1. what are protooncogenes?
    • Keeps cell behavior under control
    • --mutations can result in oncogene "amplification" (multiple copies) n-myc x poly-->blastoma
  2. What are Tumor suppressor genes?
    • Inhibit growth and control the development of tumors
    • --BRCA-1/2: defects-->decreased tumor suppression activity-->^risk of ovarian/breast cancer
    • --P-53: defects-->decreased tumor suppression activity--> ^risk of bladder/breast/colon/liver/lung cancer.
  3. How do hormone receptors influence the growth of cancer?
    • Some cancers have hormone receptors (estrogen, progesterone, androgen, etc). which, when activated-->increased replication of the cells.
    • In this case (prostate, breast), hormone suppressant therapy is indicated. (tamoxafen)
  4. What are some differences between benign and malignant tumors?
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    • Benign brain tumors will take up space-->^ICP, and are often hard to remove (deep within hemispheres or brainstem). Therefore "benign" might not be a good word to describe them
  5. Stages of cancer development?
    • Initiation
    • Promotion
    • Progression
  6. What happens at initiation?
    • Mutation in cell's genetic structure
    • Requires "two-hit" insult
    • --Mutation + some other stress (could be another mutation) to the mutated area. 
    • --Mutation is irreversible, but due to apoptosis cells may never progress to a tumor and may never cause problems.
  7. What happens during promotion?
    • Factors encourage growth of the cancer cells?
    • --tobacco smoke (1st and 2nd hand), radiation, chemical exposure (petroleum)
  8. What happens during progression?
    • Cancer cells are actively dividing, growing, getting worse.
    • --can grow by:
    • ----direct extension: invasion into surrounding tissue. 
    • ----hematogenous spread: through the blood stream-->sites of mets (bone, brain, lung, liver).
    • ----Lymphatic spread: same as hematogenous, but through the lymphatic system.
  9. Immune system's Role in cancer control and spread.
    • B-Cells resist tumor growth by anti-carcinogenic antibodies.
    • T-Cells: produce cytokines (IL-2 and interferon) that can directly kill tumor cells). 
    • --Pts with HIV/AIDS are at greater risk for cancer because v immunity.
  10. What are oncofetal antigens and tumor markers
    • cell's ability to return to a more "immature" state.
    • --carcinoembryonic antigen (CEA)
    • --AFP: Good test for testicular mass. ^AFP = positive for cancer. After resection, v AFP is expected. 
    • --VMA, HVA, dopamine: ^catecholamines appear in urine. 
    • Prostate Specific Antigen (PSA): Good test, but have higher than desired false positives.
  11. What's the difference between palliative and terminal care?
    Palliation may contain elements of control to prolong life. Terminal care is purely comfort care/quality of life remaining.
  12. Who finally makes a diagnosis of cancer?
    • The pathologist. Radiologists, and primary care cannot make it. 
    • --Will usually take 24-48 hrs to process biopsy. 
    • --Help family to understand the process to help manage anxiety and frustration.
  13. What is the Goldie-Coldman hypothesis?
    • Resistant cell growth is related to "genetic instability" of the tumor. 
    • --As long as tumor cells are present, there is a risk of those cells developing resistance to treatment. 
    • --Followup therapy includes includes similar but different drugs in an effort to eradicate any resistant cells that may have developed.
  14. What is the Norton-Simon Hypothesis?
    • Tumors contain both fast and slow-growing populations; use sequential non-cross resistant combinations of drugs. 
    • Protocols will use efficacy of treatment to evolve new/better protocols.
  15. What is TNM staging?
    • Tumor size?
    • Nodes affected? (regional lymph nodes)
    • Mets (x means cannot be determined)
  16. Nursing's role of chemo administration
    • Cross-checking orders
    • pharmacy communication
    • pt/family education (translational therapy)
    • medication admin and prep
    • monitoring for toxicity (can be acute, slow onset, and cumulative).
  17. Basics of radiation therapy
    • Total dose calculated by tissue to be treated
    • --superficial/sensitive vs. deep/tough
    • Total dose is divided into equal amounts administered over M-F for a number of weeks. 
    • Computer sims determine/prepare area to be treated
    • Weekly CBCs (hemoglobin >10 -->better outcomes. Transfuse if <10.)
    • Toxicity is a big problem: skin, hair (can be permanent if "boosted"), blood counts, GI mucosa (most uncomfortable of adverse effects), fatigue (normal; Tx with sleep).
  18. Types of radiation
    • External beam:
    • --2-D
    • --3-D conformal: multiple ports with small beams all irradiating at common site. May have smaller/fewer side effects. 
    • --usually outpatient. Work with pt to determine what time of day is preferable. 
    • Brachytherapy (Implants): 
    • --Pt will be radioactive (keep in isolation, disposable meal trays, pt boredom a problem)
    • --Inpatient
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