIENT EDUCATION

5. RADIATION
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6. Radiation Treatment
Skin reaction is the most common side effect during breast cancer radiation treatments
Over 90% of women receiving radiation for breast cancer will develop some skin changes during their course of treatment

7. Radiation Interacts with all biological materials in its path
Direct and indirect damage to cells causes DNA changes
Causes many molecular responses that induce cellular mechanisms for DNA repair, cell cycle arrests, and apoptosis

8. Radiation Major effect on dividing cells is reproductive death
Leaves cells unable to reproduce
Radiosensitivity of cell determines degree of injury and when it will happen

9. Radiation Direct Effect
DNA absorbs radiation
The atoms become ionized and damaged
Less common than indirect damage
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10. Radiation Indirect Effect
Water molecules surrounding DNA are ionized
Creates highly reactive free radicals such as hydroxyl radicals, peroxide, hydrated electrons, and oxygen radicals
These radicals interfere with DNA and cause damage and strand breakage
Common because 80% of a cell is water

11. Radiation Damage
Direct and indirect damage break bonds in DNA backbone
Results in loss of base, nucleotide, or one or both strands of DNA
Single-strand DNA breaks are repaired using the opposite strand as a template
Can result in mutation if not repaired correctly

12. Radiation Damage Double-strand DNA breaks related to cell killing
Results in mitotic death
X-rays are sparsely ionizing and cause locally clustered damage
Leads to clinically significant events
DNA Structure
United States National Library of Medicine

13. CONTROLS CANCER CELLS BY
Radiation
CONTROLS CANCER CELLS BY
Inducing apoptosis
Causing permanent cell cycle arrest or terminal differentiation
Inducing cells to die of mitotic catastrophe

14. Apoptosis Programmed cell death
Radiation damage triggers signaling cascades which causes cell self-destruct mechanisms
Characteristics are nucleus fragmentation and blebbing
Tumors undergoing apoptosis have good clinical response

15. Cell Cycle

16. Cell Cycle Death/Terminal Differentiation (Denucleation)
Cells can arrest in any phase of cell cycle
Radiation damage mainly in G1 and G2 phases
Normal cells and cancer cells retaining p53 function block in G1
Cancer cells with p53 loss or mutation block in G2 phase
G2 arrest related to cellular repair of DNA radiation-induced DNA damage

17. Radiation Effects Radiosensitive Radioresistant
Cells renewing rapidly with little or no differentiation
Examples are skin cells, mucous membranes, and hematopoietic stem cells
Cells that do not divide regularly or at all and are highly differentiated
Examples are muscle cells and nerve cells

18. Radiation Effects Radiosensitive Radioresistant Acute effects
Damage within weeks to months of exposure
Temporary
Normal cells affected are capable of repair
Dependent upon dose-time-volume factors
Late effects
Damage months or years after first exposure
Permanent
Damage becomes more severe as time goes on
Dependent upon dose-time-volume factors

19. Radiation Effects Radiosensitive Radioresistant
Higher doses over shorter periods of time to larger volumes of tissues result in more severe acute reactions
Acute damage results from depletion of actively proliferating parenchymal or stromal cells
Characteristics are vascular dilation, local edema, and inflammation
Severity of late effects more dependent upon total dose delivered and volume if tissue irradiated
Damage to endothelial cells or connective tissues results in late effects occurring as a result of narrowing or occlusion of small vasculature and fibrosis

20. Radiation Effects
Acute and late side effects from radiation therapy are LOCAL and ONLY affect tissues receiving treatment
Presence and severity of acute effects can not predict late effects of radiation
Late reactions such as tissue necrosis or dense tissue fibrosis can occur independently of acute reactions

21. SUPINE POSITION
Most common position for breast cancer radiation therapy
MUST be used if lymph nodes need to be treated
May involve radiation exposure to heart, lungs, ribs, and contralateral breast
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22. PRONE POSITION
Used for women with larger pendulous breast, cardiac and/or pulmonary comorbidities
Possible improved dose homogeneity
Potential reduction in lung and heart irradiation
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23. Patient-Related Considerations
Normal age-related changes:
thinning of the epidermis and dermis,
diminished elasticity,
decreased dermal turgor,
which results in delayed healing.
Nutritional status is also important for healing.

24. What is the effect of radiation on cells?
A. Reproductive death of cells throughout the body
B. Reproductive death of cells in the treated area only
C. Radiation skin reactions cause internal injuries.
D. Radiation helps repair DNA damage.

25. Click here to return to question
Wrong answer, try again.
Radiation only affects the area being treated and causes damage to DNA.
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26. Correct! Radiation causes the reproductive death of cells in the treated area only.

27. GENETICS
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28. Chromosome: rod-shaped molecule of DNA threaded around proteins containing specific genes that carry hereditary information Histones are proteins that act as spools around which DNA winds, as compaction is necessary to large genes inside cell nuclei; histones also function as gene regulators
United States National Library of Medicine

29. GENE: biological unit of hereditary; segment of DNA needed to contribute to a function and specifies a trait
United States Library of Medicine

30. Radiation effect on genes
Ionizing radiation causes phosphorylation of histone H2AX (forming gamma-H2AX)
Reaction dependent on ataxia telangiectesia mutated (ATM) molecule
Followed by accumulation of 53BP1, a protein acting as central mediator for critical pathways, including phosphorylating (which conveys the DNA damage signal to) tumor suppressor protein p53

31. Genetics in Radiation
Next, phosphorylating the ATM protein amplifies the damage signal
And recruits proteins critical for repair, such as the BRCA1 and HDAC4
Which allows a G2 cycle checkpoint
53BP1 important in double-strand DNA damage sensing, repair, and tumor suppression

32. Genetics in Radiation
HR (homologous repair) efficient in late S or G2 phase when sister chromatids have replicated but not separated
Repair is cell cycle dependent
Undamaged homologous chromosome or sister chromatid or replicated chromosome is used as a template to fill in missing DNA sequences in damaged chromosome

33. Genetics in Radiation
Human tumor cells block in G2 after DNA double-strand damage, when repairs are detectible, and irradiation induced G2 checkpoint allows more time for cells to undergo HR (homologous repair) and survive radiation

34. Genetics in Radiation
NHEJ (nonhomologous endjoining) is where blunt ends of chromosomes severed by radiation are directly rejoined
Less cell cycle dependent
Highly mutagenic due to template-free rejoining lacks specificity of HR
Ends of different chromosomes can be rejoined, leading to chromosomal aberrations or expression of dangerous fusion proteins

35. p53 Tumor Suppressor Gene
p53 stops activity of tumors
Loss or mutation of p53 predisposes to cancer
(e.g. inheriting only one functional copy of p53 gene from parents)
p53 protein binds DNA and stimulates another gene to produce protein p21 and blocks next stage of cell division
Mutant p53 no longer binds DNA and does not interact with p21
Results in p21 unable to act as a stop signal
Cells divide uncontrollably

36. Genetics in Radiation
Ras, Raf, and EGFR alter cellular sensitivity to radiation, but exact mechanisms unknown
Ras is a proto-oncogogene (portion of DNA that regulates normal cell proliferation and repair)
Raf is a gene coding for protein kinase
EGFR (epidermal growth factor receptor) found on surface of some cells and where epidermal growth factor binds, causing the cells to divide

37. What is a common gene that can lead to many cancers it is mutated or lost?
A. EGFR
B. p 21
C. p 53
D. Ras

38. Click here to return to question
Wrong answer, try again.
EGFR is epidermal growth factor, Ras is a proto-oncogene, and p21 is a protein influenced by p53 and acts as a stop signal in the cell cycle.
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39. Correct! p 53

40. INFLAMMATION
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41. Inflammation Reaction of vascularized tissue to local injury.
Causes are many and varied.
Commonly it results from an immune response to infection organisms.
Other causes are trauma, surgery, caustic chemicals, extremes of heat and cold, and ischemic damage to body tissues (Porth, 2005).

42. Five Cardinal Signs of Inflammation
Redness
Swelling
Heat
Pain
Loss of function
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43. Acute Inflammation Two major components VASCULAR CELLULAR
Inflammatory mediators, acting together or in sequence, amplify the initial response and influence its evolution by regulating the subsequent vascular and cellular responses (Porth, 2005).
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44. Vascular Stage Constriction of small blood vessels in injured area
Vasoconstriction followed rapidly by vasodilation of the arterioles and venules
Causes the area to becomes congested and results in redness and warmth

45. Vascular Stage
Capillary permeability increases causes swelling, pain, and impaired function
Movement of fluid from capillaries into interstitial spaces (swelling) dilutes the offending agent
Extravasation of plasma proteins into extracellular spaces causes exudate
Blood stagnation and clotting of blood in the capillaries around the injury site; aids in localizing the spread of infectious microorganisms

46. Vascular Stage FIRST is immediate transient response
SECOND is immediate sustained response which occurs with more serious injury and continues for several days and damages vessels in the area
THIRD is a delayed hemodynamic response, which increases capillary permeability that occurs 4 to 24 hours after injury, seen with RADIATION types of injuries

47. Two types of leukocytes involved--granulocytes and monocytes
Cellular Stage
Movement of phagocytic white blood cells (leukocytes) into area of injury
Two types of leukocytes involved--granulocytes and monocytes
Requires the release of chemical mediators from sentinel cells (mast cells and macrophages) already positioned in tissues

48. Cellular Stage: Granulocytes
Granulocytes divided into three types
neutrophils, eosinophils, and basophils.
Neutrophils are primary phagocytes; arrive within 90 minutes to injury site; contain enzymes and antibacterial substances that destroy and degrade engulfed particles.

49. Segmented Neutrophils

50. Cellular Stage: Monocytes
Mononuclear phagocytes are largest of white blood cells
Last 3 to 4 times longer than granulocytes and survive longer in the tissues.
Help to destroy agent, aid in signaling processes of specific immunity, and help to resolve inflammatory process.
Arrive by 24 hours and at 48 hours monocytes and macrophages are predominant cells at injury site
Engulf larger and greater quantities of foreign materials and migrate to lymph nodes.

51. Phases of Acute Inflammation Response
MARGINATION Leukocytes increase adhesion molecules, slow migration, and move along periphery of blood vessels

52. Phases of Acute Inflammation Response
EMIGRATION Leukocytes pass through capillary walls and migrate into tissue spaces

53. Phases of Acute Inflammation Response
CHEMOTAXIS Leukocytes in tissues guided by cytokines, bacteria, and cell debris

54. Phases of Acute Inflammation Response
PHAGOCYTOSIS
Neutrophils and macrophages engulf and degrade bacteria and debris
Phagocytosis
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55. Inflammatory Mediators
CYTOKINES
Polypeptide products of various cell types-
mostly lymphocytes and macrophages
modulate functions of other cell types
COLONY-STIMULATING FACTORS
directs growth of immature marrow precursor cells
INTERLEUKINS (Ils)
INTERFERONS (Ifs)
TUMOR NECROSIS FACTOR

56. Inflammation with Chemical Mediator
INFLAMMATORY RESPONSE Swelling, redness, and tissue warmth (vasodilation and increased capillary permeability)
CHEMICAL MEDIATOR Histamine (fast acting and causes dilatation and increased permeability of capillaries), Prostaglandins, Leukotrienes, Bradykinin, Platelet-activating factor (attracts neutrophils)

57. Inflammation with Chemical Mediators
INFLAMMATORY RESPONSE Tissue Damage
CHEMICAL MEDIATOR Lysomomal enzymes and products released from neutrophils, macrophages, and other inflammatory cells

58. Inflammation with Chemical Mediators
INFLAMMATORY RESPONSE Pain
CHEMICAL MEDIATOR Prostaglandins Bradykinins

59. Inflammation with Chemical Mediator
INFLAMMATORY RESPONSE Leukocytosis
CHEMICAL MEDIATOR Interleukin-1 Other Cytokines

60. What are the five major signs of inflammation?
A. Redness, pus, fever, pain, and swelling
B. Pain, swelling, numbness, tingling, and cold
C. Heat, pain, swelling, pus, and loss of function
C. Heat, pain, swelling, pus, and loss of function
D. Redness, swelling, heat, pain, and loss of function

61. Click here to return to question
Wrong answer, try again.
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62. Correct! Redness, swelling, heat, pain, and loss of function.

63. SKIN STRUCTURE AND FUNCTION
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64. SKIN Largest organ of the body
Receives approximately one-third of heart’s oxygenated blood
Body’s FIRST defense mechanism

65. Skin Three Layers Epidermis (outer layer) Dermis (middle layer)
Subcutaneous tissue (inner layer)
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66. Skin Structure

67. Epidermis Multi-layered and impermeable
Outer layer that forms a resistant cover and permeability barrier of varying thickness
Renews itself continuously through cell division in deepest (basal) layer
Undergoes keratinization to produce scales that are shed from outer layer
Avascular and receives nutrients from dermis

68. Epidermal Layers
Stratum corneum is outermost layer composed of flattened dead cells and is about 25% of total thickness
Stratum granulosum is thin transitional layer
Stratum spinosum (squamous cell) is viable layer made up of mainly post-mitotic cells
Basal cell layer is viable and deepest layer where majority of cell division occurs

69. Layers of Epidermis

70. Terminal Transition in Epidermis
Half the cells produced in basal layer undergo mitosis
After dividing, cells leave basal cell layer and enter stratum spinosum and then stratum granulosum
This is where the cells flatten, lose organelles, and become mature, keratininized cells of the stratum corneum
Cells detach and desquamate, but are continually replaced by cells produced in basal layer (turnover process is 30 days)

71. Dermis Tough and durable middle layer 1-3mm thick
Gives skin strength, elasticity, and softness
Protects deeper structures from injury
Contains blood vessels that regulate body temperature and provide nourishment to epidermis; also contains nerves, hair follicles and various glands
Interacts with epidermis during wound repair

72. Subcutaneous Tissue Composed mostly of adipose tissue
Cushion to physical trauma
Insulator to temperature change
Energy reservoir
Nerves, blood vessels, and lymphatics run through it

73. Functions of Skin PROTECTION - MOST IMPORTANT!
Regulation of body temperature
Sensory perception
Vitamin D production
Provides an active system of immunologic defense (dermal lymphocytes, mast cells, mononuclear phagocytes, Langerhans cells)
Excretion

74. Skin
First line of defense against bacteria and foreign substances, physical trauma,
heat, or rays
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Protection works by: (1) eccrine gland sweating (2) insulation by the skin and subcutaneous tissue (3) regulation of cutaneous blood flow (vasoconstriction and vasodilation) (4) muscle activity (shivering)

75. What is the major function of the skin?
A. Vitamin D Production
B. Sensory perception.
C. Regulation of body temperature.
D. Protection

76. Click here to return to picture
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77. Correct! Protection.

78. BREAST SKIN CHANGES
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79. Radiation Changes Reflect injury occurring mostly in the epidermis
Primary target for acute radiation skin reactions is the basal cell layer
Entire epidermis turns over in 30 days

80. Radiation Changes
Early erythema within few hours after radiation and subsides after hours
Inflammatory response from histamine-like substances that cause dermal edema from the permeability and dilatation of capillaries

81. Radiation Changes
Main erythematous reaction occurs 3-6 weeks after radiation begins and is due to a varying severity loss of epidermal basal cells
Basal cell density changes with higher doses of radiation
Reddening of the skin due to a secondary inflammatory reaction or hyperemia

82. Radiation Changes
Higher radiation doses reduce number of mitotic cells and increase in degenerate cells
When cells are not being reproduced at the same rate in the basal cell layer and the normal migration of cells to stratum corneum continues, epidermis is denuded in time equal to natural turnover (30 days)

83. Dry Desquamation
If enough numbers of clonogenic cells (cells giving rise to a clone of cells) remain to replace injured cells, there is atypical thickening of the stratum corneum
The populations of the basal-layer stem cells become depleted in the radiation treated area
This can result in dry flaking, scaling, and itching in the treated area

84. Dry Desquamation
Adapted with permission by Nature Publishing Group: Leukemia, volume 17, issue 7, 2003.
www. Nature.com/leu/journal/v17/n7images/240991f1.jpg

85. Moist Desquamation
If new cell proliferation is inadequate, there is exposed dermis with oozing of serum
Repopulation of the basal cell layer of epidermis after irradiation is mainly from surviving clonogenic cells (cells giving rise to a clone of cells) within the irradiated area
If the treated area is completed denuded of clonogenic epithelial cells, then healing results from division and migration of viable cells from skin around the irradiated area

86. Moist Desquamation
Used with permission , Adapted from Ostomy Wound Management , volume 51, issue 10, Managing Radiation Skin Injury

87. Acute Skin Reactions
ERYTHEMA Redness that outlines treatment field and intensifies as treatment continues Increased skin temperature Edema Follows after 2-3 weeks after standard fractionated radiation and resolves days after last treatment

88. Acute Skin Reactions
DRY DESQUAMATION Dryness Flaking Peeling Pruritus Following 3-4 weeks of standard fractionated radiation and resolves 1-2 weeks after completion of treatments

89. Acute Skin Reactions
HYPERPIGMENTATION Tanned appearance Following 2-3 weeks of standard fractionated therapy and is usually resolved in 3 months to 1 year after treatment but may be chronic

90. Acute Skin Reactions
MOIST DESQUAMATION Bright erythema Sloughing skin Exposed dermis Serous exudate Pain

91. Acute Skin Reactions
MOIST DESQUAMATION Can occur with radiation or with trauma or friction and most recovery usually 2-4 weeks after completion of treatment SKIN REGROWTH New skin is smooth, pink, thin, and dryer Depends upon severity but usually is complete 2-3 months after therapy

92. Late Skin Reactions
PHOTOSENSITIVITY Enhanced erythema over skin exposed to UV radiation from sun and tanning bed/booths Begins during treatment and is lifelong

93. What develops after 3 -4 weeks of radiation with symptoms of dry, flaking, and peeling skin?
A. Dry desquamation
B. Erythema
C. Moist desquamation
D. Hyperpigmentation

94. Click here to return to question
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95. Yes! Dry desquamation.

96. NURSING CARE AND PATIENT EDUCATION
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97. Nursing Care
Perform skin assessment before radiation treatments, at least weekly during treatments,
1 month following completion of treatment, and each follow-up appointment.
Initial assessment includes the patient’s present skin condition, preexisting skin disorders, medical conditions, medications, age-related factors, and nutritional status.
Consistency in assessment and documentation is important.

98. Patient Instructions
Use gentle soaps ONLY, such as Dove or Ivory, which do not contain additives
Use a moisturizing lotion on the treatment area twice a day
Expose the treated area to the air as much as possible
Do not wear underwire bras
Do not wear tight-fitting clothing that rubs or binds underneath the breast

99. Patient Instructions
Wear a comfortable bra. Wear cotton t-shirts underneath your bra to absorb moisture.
Drink 8-10 glasses of water a day.
Eat well-balanced meals and maintain your weight during treatment.
Continue with your normal daily activities.

100. Patient Instructions
Sexual activity may continue during treatment. You are not radioactive and there are no dangers to your partner.
Avoid extreme temperatures to the affected area. Do not use water bottles, heating pads, sun lamps, ice bags, etc.
Avoid exposing your skin to the sun, as the sun and sun rays are an additional form of radiation to the skin. Always apply sunscreen with SPF or 15 before sun exposure.

101. Patient Instructions
Do not apply tape or adhesive bandages to the treated area.
Speak with your nurse about deodorant use
Continue with the range of motion exercises for your arm and shoulder.
Report any pain or swelling to your doctor or nurse.

102. Breast Skin Products
Cleanser and moisturizer Given to every breast cancer patient being treated with radiation Have patients use twice a day

103. Breast Skin Products
Healing ointment and skin protectant Used for dry desquamation Apply to affected area

104. Breast Skin Products
MOIST DESQUAMATION Topical aluminum acetate packets (astringent) mixed with normal saline Gently debride area and apply solution to area for 20 minutes; rewet every 10 minutes and repeat once a day Apply hydrocolloid dressing over affected area and secure Do NOT use hydrocolloid dressing 4 hours before treatment

105. What is the recommended treatment for every radiation patient?
A. Soap and water once a day
B. Apply cleanser and moisturizer twice a day on the affected area
C. Apply a hydrocolloid over the treated area
D. Encourage daily sun exposure.

106. Sorry, incorrect. Try again.
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107. Yes! Apply cleanser and moisturized twice a day to the affected area.

108. Case Study
Mrs. K is a breast cancer patient who has received radiation to her left breast for the past 4 weeks. She is complaining of increasing pain and her left breast is bright red in color, with sloughing skin and a serous exudate. What is the name of this skin condition caused by radiation? What would be the nurse’s actions and interventions?

109. Case Study
Moist desquamation. The nurse would apply an aluminum acetate solution for 20 minute and gently debride the area. A hydrocolloid dressing would then be placed over this area and secured. The patient would be given instructions about this treatment once a day. Pain management will be addressed.

110. References
Abeloff, M.D., Armitage, J. O., Niederhuber, J. E., Kastan, M. B., & McKenna, W. G. (2004). Clinical oncology (3rd ed.). Philadelphia, PA: Elsevier, Inc. Bruner, D. W., Bucholtz, J. D., Iwamoto, R., & Strohl, R. (Eds.) (1998). Manual for radiation oncology nursing practice and education. Pittsburgh, PA: Oncology Nursing Society. Fox, S. I. (1996). Human physiology (5th ed.). Dubuque, IA: Wm. C. Brown Publishers. Groenwald, S.L., Frogge, M.H., Goodman, M., & Yarbro, C.H. (1993). Cancer nursing: Principles and practice (3rd ed.). Boston, MA: Jones & Bartlett. Hill, S. (2008). Managing radiation skin injury. Ostomy Wound Management, 51(10), 1-2. Retrieved May 13, 2009, from, Mahon, S. M. (Ed.). (2007). Breast cancer. Pittsburgh, PA: Oncology Nursing Society. Milojkovic, D., Short, K., Salisbury, J. R., creamer, D., du Vivier a. W. P., & Mufti, G. J. (2003). Dose-limiting dermatological toxicity secondary to imatinib mesylate (STI571) in chronic myeloid leukaemia. Leukemia, (17), Retrieved May 13, 2009, from Microsoft Clip Art 2007 retrieved on various dates in April and May of 2009, from

111. National Human Genome Research Institute (n. d. ). Chromosome
National Human Genome Research Institute (n.d.). Chromosome. Retrieved May 12, 2009, from Otto, S. E. (2001). Oncology nursing (4th ed.). St. Louis, MO: Mosby, Inc. Porth, C. M. (2005). Pathopphysiology: Concepts of altered health status (7th ed.). Philadelphia, PA: Lippincott, Williams & Wilkins. Singer, M. (1992). The Ras gene and cancer. Winding your way through DNA. Symposium conducted at the University of California. San Francisco. Retrieved May 13, 2009, from Cancer.php. United States National Library of Medicine (n.d.). DNA structure. Genetics home reference: Your guide to understanding genetic conditions. Retrieved May 9, 2009, from United States National Library of Medicine (n.d.). Chromosome structure. Genetics home reference: Your guide to understanding genetic conditions. Retrieved May 13, 2009, from United States National Library of Medicine (n.d.). Gene. Genetics home reference: Your guide to understanding genetic conditions. Retrieved May 13, 2009, from chromosome.

112. White, J., & Joiner, M. C. (2006). Toxicity from radiation in breast cancer. In W. Small Jr., & G. E. Woloschack (Eds.)., Radiation toxicity: A practical guide. Springer Science + Media Business, Inc. Wikigenetics (n.d.). The cell cycle. Retrieved May 9, 2009, from wikigenetics.org/index.php./The_Cell_Cycle. Wikimedia Commons (n.d.). Segmented neutrophils. Retrieved May 14, 2009, from Wikimedia Commons (n.d.). Skin. Retrieved May 13, 2009, from Wikimedia Commons (n.d.). Skin layers. Retrieved May 13, 2009, from Wikipedia (n.d.). Phagocytosis. Retrieved May 14, 2009, from

113. Good Job
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