Cancer: Part 1 – Flashcards
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For all ages, cancer is the ____ most common case of death in the U.S.
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2nd
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The overall 5-year survival rate for cancer is now ____%.
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66%
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Normal cells respect boundaries of surrounding cells and tissues and stay out of other territories, thus inhibiting growth of surrounding tissues unlike themselves (occurs thru barrier of physical contact); this is particularly evident during wound healing: when edges of a wound meet, the cells stop migrating until they are surrounded by other cells on all sides.
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Contact Inhibition
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Programmed cell death: occurs when cell becomes mutated or damaged. * Body's safety mechanism: normal! * Greek for "shedding of leaves from tree" Something inside or outside cell triggers "cell suicide" genes to produce damaging enzymes: cell shrinks & pulls away from other cells to be phagocytized. * Means of regulating number of cells in a tissue & eliminate cancer cells or other dangerous cells * Occurs during fetal development to remove webbing b/w digits
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Apoptosis
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Cancer cells lose contact inhibition and grow on top of one another or on top of/between normal cells; Cancer cells respond differently to body's regulating mechanisms: divide indiscriminately; proliferate despite mutations; etc.
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2 adverse effects of cancer cells
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Proliferation of cancer cells is continuous and indiscriminate: tumor grows b/c cells continue to multiply: 1x2x4x8x16
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Pyramid effect
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Normal cellular genes: regulate ordinary cell processes; "Genetic Locks" that keep cell in mature functioning state; PROMOTE growth
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Protooncogenes
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SUPPRESS growth; regulate ordinary cell growth * BRCA1 & BRCA2 (alterations cause breast & ovarian cancer * APC gene (alterations lead to colorectal cancer) * p53 (alterations cause bladder, breast, colorectal, esophageal, liver, lung, ovarian cancers)
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Tumor Suppressor genes
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Tumor-inducing genes: mutation of protooncogenes; cell becomes malignant and may produce proteins or hormones from fetal/embryonic periods that shouldn't be created.
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Oncogenes
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May be "unlocked" by: carcinogen exposure (chemical, radiation), oncogenic viruses, genetic alterations
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How might protooncogenes be altered?
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Well-differentiated, encapsulated, expansive mode of growth, characteristics similar to parent cell (fairly normal), slight vascularity
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Characteristics of benign neoplasms
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Poorly differentiated, metastatic capacity, moderate to marked vascularity, possible recurrence, mode of growth is infiltrative & expansive, rarely encapsulated, cells abnormal (unlike parent cells)
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Characteristics of malignant neoplasms
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Initiation, promotion, progression
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3 stages of cancer development
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1st stage of cancer development: IRREVERSIBLE mutation of genetic structure; may develop into clone of neoplastic cells; set off by chemical, viral, genetic, radiation factors
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Initiation
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pesticides, asbestos, radon, chemotherapy drugs, immunosuppressants, cigarette tar, diet coke
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Example of chemical carcinogens
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2nd stage of cancer development: REVERSIBLE proliferation of altered cells: increase in altered cells causes an increase in mutations
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Promotion
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Dietary fat, obesity, cigarette smoking, alcohol consumption: lifestyle behaviors that are modifiable
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Promoting Agents
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Approximately ____ of cancer-related deaths in the U.S. are related to tobacco use, physical inactivity, obesity, and unhealthy diet.
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half
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This is both an initiator and a promoter: ex: cigarette smoke
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Complete carcinogen & example
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May be between 1-40 years; between initial cellular alterations and clinical evidence of cancer (critical mass: 1 cm tumor w/ 1 billion cancer cells); length of period varies with mitotic rate of tissue of origin & other environmental factors
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Latent period
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Final stage of cancer development: increased growth rate of tumor, including invasiveness & metastasis; Metastasis begins with rapid development of a primary tumor
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Progression
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In what stage of cancer development, does a tumor develop its own blood supply (to survive) & penetrate walls of lymph or vascular vessels allowing it to metastasize elsewhere?
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Progression
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To reject or destroy cancer cells if perceived as non-self: may be inadequate if cancer cells arise from the body's own normal cells
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Role of immune system in cancer & loopholes of this function
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The response of the immune system to antigens, such as tumor-associated antigens (TAAs), of the malignant cells; occurs continuously
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Immunologic surveillance
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These cells involved in immune response monitor cell surface antigens and detect and destroy abnormal cells
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Lymphocytes
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Kill tumors (dominant role); produce cytokines, such as interferon and interleukin, which stimulate T cells, NK cells, B cells, and macrophages to get busy and fight!
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Functions of cytotoxic T cells in battling cancer:
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Lyse tumor cells indiscriminately; with stimulation from T cells' cytokines, cytotoxic activity increases
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Functions of NK cells in fighting cancer:
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When activated by interferon, lyse tumor cells; also secrete interleukin, tumor necrosis factor (cause hemorragic necrosis of tumors), and colony-stimulating factors (regulate BC production & stimulate fxn of WBCs)
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Functions of monocytes/macrophages in fighting cancer:
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Produce specific antibodies that bind to tumor cells and kill them by complement fixation & lysis
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Functions of B cells in fighting cancer:
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When cancer cells evade the immune system: occurs when cancer cells may have weak surface antigens, immune system tolerance to tumor antigens, suppression of T cell stimulating factors, antibodies binding TAAs (thus preventing recognition by T cells)
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Immunologic Escape
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antigens that are normal during fetal development, but appear in the presence of certain cancers; theory about reappearance of fetal antigens: may occur as a result of cell regaining capacity to differentiate into multiple cell types
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Oncofetal antigens
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Carcinoembryonic antigens (CEA) and Alpha-fetoprotein (AFP)
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Examples of oncofetal antigens
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Produced during fetal development, normally disappears during last 3 months of fetal life (production stops after birth); fetal protein increases in various cancers
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Carcinoembryonic antigen (CEA)
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Used to monitor effect of therapy and indicate tumor recurrence; elevated CEA titers after surgery indicates tumor was not completely removed; rise in CEA after chemo/radiation indicates recurrence or metastasis
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CEA as tumor marker
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Produced by fetal or malignant liver cells; found in developing fetus, newborns, pregnant women
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Alpha-fetoprotein (AFP)
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AFP levels found to be elevated in testicular carcinoma, viral hepatitis, nonmalignant liver disorders; AFP Dx value in hepatocellular cancer, & produced when mets liver growth occurs
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AFP as tumor marker
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Anatomic site, histology (grading), extent of disease (staging)
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3 ways tumors can be classified
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In this classification of cancer, tumors are identified by the tissue of origin, location of the body, and behavior of the tumor (benign or malignant)
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anatomic site classification
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Papilloma and adenoma are examples of benign/malignant epithelial/connective/nervous/hematopoietic tissue tumors?
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Benign epithelial tissue tumors (surface epithelium/granular epithelium)
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Carcinoma and adenocarcinoma are examples of benign/malignant epithelial/connective/nervous/hematopoietic tissue tumors?
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Malignant epithelial tissue tumors
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Fibroma, chondroma, rhabdomyoma, osteoma are examples of benign/malignant epithelial/connective/nervous/hematopoietic tissue tumors?
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Benign connective tissue tumors (fibrous tissue, cartilage, striated muscle, bone)
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Fibrosarcoma, chondrosarcoma, rhabdomyosarcoma, osteosarcoma are examples of benign/malignant epithelial/connective/nervous/hematopoietic tissue tumors?
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Malignant connective tissue tumors (fibrous tissue, cartilage, striated muscle, bone)
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Meningioma, ganglioneuroma are examples of benign or malignant epithelial/connective/nervous/hematopoietic tissue tumors?
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Benign nervous tissue tumors (meninges, nerve cells)
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Meningeal sarcoma and neuroblastoma are examples of benign or malignant epithelial/connective/nervous/hematopoietic tissue tumors?
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Malignant nervous tissue tumors (meninges, nerve cells)
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Hodgkin's lymphoma, non-Hodgkin's lymphoma, multiple myeloma, lymphocytic & myelogenous leukemia are examples of benign or malignant epithelial/connective/nervous/hematopoietic tissue tumors?
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Malignant hematopoietic tissue tumors (lymphoid tissue, plasma cells, bone marrow)
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There are no benign/malignant hematopoietic tissue tumors.
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Benign
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In this type of cancer classification, four grades are used to evaluate abnormal cells based on their resemblance to tissue of origin & degree of differentiation from tissue of origin. (The more they resemble the original tissue, the better the prognosis.
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Histologic Grading
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Mild dysplagia (cells differ slightly from normal cells); well differentiated (look most like tissue of origin): Low grade
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Grade I (Histologic Classification of Cancer)
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Moderate dysplasia (cells abnormal); moderately differentiated: intermediate grade
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Grade II (Histologic Classification of Cancer)
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Severe dysplasia (cells are very abnormal); poorly differentiated: high grade
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Grade III (Histologic Classification of Cancer)
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Anaplasia (cells are immature & primitive); undifferentiated; cell of origin is difficult to determine: high grade
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Grade IV (Histologic Classification of Cancer)
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Grade cannot be assessed
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Grade X (Histologic Classification of Cancer)
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Term for classifying the extent and spread of disease, based on anatomic extent rather than appearance of cells: clinical staging, TNM classification system
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Staging
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Cancer in situ
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Stage 0 (Clinical staging)
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Tumor limited to tissue of origin; localized tumor growth
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Stage I (Clinical staging)
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Limited local spread of tumor
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Stage II (Clinical staging)
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Extensive local and regional spread of tumor
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Stage III (Clinical staging)
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Metastasis of tumor
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Stage IV (Clinical staging)
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This system is used to determine the ANATOMIC EXTENT of disease according to tumor size and invasiveness, presence or absence of regional spread to lymph nodes, and metastasis to distant organs.
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TNM Classification System
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extent of primary tumor
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T of TNM
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absence or presence & extent of regional lymph node involvement
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N of TNM
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absence or presence of distant metastases
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M of TNM
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Family Hx of CA, dietary habits (alcohol, high fat, high carbs, etc), radiation exposure, viral exposure, carcinogenic exposure
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Risk Factors for Cancer
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Reduce/avoid exposure to known carcinogens (cigarettes, alcohol, asbestos) Balanced diet Exercise regularly Adequate rest Regular check-ups Reduce/eliminate/decrease stressors Teach CAUTION (seven warning signs of CA) Self-exams Seek care promptly if CA suspected Make time for relaxation/leisure activities Enhance coping ability
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Primary prevention & detection of cancer: What can patients be educated about?
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C: Change in bowel/bladder habits A: A sore that does not heal U: Unusual bleeding/discharge from body orifice or mole/freckle T: Thickening of tissue/lump in breast or elsewhere I: Indigestion or difficulty swallowing O: Obvious in a wart or mole N: Nagging cough or hoarseness
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Seven (late) warning signs of cancer
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Patient may experience fear & anxiety Clear & repeated explanations possible/necessary Diagnostic plan: health hx (emphasis on risk factors), physical exam, specific lab/diagnostic studies
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Secondary Prevention & Possible/Positive Dx of Cancer: Points to remember
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Cytology studies (Pap smear), Chest Xray, CBC, Guaiac for occult blood (w/ sigmoid/colonoscopy), Liver fxn test, Radiologic exam (mammogram), Radioisotope scan (bone/liver/lung/brain), CT, MRI, Oncofetal agent check: CEA/AFP, Bone marrow exam, Biopsy
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Diagnostic Tests for CA
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Removal of a tissue sample (by needle, incision, or excision) for pathological analysis; may be percutaneous, endoscopic, surgical; provides a definite Dx of CA; determines degree of differentiation
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Biopsy
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Biopsy of a small amount of tissue, thinly sliced, quickly frozen, & stained for immediate evaluation
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Frozen section
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A goal for CA Tx: may involve surgery or extended periods of systemic therapy (chemo) to provide a cure
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Curative therapy
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A goal for CA Tx: initial course & maintenance therapy (for recurrence): when cancer is incurable, but possible to live with for a time
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Control treatment plan
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A goal for CA Tx: relief or control of symptoms; maintenance of quality of life (may need to stop all therapies to feel better before imminent death)
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Palliation
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Cell type, Location/size of tumor, Extent of disease, Physiologic status, Psychological status; Finances
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Factors that determine treatment modality:
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Prevention, Cure & control, Supportive & palliative care, Rehabilitative care
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General purposes of surgical therapy
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Used for diagnosis (biopsy) Used to determine diagnostic & treatment plan Used to cure or control disease process of cancer (remove site where CA typically spreads): mastectomy, i.e.
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Uses for surgical therapy
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mastectomy, pneumonectomy, thyroidectomy, bowel resection
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Examples of prophylactic surgical therapy procedures:
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GT, colostomy, suprapubic cystostomy
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Examples of supportive care (surgical therapy) procedures:
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colostomy to relieve bowel obstruction; laminectomy to relieve spinal cord compression
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Examples of palliation (surgical therapy) procedures:
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breast reconstruction post mastectomy
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Examples of rehabilitative (surgical therapy) procedures:
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Cure, control, and palliation
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Goals of radiation therapy
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* APC (tumor-suppressor) gene is lost * Mutant RAS gene, an oncogene, keeps pumping new genes (the combination of the 2 above create cancer cell growth) * Immortality (Telomerase from embryonic cells is normally turned off, but is reactivated by cancer cells, enabling ability to replicate without limits)
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How are cancer cells different? (3 factors)
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Which tumor suppressor gene is activated by some cancer treatments and begins to work with the therapy to fight the disease?
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p53
