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Alteration in cell function and
        differentiation:
   Neoplastic Disruptions
Objectives

• Compare the characteristics of abnormal cell growth and
  reproduction processes to normal cell growth and
  reproduction.
• Describe the process of carcinogenesis, major risk factors
  and preventative measures.
• Discuss the general premise of the concept of prevention
  and early detection of cancer.
• Describe the ways a cancer can be classified.
• List the major treatment options for cancer and discuss
  each according to: indication for method, common
  complications, and medical/nursing management related to
  each method.
Epidemiology of Cancer

• Second leading cause of death in the United States (What
  is the first?)
• Leading cause of death from disease in children aged 1 to
  14 years old (leading cause of death is accidents in this age
  cohort)
• over 1.2 million cases in 2006, with over 570,000 deaths
• Approximately 62% of individuals diagnosed will be alive at
  5 years
• Most common in men is prostate cancer, and in women
  breast cancer
• Most common cause of cancer death in both men and
  women is lung cancer
• 10 million adults are cancer survivors
Cancer Incidence and Mortality
               2006 ACS Projections
                    Cases Deaths                                    Cases   Deaths
    Prostate       234,460 27,350                   Breast          212,920 40,970
    Lung & bronchus 92,700  90,330                  Lung & bronchus 81,770   72,130
    Colon & rectum 72,800   27,870                  Colon & rectum 75,810    27,300
    Urinary bladder 44,690  8,990                   Uterine corpus   41,200   7,350
    Lymphomas        34,870 10,770                  Lymphomas        31,800   9,560
    Melanoma        34,260  5,020                   Melanoma         27,930  2,890
    Kidney &        24,650  8,130                   Ovary           20,180  15,310
    renal pelvis                                    Pancreas        16,580   16,210
    Leukemia        20,000 12,470                   Urinary bladder 16,730    4,070
    Pancreas        17,150 16,090
                                                    All sites      679,510   273,560
    All sites         720,280 291,270




Data from the ACS. Cancer facts and figures 2006.
Change in the US Death Rates* by Cause,
1950 & 2005


       Rate Per 100,000


                                                                                       1950
                                                                                       2005




               Heart                Cerebrovascular              Influenza &                  Cancer
             Diseases                  Diseases                  Pneumonia

 * Age-adjusted to 2000 US standard population.
 Sources: 1950 Mortality Data - CDC/NCHS, NVSS, Mortality Revised.
 2005 Mortality Data: US Mortality Data 2005, NCHS, Centers for Disease Control and Prevention, 2008.
Cancer Death Rates* Among Men, US,1930-2004



                Rate Per 100,000

                                                                       Lung & bronchus




           Stomach                                                                         Prostate




                                                                           Colon & rectum

                                                                                           Pancreas


                             Leukemia
                                                                   Liver




*Age-adjusted to the 2000 US standard population.
Source: US Mortality Data 1960-2004, US Mortality Volumes 1930-1959,
National Center for Health Statistics, Centers for Disease Control and Prevention, 2006.
Cancer Death Rates* Among Women, US,1930-2004




                 Rate Per 100,000




                                                                                           Lung & bronchus
      Uterus
                                                                    Breast


                                               Colon & rectum
          Stomach

                  Ovary

                                                            Pancreas




*Age-adjusted to the 2000 US standard population.
Source: US Mortality Data 1960-2004, US Mortality Volumes 1930-1959,
National Center for Health Statistics, Centers for Disease Control and Prevention, 2006.
Cancer Death Rates* by Sex and Race, US, 1975-2004



                 Rate Per 100,000

                                                         African American men




                                                            White men

                                       African American women



                                                    White women




  *Age-adjusted to the 2000 US standard population.
  Source: Surveillance, Epidemiology, and End Results Program, 1975-2004, Division of Cancer Control and
  Population Sciences, National Cancer Institute, 2007.
Cancer Incidence Rates* Among Men, US, 1975-2004


       Rate Per 100,000



                                                   Prostate




                                                                Lung & bronchus



            Colon and rectum
                                                       Urinary bladder

        Non-Hodgkin lymphoma
                                                        Melanoma of the skin



*Age-adjusted to the 2000 US standard population and adjusted for delays in reporting.
Source: Surveillance, Epidemiology, and End Results Program, Delay-adjusted Incidence database:
SEER Incidence Delay-adjusted Rates, 9 Registries, 1975-2004, National Cancer Institute, 2007.
Cancer Incidence Rates* Among Women, US, 1975-2004


        Rate Per 100,000




                                                                        Breast




                                                                               Lung & bronchus
             Colon and rectum

                                                              Uterine Corpus
             Ovary
                                      Non-Hodgkin lymphoma



*Age-adjusted to the 2000 US standard population and adjusted for delays in reporting.
Source: Surveillance, Epidemiology, and End Results Program, Delay-adjusted Incidence database:
SEER Incidence Delay-adjusted Rates, 9 Registries, 1975-2004, National Cancer Institute, 2007.
Cancer Definitions

Oncology: The study of tumors and their treatment

Cancer: from the latin "crab-like"

Tumor: Swelling that can be caused by a number of
conditions, usually marked by the suffix -oma

Carcinoma: malignant tumor of epithelial tissue

Adenocarcinoma: malignant tumor of glandular epithelial
tissue

Sarcoma: Malignant tumor of mesenchymal origin
neoplastic disruptions
Host defense mechanisms against
cancer:
Tumor Antigens
   o   Tumor-Associated Antigens (TAA)
   o   Tumor-Specific Antigens (TSA)
Host defense mechanisms against
cancer:
Tumor Antigens
Click to add content
Host defense mechanisms against
cancer:
Tumor Antigens altered cell surface antigens as a
Cancer cells may display
result of their malignant transformation.

• Through immunogenic survellience our immune system
  recognizes and destroys the cells that exhibit these non-self
  tumor antigens
   o Mainly mediated by T-cells (both CD4+ and CD8+ cells)
   o Anti-tumor antibodies can be found in patients with
     cancer suggesting a role for B-cells in cancer
     surveillance (humoral immunity)
   o Macrophages and dendritic cells function as APCs to the
     Immune System and also directly phagocytize CA cells
   o NK cells engage in actual killing/lysis of the tumor cells
Host defense mechanisms against
cancer:
Tumor Antigens
Host defense mechanisms against
cancer:
Howare many theories how cancerthe immune
 There cancer cells evade cells are able to evade
system.
the immune system.
 •  Suppression of factors that stimulate T-cells to react to CA
    cells
•   Weak surface antigens allowing CA cells to "sneak through"
    immune surveillance
•   Development of tolerance to some tumor antigens
•   Suppression of the immune response by products secreted
    by CA cells
•   Induction of Suppressor T-cells by the tumor
•   Blocking antibodies that bind to Tumor Associated
    Antigens, thus preventing recognition by T-cells
Blocking Antibodies on TAA's
Cell Life Cycle and
Metabolic Activity




                      FIG. 16-1
Cell life cycle:  the alternation between
mitosis and interphase.
S phase:                      G2 phase:
 • Synthesis phase            • G=gap
 • synthesis of DNA and       • RNA and protein synthesis
   proteins for new             occur
   chromosomes                • period between the
 • Get two separate sets of     completion of DNA
   chromosomes                  synthesis and the next
                                phase which is the M
                                phase
Cell life cycle:  the alternation between
mitosis and interphase
M phase:                      G1 phase:
• Mitosis phase               • G=gap
• Nuclear and cytoplasmic     • period between the M
  division occurs producing     phase and the start of
  two daughter cells            DNA synthesis
• phases of mitosis include   • energy is generated and
  prophase, metaphase,          extra membranes and
  anaphase and telophase        cytoplasm are made
Cell life cycle:  the alternation between
mitosis and interphase
G0 phase:
• Not really part of the cell cycle
• the cell is reproductively resting
• cell is functional but not dividing
• most cells spend their time in G0
   o eg. hepatocytes (liver cells) do not divide unless some
     injury to the liver has occured.

There are some permanent cells that are unable to re-enter
the cell cycle (Neuron cells)
 • Stable cells can re-enter the cell cycle if stimulated by
   extracellular nutrients, growth factors, hormones, and other
   signals such as blood loss or tissue injury.
Cell proliferation

This is a highly regulated process by which cells divide and
reproduce. Feedback regulation of this process occurs in
normal cells and tissues.
 • Normal cells will also stop dividing based on "contact
   inhibition."
 • Normal cells keep an equal balance between cellular
   proliferation and cellular degeneration or death
 • Rate of proliferation differs in different cells and tissues
    o Bone marrow, epithelial cells of the GI tract, and hair
      follicles have a rapid rate of cellular proliferation
    o Myocardium and cartilage either have no or slow rates of
      cellular proliferation
Cellular proliferation in cancer cells

1. They divide nearly continuously with little time spent in the
   G0 phase, with some cells dividing haphazardly generating
   more than 2 daughter cells with one division.
2. They have a short "generation time" which is the period of
   time necessary for the cell to enter and complete one round
   of cell division by mitosis.
3. They can have a rapid growth rate and "doubling time."
4. They have a high proportion of cells within the tumor
   population that are in the proliferative pool undergoing cell
   division.
5. They have a loss of "contact inhibition."
Cellular differentiation in cancer cells

A mature, differentiated cell in a human is capable of
functioning only as the tissue/organ it has developed into can.
The purpose of differentiation is to provide for organization
throughout the tissues/organs/human system. Normal cells
differentiate in an orderly, stable process.
 • CA cells (neoplastic cells) lack this differentiation, and do
    not resemble or function like their parent cells
 • This differentiation is thought to be controlled by genes
    (protooncogenes and oncogenes which will be discussed
    later).
Cellular metabolism in cancer cells

Normal cells depend on aerobic metabolism for 90% of their
energy needs. Only cells without mitochondria use anaerobic
metabolism for their primary energy needs.
 • Neoplastic (CA) cells depend more on anaerobic
   metabolism
 • CA cells use higher levels of glucose
 • CA cells are engage in high levels of protein catabolism in
   order to get energy (rob normal cells of protein)
Characteristics of benign and malignant
neoplasms
Tumor: Swelling that can be caused by a number of
conditions including inflammation and trauma.

Neoplasia: These are clusters of cells that can be benign or
malignant

Benign Neoplasm: contain well differentiated cells that are
clustered together in a single mass.

Malignant Neoplasm: less well differentiated to
undifferentiated and have the ability to break loose, enter the
circulatory or lymphatic systems and form secondary
malignant tumors at other sites.
Non-neoplastic growth patterns

• Hyperplasia: Increase in the number of cells in a tissue or
  an organ
• Metaplasia: Conversion of one cell type to another
• Dysplasia: Alteration in the size, shape and organization
  of cells. Dysplastic cells can become or precede
  neoplastic/cancerous changes.

Benign and malignant neoplasms are usually differentiated by
their cell characteristics, rate of growth, manner of growth,
capacity to metastasize and spread to other parts of the body
and potential for causing death.
Examples of non-neoplastic growth
patterns
Comparison of benign and malignant
neoplasms
Comparison of benign and malignant
neoplasms
Carcinogenesis

Strictly interpreted, this is the development of cancer in
otherwise normal tissue.

• The natural development of cancer is usually an orderly
  process that comprises several stages and occurs over a
  period of time.
• Includes initiation, promotion and progression
Terms important in carcinogenesis
Oncogene:                         Proto-Oncogene:
• These are genes that can         • These are genes that
  promote the growth of cancer       regulate normal cellular
  cells                              processes (very important)
• these genes are usually          • promote normal embryonic
  derived from mutations of          cellular development
  normal genes                     • Once growth and
• Can interfere with the cells'      development ceases, they
  normal functions and protein       genes are usually "turned off"
  expression                       • Can be "turned on" by
                                     viruses, chemicals, or any
                                     carcinogen
Terms important in carcinogenesis

Tumor Suppressor Genes:        Mutations in proto-oncogenes
 • They normally function to   and tumor suppressor genes
   regulate growth             can occur in embryonic
 • Mutations to this part of   development, and this usually
   the genome can cause the    leads to an earlier
   cell to engage in           development of cancer, and a
   unregulated growth          more significant presentation
    o p53 gene in many         of the cancer
      cancers
    o BRCA-1, BRCA-2           Mutations in these genes can
    o APC gene                 also be induced by exposure
 • Can be inherited            to carcinogens.
CRC Development:
              Adenoma-to-Carcinoma Sequence

         First somatic APC Second APC K-ras Further changes
         mutation or loss mutation or loss mutation DCC loss TP53 loss eg, NM23 loss



       Normal
       mucosa
               Hyperproliferative        Adenoma, increasing
                  epithelium             in size, and dysplasia            Carcinoma



        Germline APC
        mutation (FAP)




Adapted from Bishop and Hall. Eur J Cancer. 1994;30A:1946-1956, with permission.
Carcinogenesis:  Initiation
This is a mutation in the cell's genetic structure
 • Can be inherited
 • Can be induced after exposure to a carcinogen (chemical,
   radiation, or viral agent)
    o the altered cell becomes a clone
 • This is an irreversible process, but:
    o the DNA may repair itself
    o most deranged cell can undergo apoptosis
    o cells with altered antigens are subject to immune
      surveillance
    o or the DNA alteration may not become functionally
      significant
 • Often, for the DNA alteration to be significant, more than
   one episode of genetic damage must occur
neoplastic disruptions
Carcinogenesis:  Promotion

• During this stage, the environment has to promote or favor
  the development of the "initiated" or altered cell
• There is a period of latency from 1 to 40 years, between the
  initial genetic alteration and the actual clinical evidence of
  cancer
• An important distinction between initiation and promotion is
  that the action of promoters is reversible.
   o important promoters include: dietary fat, smoking,
      obesity, and alcohol consumption

****Cigarette smoke can act as both an initiator of
malignant change and a promoter of cancer development.
Carcinogenesis:  Progression

This is the final stage in the natural history of cancer.
 • Increased growth of the tumor (Significant)
 • Increased invasiveness of the tumor
 • Spread of the cancer to a distant site
    o Metastasis: the cancer has spread from the primary site
      (where the cancer developed) to another organ or part of
      the body
        Most frequent sites: lungs, brain, bone, liver, and
         adrenal glands
        often determined or limited by angiogenesis
        get hematogenous metastases and lymphatic
         metastases
Process of Cancer Development
Process of metastatic spread




                               FIG. 16-5
What do Metastases look like?




                                FIG. 16-4
What about the Oncofetal Antigens?
Oncofetal antigens are tumor antigens that are found on the surfaces
and inside of cancer cells, as well as fetal cells.

• Appearance in cancer cells is thought to be reflective of that cell
  regaining its embryonic capability to differentiate into various types
  of cells
   o Carcinoembryonic antigen (CEA): normally found in fetal gut,
     liver, and pancreas cells and disappears during the last 3
     months of fetal life. This antigen is overexpressed in colon
     cancer and also elevated in cigarette smokers, pt's with
     ulcerative colitis and cirrhosis of the liver
   o Alpha-Fetoprotein (AFP): fetal liver cells and liver cancer
   o CA-125: Ovarian cancer
Risk factors that predispose for cancer
development
1. Heredity
2. Hormones
3. Immunologic mechanisms
4. Chemical Carcinogens
5. Radiation
6. Oncogenic viruses
Risk factors that predispose for cancer
development
Heredity:                     Hormones:
• Cancer related genes        • Hormones can
  have been identified that     overstimulate the
  increase an individual's      proliferation of certain
  susceptibility to the         cells overtime
  development of certain         o Prostate cancer is
  cancers                          thought to develop in
   o BRCA-1/BRCA-2: 40-            elder males because of
     80% lifetime risk of          lifetime exposure to
     breast cancer                 androgens
   o Accounts for approx.        o DES babies had higher
     10% of cancers                rates of Uterine cancer
Risk factors that predispose for cancer
development
Immunologic Mechanisms:          Chemical Carcinogens:
 • Mutant cells are constantly   • These include chemicals
   formed, but are destroyed       like cigarette smoke and
   by immune cells through         asbestos, drugs like
   immuno-surveillance             hormones,
 • people with depressed           immunosuppressive
   immune systems have             agents, cytotoxic drugs,
   higher rates of cancer          and dietary factors like
    o AIDS related kaposi's        fats and nitrates
      sarcoma                    • some of these compounds
                                   are either initiators or
                                   promotors, cigarette
                                   smoke is both
Risk factors that predispose for cancer
development
Radiation:                     Oncogenic Viruses:
• When cells are exposed to    • Some viruses can infect a
  radiation, there is damage     cell and inject their genetic
  to one or both strands of      material into the host
  DNA                            DNA...this can either
• This can be exposure to        disrupt a tumor
  ionizing radiation or          suppressor gene or add
  exposure to UV radiation       an oncogene to the DNA
• Melanoma is a cancer           causing malignant
  with significant               transformation
  increases in incidence          o Hep B/C and HCC
• Hiroshima survivors             o HPV and Cervical
                                    Cancer
Risk factors that predispose for cancer
development
Age:
• Advanced age is the single most significant risk factor
   o 50% of cancers occur in those >65 years of age
   o the symptoms of cancer are often perceived or
     written off as "age related changes"
   o Can be more vulnerable to complications from
     cancer treatment
Prevention and the early detection of
cancer
Preventative Measures:
 • Patient education is one of the most important nursing
   interventions that can be utilized in the prevention and
   progression of cancer. Patients should be educated in the
   following:
    o Risk factors: what are they (sun exposure, smoking,
      diet, exposure to chemicals, radiation) and how to avoid
      exposures
    o Health Promotion behaviors: quit smoking, low fat, high
      fiber, low nitrate diet, exercise, routine screening exams
Warning signs of cancer development
neoplastic disruptions
Screening Guidelines for the Early Detection
of Breast Cancer, American Cancer Society

•   Yearly mammograms are recommended starting at age 40.
•   A clinical breast exam should be part of a periodic health exam, about
    every 3 years for women in their 20s and 30s, and every year for
    women 40 and older.
•   Women should know how their breasts normally feel and report any
    breast changes promptly to their health care providers. Monthly breast
    self-exam is an option for women starting in their 20s.
•   Screening MRI is recommended for women with an approximately
    20%-25% or greater lifetime risk of breast cancer, including women
    with a strong family history of breast or ovarian cancer and women
    who were treated for Hodgkin disease.
Screening Guidelines for the Early Detection
of Cervical Cancer, American Cancer Society

•   Screening should begin approximately three years after a women
    begins having vaginal intercourse, but no later than 21 years of age.
•   Screening should be done every year with regular Pap tests or every
    two years using liquid-based tests.
•   At or after age 30, women who have had three normal test results in a
    row may get screened every 2-3 years. However, doctors may
    suggest a woman get screened more frequently if she has certain risk
    factors, such as HIV infection or a weakened immune system.
•   Women 70 and older who have had three or more consecutive Pap
    tests in the last ten years may choose to stop cervical cancer
    screening.
•   Screening after a total hysterectomy (with removal of the cervix) is not
    necessary unless the surgery was done as a treatment for cervical
    cancer.
Screening Guidelines for the Early Detection
of Prostate Cancer, American Cancer Society


The prostate-specific antigen (PSA) test and the digital rectal examination
(DRE) should be offered annually, beginning at age 50, to men who have a
life expectancy of at least 10 years.
Men at high risk (African-American men and men with a strong family
history of one or more first-degree relatives diagnosed with prostate cancer
at an early age) should begin testing at age 45.
For men at average risk and high risk, information should be provided
about what is known and what is uncertain about the benefits and
limitations of early detection and treatment of prostate cancer so that they
can make an informed decision about testing.
Screening Guidelines for the Early Detection of
Colorectal Cancer and Adenomas, American Cancer
Society 2008
 Beginning at age 50, men and women should follow one of the
 following examination schedules:
  • A flexible sigmoidoscopy (FSIG) every five years
  • A colonoscopy every ten years
  • A double-contrast barium enema every five years
  • A Computerized Tomographic (CT) colonography every five years
  • A guaiac-based fecal occult blood test (FOBT) or a fecal
      immunochemical test (FIT) every year
  • A stool DNA test (interval uncertain)




 People who are at moderate or high risk for colorectal cancer should talk with
                 a doctor about a different testing schedule
Other Diagnostic tests if cancer is
suspected or diagnosed (will depend on
primary site)examination of cells that are sloughed into the
1. Cytology studies:
various body secretions or scraped from organ cavities (i.e. pap
smear)....suspicious findings may necessitate an actual biopsy

2. Chest Xray/Mammogram: looking for radiological evidence of a
primary or a metastatic cancer site (not very sensitive, you need a
pretty big lesion to see it on chest xray)

3. CBC: evaluate the blood for anemia, alterations in WBCs,
thrombocytopenia or thrombocytosis

4. Blood tests for tumor markers/antigens: CEA, AFP, CA19-9, CA-
125, CA15-3, CA27-3, PSA
Other diagnostic tests if cancer is
suspected or diagnosed (will depend on
the primary site)
5. Biopsy: refers to the process of obtaining tissue for histologic exam
and susequent diagnosis of the disease
 • Needle Biopsy
 • Incisional
 • Excisional

6. CT Scan: Multiple xrays are done, usually from the neck to groin to
get a picture of the internal organs and look for metastatic disease
(often part of routine staging of cancer

7. PET Scan: This is a specialized test looked at the metabolic rate of
tissues. A radioactively labeled sugar solution is ingested and the
scanner looks for areas of the body that take up the sugar...good in
cancer because of the elevated glucose needs of cancerous cells
Other diagnostic tests if cancer is
suspected or diagnosed (will depend on
the primary site)
8. Sigmoidoscopy/Colonoscopy: Visualize and remove
polyps, precancerous lesions and cancerous lesions from the
colon.

9. Bone Scan: Radioisotopes are injected and looks for
increased uptake in the bone (hot spots) which indicate
metastatic disease in the bones

10. Bone Marrow Study: evaluate the progenitor cells, look
for genetic abnormalities (most often used in hematologic
malignancies, but a metastatic cancer to the bone marrow can
also be evaluated).
Ways of classifying cancer...

1. Anatomic Site
2. Histological Analysis (grading)
3. Extent of Disease (Staging)
Ways of classifying cancer:  Anatomic
site
The tumor is identified by the tissue of origin, the anatomic
site, and the behavior of the tumor.
 • Tissue of origin (embryonic):
     o Carcinomas originate from the embryonal ectoderm (skin
       and glands) and endoderm (mucous membranes of the
       resp. tract, GI tract, GU tract)
     o Sarcomas originate from embryonal mesoderm
       (connective tissue)
     o Lymphomas/Leukemias originate from the hematopoietic
       system
 • Location of primary tumor: Breast cancer in breast tissue,
    prostate cancer in prostate tissue
 • Behavior: Benign or Malignant
Ways of classifying cancer:  Histological
analysis
This is a microscopic analysis of the tumor, looking at the
appearance of cells and the degree of differentiation. Broken
down into 4 grades based on the differentiation.
 • 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
Ways of classifying cancer:  Extent of
disease
This is describing the extent of the disease in the body. They
can be broken up into the American Joint Committee on
Cancer (AJCC) and Tumor/Node/Metastases (TNM) staging.
Both these staging systems are more amenable to solid tumor
evaluation (not leukemias/lymphomas).
stage 0: cancer in situ
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
Ways of classifying cancer :  Extent of
disease
Major treatment options in cancer

1. Surgery
2. Radiation
3. Chemotherapy
4. Hormonal therapy
5. Biotherapy
6. Targeted therapy
7. Bone Marrow and peripheral blood stem cell transplantation
How do you choose an option for cancer
treatment?
Treatment option choices are dictated by the goals of therapy.

• Cure
• Control
• Palliation
Surgery

1. Indicated if the cancer is confined and well-encapsulated,
   where surgery alone can "cure" the cancer.
2. "Debulk" the tumor so other treatments can be more
   effective.
3. Prophlaxis, prevent the development of cancer
4. Diagnose or stage a tumor
5. Palliate the symptoms from a cancer
6. Reconstruction from previous cancer surgery
7. Determine if therapy if effective (very rarely the primary goal
   of surgery, but may be secondary)
Complications of surgery and nursing
care
• Loss of body part/function
• Disfigurement
• Increased risk for infection if immune suppressed
• Increased risk for bleeding if thrombocytopenic
• Increased risk for wound healing if the patient is on
  antiangiogenic therapy
Nursing Care
• Routine pre- and post-op care
• Additional psycho-social needs of cancer patients
   o Anxiety
   o Body image disturbance
• Attention to the other risk factors that accompany a patient
  with cancer
Radiation Therapy
Ionizing radiation is used for most treatments:
 • acts at the cellular level to damage or alter the cells
 • breaks chemical bonds, disrupts DNA and interferes with
   cell activity and mitosis
 • Affects the cell cycle in the following order: M-phase, G2-
   phase, G1-phase, and S-phases
 • Cells damaged by radiation either die or are unable to
   divide

Indicated as primary therapy for cancer if the tumor is in
an area that is difficult to reach surgically or where
surgery could be significantly disfiguring (H&N CA)
 • Some tumors are more radiosensitive than others
 • Can shrink the tumor for potential surgery
 • Can palliate complications from cancer
How is radiation therapy delivered?
• External Radiation:
  o teletherapy: this form of therapy is external to the patient
    and distant from the tumor.

• Internal Radiation:
   o This is known as brachytherapy, and the radiation source
     is placed in close contact with the tumor
        Sealed: radiation is contained within some sort of
         device like a needle or seed device which may be
         placed near the tumor site temporarily or permanently
        Unsealed: radiation is not contained in a device so
         the radiation is not confined to one area of the body
         (po, IV, or instilled into a body cavity)
Nursing Management of Radiation
Therapy Patients
Safety Precautions:
 • Needed when caring for patients undergoing
   brachytherapy. Remember, the patient is not radioactive
   but the implant is.
 • Handling of secretions and excretions must be done
   wearing gloves if the patient has received an unsealed
   radioactive source (the source is now systemic once in the
   body).
 • The patient who has sealed radiation implants emits
   radiation while the implant is in place but his/her body
   secretions are not radioactive
 • Remember that the patient who receives external radiation
   is not radioactive at any time
neoplastic disruptions
Nursing Management of Radiation
Therapy Patients
• Providing patient teaching based on the type of radiation
  they are to receive...teletherapy or brachytherapy
   o teletherapy: teach regarding the machinery, any braces
     or adaptive devices that will be used, what will be
     expected (positioning during therapy, side effects)
   o brachytherapy: teach regarding how this is different from
     teletherapy, what sort of care they will undergo, limiting
     of visitors, and the distance visitors need to keep during
     the therapy.
Nursing Management of Radiation
Therapy Patients
• Skin preparation prior to therapy: with teletherapy, the skin
  is marked by the radiation therapist to identify the exact
  area where the radiation should be delivered. The patient
  should be instructed not to wash these markings off.
• Prevent skin breakdown...teach the patient to avoid
  scratching...dry itchy skin is a common complication of
  teletherapy. Usually recommend aloe vera and very simple
  emoillients (no petroleum products, cause increased
  breakdown)
• Promote healing of skin after therapy: cleanse thoroughly if
  skin is broken, observe for s/s of infection and treat
  promptly if infection occurs, optimize nutrition to promote
  healing
Skin Complications with Radiation
Therapy
Skin Complications with Radiation
Therapy
Nursing Management of Radiation
Therapy Patients
• Minimize GI upset
  o Mouth XRT causes dry mouth and stomatitis
      Biotene mouthwash and gel
      warm water/baking soda rinse
      assess for and treat oral candidiasis quickly
      for taste alterations, encourage moist, bland food
  o Esophageal/Upper abdominal XRT causes
    N/V/Esophagitis
      antiemetics: teach about the medication, frequency
      bland diet
      Proton Pump Inhibitors
  o Rectal/lower abdominal radiation causes diarrhea
      teach about the use of immodium/Lomitil
      Low residue diet
Chemotherapy

This is indicated in the treatment of hematologic and solid
tumor malignancies. Can be the primary therapy or used
adjunct to another therapy (surgery or radiation).
Chemotherapy works in different ways, but primarily by
disrupting the production of essential enzymes, inhibits RNA,
DNA, and protein synthesis, and can prevent cell mitosis.

Most effective against rapidly dividing cells.
Goals of Chemotherapy

The goal of chemotherapy is to eliminate or reduce the number
of malignant cells in the primary tumor and/or the metastatic
tumor site. The response of malignant cells to chemotherapy
is determined by:
 1. Mitotic rate of the tissue from which the tumor arises.
 2. Size of the tumor
 3. Age of the tumor
 4. Location of the tumor
 5. Presence of resistant tumor cells
Chemotherapy Classifications
Cell Cycle Specific:                Cell Cycle Nonspecific:
 • these drugs are effective         • Effective on both dividing and
   during specific phases of the       resting cells (G0 phase).
   cell cycle (G1, S, G2, M)         • Damage the cell at some
   relating to cellular                point in the cycle but death
   proliferation/replication.          does not occur until the cell
 • Effective only during one           attempts to divide
   specific phase and are often      • Very dose dependent
   given over a prolonged period
   to ensure that the majority of
   cells reach the phase the drug
   acts on.
 • Very time dependent

           Cell Cycle specific and Cell Cycle Non-
            specific are often given together to
                enhance death of tumor cells
Chemotherapy Examples

Cell Cycle Specific:                Cell Cycle Non-specific:
 • Antimetabolites: mimic            • Alkalating Agents: first
   naturally occuring substances       chemotherapies used,
   thus interfering with enzyme        Damage DNA by breaking the
   function or DNA synthesis           double-stranded helix
     o capecitabine (Xeloda)         • Antitumor antibiotics: bind
     o methotrexate (Trexall)          directly to the DNA, inhibiting
 • Mitotic Inhibitors: Some act        DNA replication and
   by stabilizing microtubules so      interfering with transcription
   they aren't able to align the     • Hormone therapy: interferes
   chromosomes to divide               with the action of a hormone,
 • Topsimerase Inhibitors:             or with the enzymes that
   Inhibit the enzyme                  produce hormones
   topsimerase that function to
   make breaks in DNA for
   replication
Methods of Chemotherapy
Administration
Extravasations of Chemotherapy

Chemotherapy drugs can have direct affects on the tissue it's
exposed to upon administration. One of the major routes of
administration for chemotherapy is the IV route. Since most
chemotherapy drugs are either irritants or vesicants, a major
risk of peripheral IV chemotherapy is Extravasation.

 • This is the infiltration of drugs into the tissues surrounding
   the infusion site
    o Can cause local tissue damage
    o Can lead to permanent damage and loss of function
All vesicant chemotherapy should be administered using
a central venous access device (CVAD)
Why?
If extravasation occurs...

• Stop the infusion immediately, notify the MD
• Remove the IV infusion tubing and try and aspirate any
  remaining drug in the catheter with a new syringe
• Inject the prescribed antidote, if one exists, in the infusion
  needle or in a pincushion fashion in the skin around the
  extravasation (the MD will direct the route/order)
• Topical corticosteroids may be applied if ordered
• Elevate the site
• Cold Compresses for 1st 24/48 hours unless an alkaloid or
  oxaliplatin has been infiltrated (use heat with alkaloids or
  oxaliplatin)
• Document the extravasation
• Observe the site at designated intervals
Examples of CVADs
Examples of CVADs
Toxicities/Side Effects from
Chemotherapy
Chemotherapy does not distinguish between normal cells and
cancer cells so toxicity to normal tissues is expected.

Acute Toxicity: Nausea, vomiting, allergic reactions,
dysrhythmias, cold sensitivity

Delayed Toxicity: mucositis, diarrhea, stomatitis, alopecia,
neutropenia, anemia, pancytopenia

Chronic Toxicity: damage to organ systems such as the
heart, liver, kidneys, lungs, nervous system, and bone marrow.

    Of all of the above, the most life threatening is the
                  neutropenia/pancytopenia
Nursing Management and
Considerations
• Knowledge of safe administration and disposal of chemo
  agents. Each hospital will have protocols for both
  administration and disposal of the chemo agents.
• Know how to differentiate between tolerable side effects
  and toxic effects (nausea and vomiting vs. pulmonary
  fibrosis or cardiotoxicity) and how to deal with affects as
  they occur.
• Lab Results need to be considered and followed prior to,
  during and post chemotherapy administration (CBC and
  other's per the chemo toxicity)
• Patient education is important during administration re: drug
  action, how to deal with side effects. Remember that
  information can decrease anxiety.
Hormonal Therapy

Some tumors are very hormone dependent, and can grow at
an increased rate in the presence of certain hormones (eg
breast, uterine, prostate cancers)
 • Altering the level of hormone available can decrease or
   stop the growth of a particular tumor.
    o tamoxifen for breast cancer: blocks the estrogen
      receptors on breast cancer cells
    o letrozole for breast cancer: inhibits the enzyme that
      converts androgen to estrogen
    o Lupon for prostate: inhibits the production of
      testosterone by the testicles
    o Extreme hormone manipulation: orchiectomy/
      oophorectomy
Side Effects of Hormone Therapy

• Hypercoagulability: more prone to DVTs/PEs
• Selective Estrogen Receptor Modulators: increased risk of
  uterine cancer
• Weight gain
• Lupron: emotional lability, gynecomastia
Biotherapy/Targeted Therapy:

This consists of agents that modify the relationship between
the biologic response of the host to the tumor cells. Includes
immunotherapy, monoclonal antibodies, antiangiogenic agents
and tyrosine kinase inhibitors. Work 3 ways:
 1. Have direct anti-tumor effects
 2. They restore, augment, or modulate host immune system
    mechanisms
 3. They have other effects, like inhibiting the cancer's ability to
    metastasize or differentiate.
Immunotherapy
Interferon:
 • Naturally occuring protein that is produced by WBCs and
   other body cells in response to a variety of stimuli including
   viral infections
 • Exposure of cells to interferon causes production of antiviral
   proteins which then help to protect the neighboring cells
   from attack by viruses.
 • Other functions of interferon are:
    o inhibition of viral DNA
    o stimulates the expression of TAA's on the cell surface so
      that the chance of an immune response against the
      cancer is increased.
 • Cannot be administered orally because of the protein
   nature
 • Significant side effects include depression and
   Significant Fatigue
Immunotherapy
Interleukin 2:
 • Approved for use in Renal cell cancer and melanoma
 • Help the immune system cells recognize and destroy
   abnormal cells
 • IL-2 is produced by the helper T-lymphocytes and
   stimulates the proliferation of other T-lymphocytes,
   activates NK cells, stimulates the release of other cytokines
   like gamma interferon, TNF, IL-1 and IL-6
 • Side effects area also significant, IL-2 is given IV as an
   inpatient. Causes "Shake and Bake" syndrome with
   high fevers and rigors. Also can cause damage the
   kidneys and a careful balance of hydration and
   diuretics is needed....VERY SPECIALIZED NURSING
   CARE
Monoclonal Antibodies

These are antibodies or immunoglobulins that are produced to
bind antigens that are overexpressed on cancer cells. This
blocks the "downstream activity" of these receptors in
stimulating the growth of these tumor cells
 • Herceptin binds the Her2Neu molecule that is
   overexpressed in some breast cancer tumors
 • Cetuximab binds the EGFR receptor that is overproduced in
   many cells, but is FDA approved for use in colon and head
   and neck cancer
 • Tarceva (erlotenib) is an oral agent that binds the EGFR
   receptor and is approved in pancreatic cancer. (big side
   effect is a significant dose limiting rash for erlotenib and
   cetuximab)
Sites of Action of Targeted
Therapy




                       FIG. 16-21
Targeted Therapies (which can be
interchanged often with monoclonal
antibodies)
Interferes with cancer growth by targeting specific cellular
receptors and pathways that are important in tumor growth.
They have a very different side effect profile than chemo and
are often successful at improving the outcome of
chemotherapy without increasing the toxicity.
 • Antiangiogenic therapies: block the circulating vascular
   endothelial growth factor, leading to decreased blood
   vessel formation to tumors/metastases
 • Tyrosine Kinase Inihibitors: block the phosphorylation of
   proteins in the cell leading to decreased growth.
Bone marrow and peripheral blood
stem cell transplantation
Life saving treatment option for malignant and non-malignant
conditions. Involves giving high dose chemotherapy with the
goal of clearing all the malignant cells and then "rescuing" the
patient with new hematopoietic stem cells that can repopulate
the bone marrow.
 • Can be a donor that is HLA matched (preferably 6/6 match)
   (Matched Unrelated Donor)
 • Can be a syngenic donor (identical twin)
 • Can be cord blood (only a small recipient) (again, Matched
   Unrelated)
 • Can be from your own stem cells harvested ahead of the
   procedure (Auto)
Harvesting of Peripheral Blood for Stem
Cell
• Donor is given Colony stimulating factors that boost the
  release of stem cells into the peripheral circulation
• May also be given chemotherapy to stimulate the release of
  the stem cells
• Donor is then hooked up to a pheresis machine that takes
  the blood out of one vein, filters out the stem cells, and
  returns the blood back to the donor through another vein
• Those stem cells are collected over a week period and then
  infused (IV) into the patient once they are completed with
  their chemotherapy conditioning.
Stem Cell Transplant
Complications of Stem Cell Transplants

• The biggest complication of stem cell transplants is the risk
  of infection.
   o patients are usually on protective isolation
   o may have standing orders if a fever occurs
   o +/- neutropenic diet (no raw fruits of vegetables, no
     uncooked or undercooked meat)
• Graft vs. Host Disease is an often chronic complication: the
  patient's new bone marrow if from an unrelated donor may
  mount an immune response against the host (t-cell
  mediated)
   o instruct on the importance of adherence to the
     immunosuppressive regimen.
What's upcoming in cancer care?

• Genetic profiling of individual tumors to determine the
  effectiveness of potential chemotherapy drugs.
   o ERCC1 in lung cancer for Irinotecan and platnim activity
   o DPD in colon cancer to determine the responsiveness of
     the tumor to fluropyrimidines
• More aggressive surgical and chemotherapy management
  of metastatic disease rendering patients disease free who
  were previously uncurable
• More targeted treatment and radiation, making cancer more
  of a chronic disease
• Further advancements in the knowledge of prevention
  leading to a lower incidence of cancer
Thank you for your attention

        Good luck studying!!!
   See you on Tues, Dec. 6th in the
         Little theater at 7am

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neoplastic disruptions

  • 1. Alteration in cell function and differentiation: Neoplastic Disruptions
  • 2. Objectives • Compare the characteristics of abnormal cell growth and reproduction processes to normal cell growth and reproduction. • Describe the process of carcinogenesis, major risk factors and preventative measures. • Discuss the general premise of the concept of prevention and early detection of cancer. • Describe the ways a cancer can be classified. • List the major treatment options for cancer and discuss each according to: indication for method, common complications, and medical/nursing management related to each method.
  • 3. Epidemiology of Cancer • Second leading cause of death in the United States (What is the first?) • Leading cause of death from disease in children aged 1 to 14 years old (leading cause of death is accidents in this age cohort) • over 1.2 million cases in 2006, with over 570,000 deaths • Approximately 62% of individuals diagnosed will be alive at 5 years • Most common in men is prostate cancer, and in women breast cancer • Most common cause of cancer death in both men and women is lung cancer • 10 million adults are cancer survivors
  • 4. Cancer Incidence and Mortality 2006 ACS Projections Cases Deaths Cases Deaths Prostate 234,460 27,350 Breast 212,920 40,970 Lung & bronchus 92,700 90,330 Lung & bronchus 81,770 72,130 Colon & rectum 72,800 27,870 Colon & rectum 75,810 27,300 Urinary bladder 44,690 8,990 Uterine corpus 41,200 7,350 Lymphomas 34,870 10,770 Lymphomas 31,800 9,560 Melanoma 34,260 5,020 Melanoma 27,930 2,890 Kidney & 24,650 8,130 Ovary 20,180 15,310 renal pelvis Pancreas 16,580 16,210 Leukemia 20,000 12,470 Urinary bladder 16,730 4,070 Pancreas 17,150 16,090 All sites 679,510 273,560 All sites 720,280 291,270 Data from the ACS. Cancer facts and figures 2006.
  • 5. Change in the US Death Rates* by Cause, 1950 & 2005 Rate Per 100,000 1950 2005 Heart Cerebrovascular Influenza & Cancer Diseases Diseases Pneumonia * Age-adjusted to 2000 US standard population. Sources: 1950 Mortality Data - CDC/NCHS, NVSS, Mortality Revised. 2005 Mortality Data: US Mortality Data 2005, NCHS, Centers for Disease Control and Prevention, 2008.
  • 6. Cancer Death Rates* Among Men, US,1930-2004 Rate Per 100,000 Lung & bronchus Stomach Prostate Colon & rectum Pancreas Leukemia Liver *Age-adjusted to the 2000 US standard population. Source: US Mortality Data 1960-2004, US Mortality Volumes 1930-1959, National Center for Health Statistics, Centers for Disease Control and Prevention, 2006.
  • 7. Cancer Death Rates* Among Women, US,1930-2004 Rate Per 100,000 Lung & bronchus Uterus Breast Colon & rectum Stomach Ovary Pancreas *Age-adjusted to the 2000 US standard population. Source: US Mortality Data 1960-2004, US Mortality Volumes 1930-1959, National Center for Health Statistics, Centers for Disease Control and Prevention, 2006.
  • 8. Cancer Death Rates* by Sex and Race, US, 1975-2004 Rate Per 100,000 African American men White men African American women White women *Age-adjusted to the 2000 US standard population. Source: Surveillance, Epidemiology, and End Results Program, 1975-2004, Division of Cancer Control and Population Sciences, National Cancer Institute, 2007.
  • 9. Cancer Incidence Rates* Among Men, US, 1975-2004 Rate Per 100,000 Prostate Lung & bronchus Colon and rectum Urinary bladder Non-Hodgkin lymphoma Melanoma of the skin *Age-adjusted to the 2000 US standard population and adjusted for delays in reporting. Source: Surveillance, Epidemiology, and End Results Program, Delay-adjusted Incidence database: SEER Incidence Delay-adjusted Rates, 9 Registries, 1975-2004, National Cancer Institute, 2007.
  • 10. Cancer Incidence Rates* Among Women, US, 1975-2004 Rate Per 100,000 Breast Lung & bronchus Colon and rectum Uterine Corpus Ovary Non-Hodgkin lymphoma *Age-adjusted to the 2000 US standard population and adjusted for delays in reporting. Source: Surveillance, Epidemiology, and End Results Program, Delay-adjusted Incidence database: SEER Incidence Delay-adjusted Rates, 9 Registries, 1975-2004, National Cancer Institute, 2007.
  • 11. Cancer Definitions Oncology: The study of tumors and their treatment Cancer: from the latin "crab-like" Tumor: Swelling that can be caused by a number of conditions, usually marked by the suffix -oma Carcinoma: malignant tumor of epithelial tissue Adenocarcinoma: malignant tumor of glandular epithelial tissue Sarcoma: Malignant tumor of mesenchymal origin
  • 13. Host defense mechanisms against cancer: Tumor Antigens o Tumor-Associated Antigens (TAA) o Tumor-Specific Antigens (TSA) Host defense mechanisms against cancer: Tumor Antigens Click to add content
  • 14. Host defense mechanisms against cancer: Tumor Antigens altered cell surface antigens as a Cancer cells may display result of their malignant transformation. • Through immunogenic survellience our immune system recognizes and destroys the cells that exhibit these non-self tumor antigens o Mainly mediated by T-cells (both CD4+ and CD8+ cells) o Anti-tumor antibodies can be found in patients with cancer suggesting a role for B-cells in cancer surveillance (humoral immunity) o Macrophages and dendritic cells function as APCs to the Immune System and also directly phagocytize CA cells o NK cells engage in actual killing/lysis of the tumor cells
  • 15. Host defense mechanisms against cancer: Tumor Antigens
  • 16. Host defense mechanisms against cancer: Howare many theories how cancerthe immune There cancer cells evade cells are able to evade system. the immune system. • Suppression of factors that stimulate T-cells to react to CA cells • Weak surface antigens allowing CA cells to "sneak through" immune surveillance • Development of tolerance to some tumor antigens • Suppression of the immune response by products secreted by CA cells • Induction of Suppressor T-cells by the tumor • Blocking antibodies that bind to Tumor Associated Antigens, thus preventing recognition by T-cells
  • 18. Cell Life Cycle and Metabolic Activity FIG. 16-1
  • 19. Cell life cycle:  the alternation between mitosis and interphase. S phase: G2 phase: • Synthesis phase • G=gap • synthesis of DNA and • RNA and protein synthesis proteins for new occur chromosomes • period between the • Get two separate sets of completion of DNA chromosomes synthesis and the next phase which is the M phase
  • 20. Cell life cycle:  the alternation between mitosis and interphase M phase: G1 phase: • Mitosis phase • G=gap • Nuclear and cytoplasmic • period between the M division occurs producing phase and the start of two daughter cells DNA synthesis • phases of mitosis include • energy is generated and prophase, metaphase, extra membranes and anaphase and telophase cytoplasm are made
  • 21. Cell life cycle:  the alternation between mitosis and interphase G0 phase: • Not really part of the cell cycle • the cell is reproductively resting • cell is functional but not dividing • most cells spend their time in G0 o eg. hepatocytes (liver cells) do not divide unless some injury to the liver has occured. There are some permanent cells that are unable to re-enter the cell cycle (Neuron cells) • Stable cells can re-enter the cell cycle if stimulated by extracellular nutrients, growth factors, hormones, and other signals such as blood loss or tissue injury.
  • 22. Cell proliferation This is a highly regulated process by which cells divide and reproduce. Feedback regulation of this process occurs in normal cells and tissues. • Normal cells will also stop dividing based on "contact inhibition." • Normal cells keep an equal balance between cellular proliferation and cellular degeneration or death • Rate of proliferation differs in different cells and tissues o Bone marrow, epithelial cells of the GI tract, and hair follicles have a rapid rate of cellular proliferation o Myocardium and cartilage either have no or slow rates of cellular proliferation
  • 23. Cellular proliferation in cancer cells 1. They divide nearly continuously with little time spent in the G0 phase, with some cells dividing haphazardly generating more than 2 daughter cells with one division. 2. They have a short "generation time" which is the period of time necessary for the cell to enter and complete one round of cell division by mitosis. 3. They can have a rapid growth rate and "doubling time." 4. They have a high proportion of cells within the tumor population that are in the proliferative pool undergoing cell division. 5. They have a loss of "contact inhibition."
  • 24. Cellular differentiation in cancer cells A mature, differentiated cell in a human is capable of functioning only as the tissue/organ it has developed into can. The purpose of differentiation is to provide for organization throughout the tissues/organs/human system. Normal cells differentiate in an orderly, stable process. • CA cells (neoplastic cells) lack this differentiation, and do not resemble or function like their parent cells • This differentiation is thought to be controlled by genes (protooncogenes and oncogenes which will be discussed later).
  • 25. Cellular metabolism in cancer cells Normal cells depend on aerobic metabolism for 90% of their energy needs. Only cells without mitochondria use anaerobic metabolism for their primary energy needs. • Neoplastic (CA) cells depend more on anaerobic metabolism • CA cells use higher levels of glucose • CA cells are engage in high levels of protein catabolism in order to get energy (rob normal cells of protein)
  • 26. Characteristics of benign and malignant neoplasms Tumor: Swelling that can be caused by a number of conditions including inflammation and trauma. Neoplasia: These are clusters of cells that can be benign or malignant Benign Neoplasm: contain well differentiated cells that are clustered together in a single mass. Malignant Neoplasm: less well differentiated to undifferentiated and have the ability to break loose, enter the circulatory or lymphatic systems and form secondary malignant tumors at other sites.
  • 27. Non-neoplastic growth patterns • Hyperplasia: Increase in the number of cells in a tissue or an organ • Metaplasia: Conversion of one cell type to another • Dysplasia: Alteration in the size, shape and organization of cells. Dysplastic cells can become or precede neoplastic/cancerous changes. Benign and malignant neoplasms are usually differentiated by their cell characteristics, rate of growth, manner of growth, capacity to metastasize and spread to other parts of the body and potential for causing death.
  • 28. Examples of non-neoplastic growth patterns
  • 29. Comparison of benign and malignant neoplasms
  • 30. Comparison of benign and malignant neoplasms
  • 31. Carcinogenesis Strictly interpreted, this is the development of cancer in otherwise normal tissue. • The natural development of cancer is usually an orderly process that comprises several stages and occurs over a period of time. • Includes initiation, promotion and progression
  • 32. Terms important in carcinogenesis Oncogene: Proto-Oncogene: • These are genes that can • These are genes that promote the growth of cancer regulate normal cellular cells processes (very important) • these genes are usually • promote normal embryonic derived from mutations of cellular development normal genes • Once growth and • Can interfere with the cells' development ceases, they normal functions and protein genes are usually "turned off" expression • Can be "turned on" by viruses, chemicals, or any carcinogen
  • 33. Terms important in carcinogenesis Tumor Suppressor Genes: Mutations in proto-oncogenes • They normally function to and tumor suppressor genes regulate growth can occur in embryonic • Mutations to this part of development, and this usually the genome can cause the leads to an earlier cell to engage in development of cancer, and a unregulated growth more significant presentation o p53 gene in many of the cancer cancers o BRCA-1, BRCA-2 Mutations in these genes can o APC gene also be induced by exposure • Can be inherited to carcinogens.
  • 34. CRC Development: Adenoma-to-Carcinoma Sequence First somatic APC Second APC K-ras Further changes mutation or loss mutation or loss mutation DCC loss TP53 loss eg, NM23 loss Normal mucosa Hyperproliferative Adenoma, increasing epithelium in size, and dysplasia Carcinoma Germline APC mutation (FAP) Adapted from Bishop and Hall. Eur J Cancer. 1994;30A:1946-1956, with permission.
  • 35. Carcinogenesis:  Initiation This is a mutation in the cell's genetic structure • Can be inherited • Can be induced after exposure to a carcinogen (chemical, radiation, or viral agent) o the altered cell becomes a clone • This is an irreversible process, but: o the DNA may repair itself o most deranged cell can undergo apoptosis o cells with altered antigens are subject to immune surveillance o or the DNA alteration may not become functionally significant • Often, for the DNA alteration to be significant, more than one episode of genetic damage must occur
  • 37. Carcinogenesis:  Promotion • During this stage, the environment has to promote or favor the development of the "initiated" or altered cell • There is a period of latency from 1 to 40 years, between the initial genetic alteration and the actual clinical evidence of cancer • An important distinction between initiation and promotion is that the action of promoters is reversible. o important promoters include: dietary fat, smoking, obesity, and alcohol consumption ****Cigarette smoke can act as both an initiator of malignant change and a promoter of cancer development.
  • 38. Carcinogenesis:  Progression This is the final stage in the natural history of cancer. • Increased growth of the tumor (Significant) • Increased invasiveness of the tumor • Spread of the cancer to a distant site o Metastasis: the cancer has spread from the primary site (where the cancer developed) to another organ or part of the body  Most frequent sites: lungs, brain, bone, liver, and adrenal glands  often determined or limited by angiogenesis  get hematogenous metastases and lymphatic metastases
  • 39. Process of Cancer Development
  • 40. Process of metastatic spread FIG. 16-5
  • 41. What do Metastases look like? FIG. 16-4
  • 42. What about the Oncofetal Antigens? Oncofetal antigens are tumor antigens that are found on the surfaces and inside of cancer cells, as well as fetal cells. • Appearance in cancer cells is thought to be reflective of that cell regaining its embryonic capability to differentiate into various types of cells o Carcinoembryonic antigen (CEA): normally found in fetal gut, liver, and pancreas cells and disappears during the last 3 months of fetal life. This antigen is overexpressed in colon cancer and also elevated in cigarette smokers, pt's with ulcerative colitis and cirrhosis of the liver o Alpha-Fetoprotein (AFP): fetal liver cells and liver cancer o CA-125: Ovarian cancer
  • 43. Risk factors that predispose for cancer development 1. Heredity 2. Hormones 3. Immunologic mechanisms 4. Chemical Carcinogens 5. Radiation 6. Oncogenic viruses
  • 44. Risk factors that predispose for cancer development Heredity: Hormones: • Cancer related genes • Hormones can have been identified that overstimulate the increase an individual's proliferation of certain susceptibility to the cells overtime development of certain o Prostate cancer is cancers thought to develop in o BRCA-1/BRCA-2: 40- elder males because of 80% lifetime risk of lifetime exposure to breast cancer androgens o Accounts for approx. o DES babies had higher 10% of cancers rates of Uterine cancer
  • 45. Risk factors that predispose for cancer development Immunologic Mechanisms: Chemical Carcinogens: • Mutant cells are constantly • These include chemicals formed, but are destroyed like cigarette smoke and by immune cells through asbestos, drugs like immuno-surveillance hormones, • people with depressed immunosuppressive immune systems have agents, cytotoxic drugs, higher rates of cancer and dietary factors like o AIDS related kaposi's fats and nitrates sarcoma • some of these compounds are either initiators or promotors, cigarette smoke is both
  • 46. Risk factors that predispose for cancer development Radiation: Oncogenic Viruses: • When cells are exposed to • Some viruses can infect a radiation, there is damage cell and inject their genetic to one or both strands of material into the host DNA DNA...this can either • This can be exposure to disrupt a tumor ionizing radiation or suppressor gene or add exposure to UV radiation an oncogene to the DNA • Melanoma is a cancer causing malignant with significant transformation increases in incidence o Hep B/C and HCC • Hiroshima survivors o HPV and Cervical Cancer
  • 47. Risk factors that predispose for cancer development Age: • Advanced age is the single most significant risk factor o 50% of cancers occur in those >65 years of age o the symptoms of cancer are often perceived or written off as "age related changes" o Can be more vulnerable to complications from cancer treatment
  • 48. Prevention and the early detection of cancer Preventative Measures: • Patient education is one of the most important nursing interventions that can be utilized in the prevention and progression of cancer. Patients should be educated in the following: o Risk factors: what are they (sun exposure, smoking, diet, exposure to chemicals, radiation) and how to avoid exposures o Health Promotion behaviors: quit smoking, low fat, high fiber, low nitrate diet, exercise, routine screening exams
  • 49. Warning signs of cancer development
  • 51. Screening Guidelines for the Early Detection of Breast Cancer, American Cancer Society • Yearly mammograms are recommended starting at age 40. • A clinical breast exam should be part of a periodic health exam, about every 3 years for women in their 20s and 30s, and every year for women 40 and older. • Women should know how their breasts normally feel and report any breast changes promptly to their health care providers. Monthly breast self-exam is an option for women starting in their 20s. • Screening MRI is recommended for women with an approximately 20%-25% or greater lifetime risk of breast cancer, including women with a strong family history of breast or ovarian cancer and women who were treated for Hodgkin disease.
  • 52. Screening Guidelines for the Early Detection of Cervical Cancer, American Cancer Society • Screening should begin approximately three years after a women begins having vaginal intercourse, but no later than 21 years of age. • Screening should be done every year with regular Pap tests or every two years using liquid-based tests. • At or after age 30, women who have had three normal test results in a row may get screened every 2-3 years. However, doctors may suggest a woman get screened more frequently if she has certain risk factors, such as HIV infection or a weakened immune system. • Women 70 and older who have had three or more consecutive Pap tests in the last ten years may choose to stop cervical cancer screening. • Screening after a total hysterectomy (with removal of the cervix) is not necessary unless the surgery was done as a treatment for cervical cancer.
  • 53. Screening Guidelines for the Early Detection of Prostate Cancer, American Cancer Society The prostate-specific antigen (PSA) test and the digital rectal examination (DRE) should be offered annually, beginning at age 50, to men who have a life expectancy of at least 10 years. Men at high risk (African-American men and men with a strong family history of one or more first-degree relatives diagnosed with prostate cancer at an early age) should begin testing at age 45. For men at average risk and high risk, information should be provided about what is known and what is uncertain about the benefits and limitations of early detection and treatment of prostate cancer so that they can make an informed decision about testing.
  • 54. Screening Guidelines for the Early Detection of Colorectal Cancer and Adenomas, American Cancer Society 2008 Beginning at age 50, men and women should follow one of the following examination schedules: • A flexible sigmoidoscopy (FSIG) every five years • A colonoscopy every ten years • A double-contrast barium enema every five years • A Computerized Tomographic (CT) colonography every five years • A guaiac-based fecal occult blood test (FOBT) or a fecal immunochemical test (FIT) every year • A stool DNA test (interval uncertain) People who are at moderate or high risk for colorectal cancer should talk with a doctor about a different testing schedule
  • 55. Other Diagnostic tests if cancer is suspected or diagnosed (will depend on primary site)examination of cells that are sloughed into the 1. Cytology studies: various body secretions or scraped from organ cavities (i.e. pap smear)....suspicious findings may necessitate an actual biopsy 2. Chest Xray/Mammogram: looking for radiological evidence of a primary or a metastatic cancer site (not very sensitive, you need a pretty big lesion to see it on chest xray) 3. CBC: evaluate the blood for anemia, alterations in WBCs, thrombocytopenia or thrombocytosis 4. Blood tests for tumor markers/antigens: CEA, AFP, CA19-9, CA- 125, CA15-3, CA27-3, PSA
  • 56. Other diagnostic tests if cancer is suspected or diagnosed (will depend on the primary site) 5. Biopsy: refers to the process of obtaining tissue for histologic exam and susequent diagnosis of the disease • Needle Biopsy • Incisional • Excisional 6. CT Scan: Multiple xrays are done, usually from the neck to groin to get a picture of the internal organs and look for metastatic disease (often part of routine staging of cancer 7. PET Scan: This is a specialized test looked at the metabolic rate of tissues. A radioactively labeled sugar solution is ingested and the scanner looks for areas of the body that take up the sugar...good in cancer because of the elevated glucose needs of cancerous cells
  • 57. Other diagnostic tests if cancer is suspected or diagnosed (will depend on the primary site) 8. Sigmoidoscopy/Colonoscopy: Visualize and remove polyps, precancerous lesions and cancerous lesions from the colon. 9. Bone Scan: Radioisotopes are injected and looks for increased uptake in the bone (hot spots) which indicate metastatic disease in the bones 10. Bone Marrow Study: evaluate the progenitor cells, look for genetic abnormalities (most often used in hematologic malignancies, but a metastatic cancer to the bone marrow can also be evaluated).
  • 58. Ways of classifying cancer... 1. Anatomic Site 2. Histological Analysis (grading) 3. Extent of Disease (Staging)
  • 59. Ways of classifying cancer:  Anatomic site The tumor is identified by the tissue of origin, the anatomic site, and the behavior of the tumor. • Tissue of origin (embryonic): o Carcinomas originate from the embryonal ectoderm (skin and glands) and endoderm (mucous membranes of the resp. tract, GI tract, GU tract) o Sarcomas originate from embryonal mesoderm (connective tissue) o Lymphomas/Leukemias originate from the hematopoietic system • Location of primary tumor: Breast cancer in breast tissue, prostate cancer in prostate tissue • Behavior: Benign or Malignant
  • 60. Ways of classifying cancer:  Histological analysis This is a microscopic analysis of the tumor, looking at the appearance of cells and the degree of differentiation. Broken down into 4 grades based on the differentiation. • 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
  • 61. Ways of classifying cancer:  Extent of disease This is describing the extent of the disease in the body. They can be broken up into the American Joint Committee on Cancer (AJCC) and Tumor/Node/Metastases (TNM) staging. Both these staging systems are more amenable to solid tumor evaluation (not leukemias/lymphomas). stage 0: cancer in situ 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
  • 62. Ways of classifying cancer :  Extent of disease
  • 63. Major treatment options in cancer 1. Surgery 2. Radiation 3. Chemotherapy 4. Hormonal therapy 5. Biotherapy 6. Targeted therapy 7. Bone Marrow and peripheral blood stem cell transplantation
  • 64. How do you choose an option for cancer treatment? Treatment option choices are dictated by the goals of therapy. • Cure • Control • Palliation
  • 65. Surgery 1. Indicated if the cancer is confined and well-encapsulated, where surgery alone can "cure" the cancer. 2. "Debulk" the tumor so other treatments can be more effective. 3. Prophlaxis, prevent the development of cancer 4. Diagnose or stage a tumor 5. Palliate the symptoms from a cancer 6. Reconstruction from previous cancer surgery 7. Determine if therapy if effective (very rarely the primary goal of surgery, but may be secondary)
  • 66. Complications of surgery and nursing care • Loss of body part/function • Disfigurement • Increased risk for infection if immune suppressed • Increased risk for bleeding if thrombocytopenic • Increased risk for wound healing if the patient is on antiangiogenic therapy Nursing Care • Routine pre- and post-op care • Additional psycho-social needs of cancer patients o Anxiety o Body image disturbance • Attention to the other risk factors that accompany a patient with cancer
  • 67. Radiation Therapy Ionizing radiation is used for most treatments: • acts at the cellular level to damage or alter the cells • breaks chemical bonds, disrupts DNA and interferes with cell activity and mitosis • Affects the cell cycle in the following order: M-phase, G2- phase, G1-phase, and S-phases • Cells damaged by radiation either die or are unable to divide Indicated as primary therapy for cancer if the tumor is in an area that is difficult to reach surgically or where surgery could be significantly disfiguring (H&N CA) • Some tumors are more radiosensitive than others • Can shrink the tumor for potential surgery • Can palliate complications from cancer
  • 68. How is radiation therapy delivered? • External Radiation: o teletherapy: this form of therapy is external to the patient and distant from the tumor. • Internal Radiation: o This is known as brachytherapy, and the radiation source is placed in close contact with the tumor  Sealed: radiation is contained within some sort of device like a needle or seed device which may be placed near the tumor site temporarily or permanently  Unsealed: radiation is not contained in a device so the radiation is not confined to one area of the body (po, IV, or instilled into a body cavity)
  • 69. Nursing Management of Radiation Therapy Patients Safety Precautions: • Needed when caring for patients undergoing brachytherapy. Remember, the patient is not radioactive but the implant is. • Handling of secretions and excretions must be done wearing gloves if the patient has received an unsealed radioactive source (the source is now systemic once in the body). • The patient who has sealed radiation implants emits radiation while the implant is in place but his/her body secretions are not radioactive • Remember that the patient who receives external radiation is not radioactive at any time
  • 71. Nursing Management of Radiation Therapy Patients • Providing patient teaching based on the type of radiation they are to receive...teletherapy or brachytherapy o teletherapy: teach regarding the machinery, any braces or adaptive devices that will be used, what will be expected (positioning during therapy, side effects) o brachytherapy: teach regarding how this is different from teletherapy, what sort of care they will undergo, limiting of visitors, and the distance visitors need to keep during the therapy.
  • 72. Nursing Management of Radiation Therapy Patients • Skin preparation prior to therapy: with teletherapy, the skin is marked by the radiation therapist to identify the exact area where the radiation should be delivered. The patient should be instructed not to wash these markings off. • Prevent skin breakdown...teach the patient to avoid scratching...dry itchy skin is a common complication of teletherapy. Usually recommend aloe vera and very simple emoillients (no petroleum products, cause increased breakdown) • Promote healing of skin after therapy: cleanse thoroughly if skin is broken, observe for s/s of infection and treat promptly if infection occurs, optimize nutrition to promote healing
  • 73. Skin Complications with Radiation Therapy
  • 74. Skin Complications with Radiation Therapy
  • 75. Nursing Management of Radiation Therapy Patients • Minimize GI upset o Mouth XRT causes dry mouth and stomatitis  Biotene mouthwash and gel  warm water/baking soda rinse  assess for and treat oral candidiasis quickly  for taste alterations, encourage moist, bland food o Esophageal/Upper abdominal XRT causes N/V/Esophagitis  antiemetics: teach about the medication, frequency  bland diet  Proton Pump Inhibitors o Rectal/lower abdominal radiation causes diarrhea  teach about the use of immodium/Lomitil  Low residue diet
  • 76. Chemotherapy This is indicated in the treatment of hematologic and solid tumor malignancies. Can be the primary therapy or used adjunct to another therapy (surgery or radiation). Chemotherapy works in different ways, but primarily by disrupting the production of essential enzymes, inhibits RNA, DNA, and protein synthesis, and can prevent cell mitosis. Most effective against rapidly dividing cells.
  • 77. Goals of Chemotherapy The goal of chemotherapy is to eliminate or reduce the number of malignant cells in the primary tumor and/or the metastatic tumor site. The response of malignant cells to chemotherapy is determined by: 1. Mitotic rate of the tissue from which the tumor arises. 2. Size of the tumor 3. Age of the tumor 4. Location of the tumor 5. Presence of resistant tumor cells
  • 78. Chemotherapy Classifications Cell Cycle Specific: Cell Cycle Nonspecific: • these drugs are effective • Effective on both dividing and during specific phases of the resting cells (G0 phase). cell cycle (G1, S, G2, M) • Damage the cell at some relating to cellular point in the cycle but death proliferation/replication. does not occur until the cell • Effective only during one attempts to divide specific phase and are often • Very dose dependent given over a prolonged period to ensure that the majority of cells reach the phase the drug acts on. • Very time dependent Cell Cycle specific and Cell Cycle Non- specific are often given together to enhance death of tumor cells
  • 79. Chemotherapy Examples Cell Cycle Specific: Cell Cycle Non-specific: • Antimetabolites: mimic • Alkalating Agents: first naturally occuring substances chemotherapies used, thus interfering with enzyme Damage DNA by breaking the function or DNA synthesis double-stranded helix o capecitabine (Xeloda) • Antitumor antibiotics: bind o methotrexate (Trexall) directly to the DNA, inhibiting • Mitotic Inhibitors: Some act DNA replication and by stabilizing microtubules so interfering with transcription they aren't able to align the • Hormone therapy: interferes chromosomes to divide with the action of a hormone, • Topsimerase Inhibitors: or with the enzymes that Inhibit the enzyme produce hormones topsimerase that function to make breaks in DNA for replication
  • 81. Extravasations of Chemotherapy Chemotherapy drugs can have direct affects on the tissue it's exposed to upon administration. One of the major routes of administration for chemotherapy is the IV route. Since most chemotherapy drugs are either irritants or vesicants, a major risk of peripheral IV chemotherapy is Extravasation. • This is the infiltration of drugs into the tissues surrounding the infusion site o Can cause local tissue damage o Can lead to permanent damage and loss of function All vesicant chemotherapy should be administered using a central venous access device (CVAD)
  • 82. Why?
  • 83. If extravasation occurs... • Stop the infusion immediately, notify the MD • Remove the IV infusion tubing and try and aspirate any remaining drug in the catheter with a new syringe • Inject the prescribed antidote, if one exists, in the infusion needle or in a pincushion fashion in the skin around the extravasation (the MD will direct the route/order) • Topical corticosteroids may be applied if ordered • Elevate the site • Cold Compresses for 1st 24/48 hours unless an alkaloid or oxaliplatin has been infiltrated (use heat with alkaloids or oxaliplatin) • Document the extravasation • Observe the site at designated intervals
  • 86. Toxicities/Side Effects from Chemotherapy Chemotherapy does not distinguish between normal cells and cancer cells so toxicity to normal tissues is expected. Acute Toxicity: Nausea, vomiting, allergic reactions, dysrhythmias, cold sensitivity Delayed Toxicity: mucositis, diarrhea, stomatitis, alopecia, neutropenia, anemia, pancytopenia Chronic Toxicity: damage to organ systems such as the heart, liver, kidneys, lungs, nervous system, and bone marrow. Of all of the above, the most life threatening is the neutropenia/pancytopenia
  • 87. Nursing Management and Considerations • Knowledge of safe administration and disposal of chemo agents. Each hospital will have protocols for both administration and disposal of the chemo agents. • Know how to differentiate between tolerable side effects and toxic effects (nausea and vomiting vs. pulmonary fibrosis or cardiotoxicity) and how to deal with affects as they occur. • Lab Results need to be considered and followed prior to, during and post chemotherapy administration (CBC and other's per the chemo toxicity) • Patient education is important during administration re: drug action, how to deal with side effects. Remember that information can decrease anxiety.
  • 88. Hormonal Therapy Some tumors are very hormone dependent, and can grow at an increased rate in the presence of certain hormones (eg breast, uterine, prostate cancers) • Altering the level of hormone available can decrease or stop the growth of a particular tumor. o tamoxifen for breast cancer: blocks the estrogen receptors on breast cancer cells o letrozole for breast cancer: inhibits the enzyme that converts androgen to estrogen o Lupon for prostate: inhibits the production of testosterone by the testicles o Extreme hormone manipulation: orchiectomy/ oophorectomy
  • 89. Side Effects of Hormone Therapy • Hypercoagulability: more prone to DVTs/PEs • Selective Estrogen Receptor Modulators: increased risk of uterine cancer • Weight gain • Lupron: emotional lability, gynecomastia
  • 90. Biotherapy/Targeted Therapy: This consists of agents that modify the relationship between the biologic response of the host to the tumor cells. Includes immunotherapy, monoclonal antibodies, antiangiogenic agents and tyrosine kinase inhibitors. Work 3 ways: 1. Have direct anti-tumor effects 2. They restore, augment, or modulate host immune system mechanisms 3. They have other effects, like inhibiting the cancer's ability to metastasize or differentiate.
  • 91. Immunotherapy Interferon: • Naturally occuring protein that is produced by WBCs and other body cells in response to a variety of stimuli including viral infections • Exposure of cells to interferon causes production of antiviral proteins which then help to protect the neighboring cells from attack by viruses. • Other functions of interferon are: o inhibition of viral DNA o stimulates the expression of TAA's on the cell surface so that the chance of an immune response against the cancer is increased. • Cannot be administered orally because of the protein nature • Significant side effects include depression and Significant Fatigue
  • 92. Immunotherapy Interleukin 2: • Approved for use in Renal cell cancer and melanoma • Help the immune system cells recognize and destroy abnormal cells • IL-2 is produced by the helper T-lymphocytes and stimulates the proliferation of other T-lymphocytes, activates NK cells, stimulates the release of other cytokines like gamma interferon, TNF, IL-1 and IL-6 • Side effects area also significant, IL-2 is given IV as an inpatient. Causes "Shake and Bake" syndrome with high fevers and rigors. Also can cause damage the kidneys and a careful balance of hydration and diuretics is needed....VERY SPECIALIZED NURSING CARE
  • 93. Monoclonal Antibodies These are antibodies or immunoglobulins that are produced to bind antigens that are overexpressed on cancer cells. This blocks the "downstream activity" of these receptors in stimulating the growth of these tumor cells • Herceptin binds the Her2Neu molecule that is overexpressed in some breast cancer tumors • Cetuximab binds the EGFR receptor that is overproduced in many cells, but is FDA approved for use in colon and head and neck cancer • Tarceva (erlotenib) is an oral agent that binds the EGFR receptor and is approved in pancreatic cancer. (big side effect is a significant dose limiting rash for erlotenib and cetuximab)
  • 94. Sites of Action of Targeted Therapy FIG. 16-21
  • 95. Targeted Therapies (which can be interchanged often with monoclonal antibodies) Interferes with cancer growth by targeting specific cellular receptors and pathways that are important in tumor growth. They have a very different side effect profile than chemo and are often successful at improving the outcome of chemotherapy without increasing the toxicity. • Antiangiogenic therapies: block the circulating vascular endothelial growth factor, leading to decreased blood vessel formation to tumors/metastases • Tyrosine Kinase Inihibitors: block the phosphorylation of proteins in the cell leading to decreased growth.
  • 96. Bone marrow and peripheral blood stem cell transplantation Life saving treatment option for malignant and non-malignant conditions. Involves giving high dose chemotherapy with the goal of clearing all the malignant cells and then "rescuing" the patient with new hematopoietic stem cells that can repopulate the bone marrow. • Can be a donor that is HLA matched (preferably 6/6 match) (Matched Unrelated Donor) • Can be a syngenic donor (identical twin) • Can be cord blood (only a small recipient) (again, Matched Unrelated) • Can be from your own stem cells harvested ahead of the procedure (Auto)
  • 97. Harvesting of Peripheral Blood for Stem Cell • Donor is given Colony stimulating factors that boost the release of stem cells into the peripheral circulation • May also be given chemotherapy to stimulate the release of the stem cells • Donor is then hooked up to a pheresis machine that takes the blood out of one vein, filters out the stem cells, and returns the blood back to the donor through another vein • Those stem cells are collected over a week period and then infused (IV) into the patient once they are completed with their chemotherapy conditioning.
  • 99. Complications of Stem Cell Transplants • The biggest complication of stem cell transplants is the risk of infection. o patients are usually on protective isolation o may have standing orders if a fever occurs o +/- neutropenic diet (no raw fruits of vegetables, no uncooked or undercooked meat) • Graft vs. Host Disease is an often chronic complication: the patient's new bone marrow if from an unrelated donor may mount an immune response against the host (t-cell mediated) o instruct on the importance of adherence to the immunosuppressive regimen.
  • 100. What's upcoming in cancer care? • Genetic profiling of individual tumors to determine the effectiveness of potential chemotherapy drugs. o ERCC1 in lung cancer for Irinotecan and platnim activity o DPD in colon cancer to determine the responsiveness of the tumor to fluropyrimidines • More aggressive surgical and chemotherapy management of metastatic disease rendering patients disease free who were previously uncurable • More targeted treatment and radiation, making cancer more of a chronic disease • Further advancements in the knowledge of prevention leading to a lower incidence of cancer
  • 101. Thank you for your attention Good luck studying!!! See you on Tues, Dec. 6th in the Little theater at 7am