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A. Oncology Overviewnavigator

  1. Second leading cause of death in developed countries
    1. Lung
    2. Colorectal
    3. Breast
    4. Prostate
    5. Ovarian
    6. About 900,000 new cases and 400,000 deaths per year in USA
    7. Long term survival rates for many cancers have improved 1973 to 1998 [1]
  2. Leading cause of death worldwide
    1. Hepatocellular
    2. Cervical
    3. Gastric
  3. General Risk Factors
    1. Environmental factors are more important than heritable factors [2]
    2. Genetic Contribution / Family History: 5-40% of risk for major cancers [2]
    3. Smoking and Smoke Exposure
    4. Alcohol Consumption
    5. Chronic Viral Infections (such as hepatitis viruses B and C, human papillomavirus)
    6. Chronic bacterial infections (such as Helicobacter pylori)
    7. Exposure to electrical currents and magnetic fields does not cause cancer [3]
    8. Chronic exposure to high doses of electrical currents may increase risk of childhood leukemia [3]
    9. Significantly increased and similar risk of cancer, including types, in transplant recipients and HIV/AIDS infected persons [11]
  4. Definitions
    1. Progression from normal to malignant cell is called transformation
    2. Transformation is believed to occur over 5 or more years (>15 years in some)
    3. Many tumors progress from benign growths to malignant
    4. Tumor simply refers to an abnormal mass of cells
    5. Benign tumors enlarge but to not invade surrounding tissues
    6. Malignant tumors, also called neoplasms, have the capacity to invade normal tissue
    7. Malignant tumors also have the capacity to break off from primary tumor, migrate around the body through blood or lymph, and establish distant growths
    8. These distant growths are called metastases
    9. Death from cancer usually due to interference of normal tissue/organ function by metastatic tumors
  5. Cell Growth Histopathology
    1. The suffix "plasia" means growth
    2. Dysplasia means abnormal growth of a specific cell type
    3. Dysplastic cells retain some histological and molecular markers of original cell type
    4. Metaplasia refers to growths which are abnormal for specific anatomic area, but do not possess invasive or metastatic potential
    5. Metaplastic cells usually appear completely different from the original cell type
    6. Neoplasia, or "new growth", refers specifically to tumors (benign or malignant)
  6. Types of Cancers
    1. Carcinoma - tumors of epithelial tissues
    2. Adenocarcinoma - tumors of glandular (epithelial) tissue
    3. Sarcoma - tumors of connective tissue (such as muscle, bone, fibroblasts)
    4. Lymphoma - tumors of lymph nodes, usually B or T lymphocytes
    5. Leukemia - tumors of blood cells, usually granulocytes or lymphocytes
    6. Carcinosarcoma - mixed tumor types
    7. Teratoma - tumors of progenitor cells with multipotent differention capacity
  7. Issues in Clinical Oncology
    1. Screening - detection of disease prior to onset of symptoms or signs
    2. Diagnosis - presence of disease and accurate (molecular) subtype
    3. Staging - extent of spread of disease
    4. Prognosis - aggressiveness versus indolence of cancers
    5. Treatment - combined modalities are nearly always used
    6. Quality of Life - drug toxicities, palliative measures, patient activities all critical
    7. Death from Cancer
    8. Prevention of Cancer - lifestyle modifications, chemoprevention, environmental risk reduction

B. Malignant Tumor Progression [4] navigator

  1. Acquired Capabilities of Cancer Cells
    1. Evading apoptosis
    2. Self-sufficiency in growth signals (autocrine and paracrine)
    3. Insensitivity to anti-growth signals
    4. Limitless replicative potential
    5. Sustained angiogenesis
    6. Tissue invasion and metastasis
  2. Most neoplasms arise from a single clone of transformed (malignant) cells
    1. Over 5 years is required for growth of cloned transformed cell into apparent tumor
    2. Chronic inflammation may aide in tumor initiation and/or progression (see below) [5,39]
    3. Additional time is required for tumor mass to overwhelm the host
    4. This additional time is highly variable depending on the aggressiveness of the tumor
  3. Five Distinct Alterations for Neoplastic Transformation of Human Cells (see below) [4]
  4. Overview of Tumor Growth Stages
    1. Clonal cell population grows to a mass 3-4mm in diameter called primary tumor
    2. Primary tumors >3-4mm in diameter require specific blood supply for further growth
    3. Angiogenesis, the growth of new blood vessels, is a critical step in tumor growth
    4. As malignant tumors increase in size, they invade basement membrane and/or stroma
    5. This requires specific enzymes and receptors to degrade surrounding tissue
    6. Tumors can also enter blood vessels and/or lymph nodes
    7. Tumor metastasis to LN is a "marker" for development of cells which have left primary tumor site
    8. It is not known whether tumor cells in normal LN are able to escape the node
  5. Most small (<0.5mL or <5x10e8 cells) tumors are curable by surgical removal [6]
    1. Most small neoplasms are contained (Stage 1)
    2. In some tumors, even small neoplasms have invaded tissues and metastasized
    3. Tumors as small as 1-2 mm in diameter have the potential to metastasize
    4. Possible that a 1cm tumor can shed 3-5 million cells into blood every 24 hours
    5. Detection of small tumors, however, nearly always improves survival
    6. Thus, development and use of tests for screening for early stage (small tumors) is a major priority in cancer research
  6. Tumors of >10e8 to >10e9 cells usually invade surrounding tissue
    1. This requires various proteases and other destructive enzymes
    2. Matrix metalloproteinases and other enzymes have been implicated in the process
    3. Tumors then enter stromal areas where they invade blood vessels and LN
  7. Telomeres and Telomerase [7,35,38]
    1. Many cancer cells are believed to be able to proliferate indefinitely
    2. Normal cells die after ~50-60 generations, at least in part due to shortened telomeres
    3. Cancer cells appear to have overcome telomere shortening during cell division
    4. About 90% of cancers (over)-express telomerase, which replicates telomeres
    5. Telomerase is normally only expressed in germ cells and early embryo cells
    6. Telomerase consists of an RNA component and a set of proteins
    7. Proteins include TERT (active enzyme), dyskerin, chaperones, other proteins
    8. Elevated levels of telomerase in cancer cells is a poor prognostic factor
    9. Inhibition of telomerase activity may provide a novel mechanism for cancer therapy
  8. Tumor Immunity [39,43]
    1. Inflammation as a response to tumors does occur, perhaps as a response to "tumor antigens"
    2. In most cases, it is "low-grade", chronic inflammation
    3. The low-grade inflammation likely because tumor antigens are similar to host proteins
    4. Includes production of growth and angiogenic factors that stimulate tissue repair
    5. These factors can also promote tumor survival, growth, and proliferation
    6. Occasionally, inflammation becomes more rubust, similar to acute inflammatory processes
    7. In these cases, the immune response can induce a regression in the cancer
    8. Converting a pro-tumorigenic to an anti-tumorigenic environment is under study
    9. Most cancer related inflammation is due to innate immune system
    10. B lymphocytes, of the adaptive immune system, can contribute to carcinogenesis
    11. However, many immunodeficiency syndromes are associated with increased cancer risk
    12. This may be driven by high rates of chornic inflammation in immunodeficiency
    13. Stimulating the immune system has been modestly successful in reducing cancers
  9. Tumor Angiogenesis [36,42]
    1. New blood vessel growth (angiogenesis) is essential to tumor growth
    2. Tumors secrete a variety of angiogenic factors including TGFß [8]
    3. Local endothelial cells are activated and express integrin alpha v beta 3 (aVß3)
    4. Vascular endothelial growth factors (VEGF) play a major role [28]
    5. VEGF family includes VEGF-A, -B, -C, -D and placental growth factor (PlGF)
    6. The major mediator of tumor growth is VEGF-A; PlGF may also play an important role [42]
    7. VEGF-A binds to VEGF receptor 2 (VEGF-R2) initiating a cascade of signaling pathways
    8. Anti-VEGF antibodies
    9. Leads to activation of MAP kinase, PI3K/Akt, migration, and vascular permeability
    10. Anti-VEGF monoclonal Ab (bevacizumab, Avastin®) approved for colorectal, lung, breast ca
    11. An additional key angiogenesis pathway involved notch-deltalike ligand 4 (Dll4) pathways
    12. Circulating endothelial-derived progenitors may restore tumor vessels after chemotherapy
    13. Endothelial cells in some tumors contain similar genetic mutations to the tumor cells [33]
    14. Some aggressive tumors can mimic activities of endothelial cells by creating fluid- conducting, vascular-like networks
    15. Tumor and stromal derived angiogenic factors mediate neovascularization of tumors
    16. Neovascularized tumors can then grow
  10. Tumor Metastasis
    1. Once tumor cells are in blood, they "home" to specific organs based on surface receptors
    2. Tumor homing requires typical adhesion molecules including integrins and others
    3. Tumors then bind to endothelium in organ to which they have homed
    4. They traverse endothelium (destruction and/or migration) and establish new sites
    5. Extracellular matrix breakdown is required for metastatic invasion
    6. Most tumors establish multiple metastases
    7. Immune system may help select for metastatic tumor phenotypes [9]
    8. Metastatic tumor cells display marked genetic heterogeneity [10]

C. Molecular Biology of Cancer [4] navigator

  1. Progression of normal cells to metastatic tumor caused by dysfunction of ~5 pathways [4]
    1. Retinoblastoma (pRB) pathway
    2. p53 pathway
    3. Telomerase (hTERT) pathway
    4. Ras pathway
    5. Unknown pathway in humans equivalent to SV40 small t antigen
    6. The acquired capabilities discussed above are provided by dysfunction in these pathways
  2. Thus, cancer is now known to be a disease of gene mutation and dysregulation
  3. In general, mutations in genes regulating growth, cell cycle, and differentiation occur [12]
  4. Two major classes of genes involved in cancer have been identified [38]
    1. Oncogenes
    2. Tumor suppressor genes (anti-oncogenes)
    3. Mutations in these genes may lead to abnormal growth and cell cycle control [12]
    4. Genomic profiling has aided in understanding gene expression changes in various cancers [13,14]
    5. Epigenetic alterations such as DNA methylation changes, histone alterations contribute to abnormal gene expression in cancer [34]
    6. Generalized genomic hypomethylation very common in cancers []
    7. Promoter-specific hypermethylation, leading to gene silencing, found for tumor suppressor genes as well as for certain microRNAs [34]
    8. MicroRNA dysregulation increasingly reported in cancer; potentially prognostic [40,41]
    9. Cancers will likely be reclassified in the future based on gene expression profiles
  5. Causes of DNA Mutation
    1. Loss of DNA replication fidelity during (normal) aging
    2. Chronic inflammation and reactive oxygen species [15]
    3. Environmental carcinogens
    4. Various chemotherapeutic agents that damage DNA
    5. Ionizing radiation
    6. Dysfunction of endogenous DNA repair systems (due to genetic or acquired mutations)
  6. Oncogenes [38]
    1. Mutations in these genes have been shown to cause or contribute to tumors
    2. In humans, most oncogenes are mutated versions of normal genes
    3. In some cases, viruses contain genes which are "oncogenic"
    4. For example, hepatitis B virus contains one or more genes which can cause liver cancer
    5. Ras, a normal signal transduction protein which binds GTP, is mutated in >50% of human tumors
    6. A large variety of oncogenes within >5 classes have been idenitfied
    7. In some cases, specific chromosomal translocations cause oncogene activation
    8. These chromosomal translocations are most common in leukemias and some lymphomas
    9. In general, single copies of specifically mutated oncogenes cause cancer ("dominant")
    10. Dysregulation of micro RNAs, which regulate specific mRNA transcription, are increasingly recognized in cancer [40,41]
  7. Classificaiton of Oncogenes [40]
    1. Transcription factors
    2. Chromatin remodelers
    3. Growth factors and growth factor receptors
    4. Signal transducers
    5. Apoptosis regulators
  8. Tumor Suppressor Genes (TSG) [38]
    1. Inactivating mutations in TSG have been shown to cause or contribute to tumors
    2. DNA methylation reduces gene expression and may down regulate TSG mRNA [16,31]
    3. DNA hypermethylation associated with increased DNA methylases, histone acetylation [31]
    4. Some TSG such as FHIT occur at fragile sites and are inactivated by chromsome breaks [17]
    5. In humans, most TSG are inactive versions of normal cell cycle inhibitory genes
    6. In some cases, TSG are DNA repair genes
    7. In other cases, viruses contain proteins which directly inactivate TSG
    8. For example, human papilloma virus E6 protein binds to and inactivates p53, a TSG
    9. In general, both normal copies of TSG must be inactivated in order to develop cancer
  9. MicroRNAs and Cancer
    1. MicroRNAs potential as diagnostic / prognostic biomarkers
    2. Regulate gene expression by altering transcription of complimentary mRNAs
    3. High expression of microRNA mi-21 associated with poor survival (2.4X risk) and poor therapeutic outcome, independent of TNM staging and other clinical variables in colon ca
    4. Overexpression of mi-21 associated with reduced apoptosis in experimental systems
    5. mi-21 overexpression may reduce tumor suppressor gene expression including PTEN (phosphatase and tensin homologue) and tropomyosin 1
  10. Certain Viruses Clearly Cause Human Cancers
    1. Hepatitis B Virus (HBV) - hepatocellular carcinoma
    2. Hepatitis C Virus (HCV) - hepatocellular carcinoma
    3. Epstein-Barr Virus (EBV) - lymphoreticular malignancy, nasopharyngeal carcinoma
    4. Human Herpesvirus 8 - Kaposi's Sarcoma
    5. Human Papilloma Virus (HPV) - cervical cancer, some vaginal cancer
    6. HTLV-I and HTLV-II - adult T cell leukemia
  11. Helicobacter Pylori [19]
    1. Chronic bacterial infection in stomach linked with peptic ulcer disease
    2. Associated with cancers
    3. Gastric Carcinoma
    4. Mucosa-Associated Lymphoid Tissue (MALT) Neoplasms
  12. Molecular Genetic Defects Accumulate as Tumors Increase in Size
    1. Tumors are characterized by highly unstable DNA replication and repair
    2. Chromosome numbers and ultrastructure are highly abnormal
    3. In late stage tumors, essentially all tumor cells are aneuploid
    4. DNA proofreading and repair capabilities are essentially lost
    5. Therefore, germline DNA in tumors is highly abnormal
    6. Disseminated single metastatic cells show marked genetic heterogeneity [10]
    7. Alterations in five pathways are likely sufficient to transform human cells (see above) [4]
    8. Tumor gene expression profile can be used for classification [26] and drug response [27]
  13. Metastatic Potential [25,26]
    1. Originally believed that tumors acquired metastatic potential as they grow
    2. Whole genome analysis of early breast cancers (Stage I or II) suggests metatastic potential via hematogenous dissemination is a property of early tumors
    3. Primary tumor gene expression profile used to predict clinical outcome, drug response [27]
    4. Out of 25,000 genes, a 70-gene prognosis profile was created
    5. This prognosis profile was superior to all standard systems, including LN status
    6. Data indicate that primary tumor contains critical metastatic potential
  14. Genomic profiling of tumor cells is increasingly used in molecular diagnosis, prognosis, and therapy selection [37,40]

D. Cancer Screening [1,20] navigator

  1. Goal is to develop sensitive and specific screening tests
  2. These tests should be inexpensive, easily administered, and reduce mortality/morbidity
  3. For many neoplasms, there is controversy over screening
  4. The screening tests below are directed at asymptomatic, low risk patients
  5. Patients with a family history of specific cancers are automatically not low risk
  6. Screening in patients >65 years old is generally of unclear benefit
  7. Screening recommendations for genetic cancer syndromes are not covered here
  8. Whole-body 19F-flurodeoxyglucose PET scanning has been used to detect occult disease
  9. Screening Tests With Proven Cancer Death Reduction
    1. Cervical And Vaginal Cancer - Pap Smear, pelvic and external genitalia exam
    2. Breast Cancer - mammography and possibly self examination
    3. Colon Cancer - screening sigmoidoscopy and stool occult blood testing
    4. Prostate Cancer - serum PSA test (likely), digital rectal examination (unclear)

E. Cancer Diagnosisnavigator

  1. Mainly involves initial suspicion
    1. Positive cancer screening test
    2. Presence of suspicious systemic or local signs
    3. Inadvertent detection by diagnostic test done for another reason
  2. Radiologic Evaluation Generally Follows
    1. In the past, plain radiography was commonly performed
    2. However, computerized tomography and/or magnetic resonance imaging now preferred
  3. Tissue must be obtained
    1. Fine needle biopsy often replaces more extensive surgical biopsy
    2. Open surgery indicated for deep cancers and where debulking required
    3. Cancer diagnosis depends on proven pathology
    4. Tissue from lymph node (LN) metastases may be used for diagnosis
  4. Prognostic Markers
    1. Clinical Stage, or extent of detectable disease, is best single prognostic marker
    2. Tumor grade is generally considered second best prognostic marker
    3. Molecular markers are being developed to augment (replace) histopathologic markers
  5. Gene Expression Profile
    1. Most transciptional profiles derived from tumor cells themselves
    2. Increasing interest in expression profiles from tumor microenvironment and tumor infiltrating immune / inflammatory cells
    3. Increasing interest in gene expression profiles of subpopulations of tumor cells
    4. Profiles are used for definitive molecular classification [26,37]
    5. Improved Prognosis - overall and disease-free survival
    6. Response to drugs [27,37]
    7. Invasiveness 186-gene signature derived from CD44+CD24- breast ca cells independently associated with overall and disease-free survival in breast and other cancers [18]
  6. Tumor proteomic pattern (protein profile) for classification and prognosis [29]

F. Cancer Stagingnavigator

  1. Definitions here are generalized; specific staging has been developed for each tumor
  2. Stage 0 - no clinical evidence for cancer; screening test for specific cancer positive
  3. Stage 1 - single tumor mass, no lymph node (N) or distant metastases (M)
  4. Stage 2 - tumor mass (often larger than stage 1), local N spread may be present
  5. Stage 3 - tumor mass of any size with distant N spread and/or other organ invasion
  6. Stage 4 - any tumor mass size, any N spread, but with distant M disease
  7. Survival decreases with increasing tumor stage
  8. Methods for Staging
    1. Surgical pathology remains the gold standard
    2. Primary tumors (T) are often removed and can be measured
    3. Nodal (N) disease can be assessed by gross dissection or sentinal N analysis
    4. CT, MRI, or PET with CT can be used for whole body detection of distant M
    5. PET(FDG) combined with CT is more accurate than MRI for tumor staging [32]

G. Cancer Treatment navigator

  1. Modalities
    1. Surgery [22]
    2. Radiation Therapy
    3. Chemotherapy
    4. Hormonal Therapy
    5. Immunotherapy
  2. Treatment is based on tumor type and extent of disease
  3. Surgery
    1. Curative in localized and some locally advanced diseases
    2. Used to debulk tumors - reduce tumor mass
    3. For specific metastatic disease to reduce morbidity
  4. Radiation Therapy
    1. Potential alternative to surgery for localized disease (particularly indolent forms)
    2. Also used for locally advanced disease (including LN irradiation)
    3. Specifically for masses causing serious morbidity (oncologic emergencies)
    4. Combination with surgery and/or chemotherapy for local control of disease
    5. Radioactive implants can be used to control local and some metastatic disease
  5. Chemotherapy
    1. Mainstay of treatment for metastatic disease (Stage IV)
    2. Commonly used in "adjuvant" setting for LN positive disease
    3. Also used in adjuvant setting for tumors with known early metastatic potential
    4. Generally cytotoxic and some cytostatic agents with poor therapeutic windows
  6. Hormonal Therapy
    1. Specifically for hormone responsive tumors
    2. Mainstay of therapy for metastatic prostate and breast cancers
    3. Increasing use of non-sex steroids for other kinds of cancers (APML, lung)
    4. Induce apoptosis and/or differentiation of tumor cells
    5. Generally better tolerated than chemotherapeutic agents
  7. Immunotherapy
    1. Considered experimental for most tumor types
    2. Biological agents (interferons, interleukin 2, others) approved for some tumors
    3. Active and passive immunotherapy under investigation
    4. Tumor vaccines are also being developed
  8. Response to Therapy
    1. Usually measured initially by radiographic reduction (usually CT scan) of tumor size
    2. Complete response (CR) for solid tumors means "no detectable disease" on CT scan
    3. Partial response (PR) is usually >50% reduction in diameter of largest lesion
    4. Stable disease (SD) means no progression (or <50% reduction) in tumor growth
    5. Progressive disease (PD) means increase in tumor size during therapy
    6. Increase in tumor response rates translates into an overall survival advantage
    7. However, for individual (small) trials, and for individual patients, tumor size response does not allow for accurate prediction of ultimate survival benefit [23]
    8. Gene expression profiling will be used in future to predict tumor response [26,27]
  9. Depression is common in cancer patients, and should be aggressively treated [44]

H. Cancer Preventionnavigator

  1. Major Behavioral Contributions to Cancer [21]
    1. Smoking
    2. Excessive alcohol intake
    3. Overweight / obesity
    4. Low fruit and vegetable intake
  2. Lifestyle Modification
    1. Stop smoking
    2. Moderate alcohol consumption
    3. Proper diet: folate, bioflavenoids (fruits / vegetables), others
    4. Maintain normal weight - exercise and proper diet
  3. Diet
    1. Low fat diet linked with reduced risk of colon cancer
    2. Certain plant derived molecules may reduce cancer risk
    3. Avoid overweight
  4. Environmental
    1. Reduce environmental exposure to toxins and poisons
    2. Second hand smoke is major source of exposure
    3. Industrial process chemicals are now routinely evaluated
  5. Genetic Screening
    1. Familial cancer syndromes
    2. Prophylactic surgical removal when indicated
    3. Heritable factors are minor contributions to cancer risk [2]
  6. Chemoprevention Drugs
    1. Tamoxifen clearly reduces the risk of breast cancer
    2. Raloxifene also appears to reduce the risk of breast cancer
    3. Oral contraceptives reduce the risk of ovarian cancer
    4. Aspirin and other NSAIDs appear to reduce the risk of colon cancer
  7. Treatment of Chronic Viral Infections
    1. Treatment of infections generally reduces risk of developing cancers
    2. Hepatitis B Virus (HBV)
    3. Hepatitis C Virus (HCV)

I. Cancer Morbidity and Mortality navigator

  1. Early stage localized cancers do not cause death
    1. Most early stage (Stage I and most Stage II) cancers do not cause symptoms or signs
    2. Some early stage cancers can cause localized or systemic symptoms
    3. Localized symptoms due to direct impact of tumor on critical structure
    4. Systemic symptoms are due to release of bioactive compounds
  2. Paraneoplastic Syndromes
    1. Small tumors Infrequently produce biologically active products
    2. These products can have potent clinically apparent effects
    3. The effects of these tumor products cause "paraneoplastic syndromes"
    4. Many tumors secrete or induce inflammatory cytokines
    5. These cytokines, such as interleukin 6, cause systemic symptoms
    6. Systemic symptoms sometimes attributable to tumors include fever, night sweats, and weight loss
    7. As tumors progress, weight loss increases and anorexia becomes prominant
    8. Weight loss due to tumors is often called "cancer cachexia" or "wasting"
    9. Metastatic tumors interfere with normal tissue and organ function
    10. Interference with lung function, common with late stage tumors, can be fatal
    11. Cancer chemotherapy itself is highly morbid and induces wasting and immunosuppression
    12. Immunosuppression (usually neutropenia) increases risk of severe infection
    13. Neoplasms themselves induce immunosuppression
    14. Many patients succumb to infection secondary to the tumor and chemotherapy
  3. Systemic Symptoms
    1. Fatigue - most frequent symptom associated with cancer and therapy
    2. Fevers - mainly IL6, IL1, possibly tumor necrosis factor alpha (TNFa)
    3. Weight Loss - mainly TNFa (formerly called "cachexin"), catabolic state
    4. Night Sweats - IL6, IL1
    5. Anorexia - chronic inflammation
    6. Induction of acute phase reactants - catabolic state
    7. Cancer Pain - often associated with bony metastases, but may vary
  4. Fatigue [30]
    1. Likely related to chronic inflammation, catabolic state, anemia, acute phase reactants
    2. Except for anemia, etiology is poorly studied
    3. Erythropoietin (Epogen® and others) improves cancer associated fatigue in anemic patients
    4. Megesterol acetate (Megace®) alleviates anorexia and improves weight
    5. Prednisone reduces fatigue, improves quality of life in prostate cancer patients
    6. Methylphenidate (Ritalin® and others) can improve sleepiness and fatigue
    7. Cancer fatigue scale has been validated and studies are underway
  5. Quality of Life (QOL)
    1. Cancer patients are debilitated for various reasons:
    2. Problems associated with the neoplasm itself including pain, fatigue, malnourishment
    3. Problems associated with chemotherapy, surgery and/or radiation therapy
    4. Comorbid conditions
    5. Measurement of QOL is critical in assessment of all cancer treatments
    6. Often, performance status (PS) of patients is included in assessments
    7. Usually, PS rated from 0 to 4 (Southwest Oncology Group Definitions Used)
    8. PS 0 - fully active
    9. PS 1 - restricted in strenuous activity but fully ambulatory
    10. PS 2 - ambulatory and capable of self-care, but unable to do work
    11. PS 3 - capable of only limited self-care, confined to bed or chair >50% of time
    12. PS 4 - totaly disabled, incapable of self-care, totally confined to bed or chair
  6. Common Cancers (Descending Incidence)
    1. Lung
    2. Breast
    3. Prostate
    4. Colorectal
    5. Ovary
    6. Pancreas
    7. Lymphoma
    8. Leukemia
    9. Uterine
    10. Stomach
    11. Liver
    12. Esophagus
    13. Bladder
    14. Brain
    15. Myeloma
    16. Kidney
  7. Incidence of Hematologic Malignancies (1998) [24]
    1. Numbers are per 100,000 in USA
    2. Acute Myeloid Leukemia (AML) 2.3
    3. Acute Lymphoblastic Leukemia (ALL) 1.5
    4. Myelodysplastic Syndromes (MDS) 9.3
    5. Multiple Myeloma 4.3
    6. Hodgkin's Lymphoma 2.8
    7. Non-Hodgkin's Lymphoma 13.9
    8. Chronic Myeloid Leukemia (CML) 1.3
    9. Chronic Lympyocytic Leukemia (CLL) 6.0
    10. Hairy Cell Leukemia 0.2
    11. Mycosis Fungoides / Sezary Syndrome 0.4
    12. Polycythemia Vera (Myeloproliferative Syndrome) 1.9
    13. Essential Thrombocythemia (Myeloproliferative Syndrome) 0.7
    14. Waldenstrom's Macroglobulinemia 0.3

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