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Bio217F12Unit3Ch910HandoutCancerEpidem.ppt
- 1. Biology, Clinical Manifestations, and Treatment of Cancer Chapter 9 Unit III: Cell Proliferation: Cancer Cancer Epidemiology Chapter 10
- 2. Cancer Derived from Greek word for crab, karkinoma Malignant tumor Tumor Also referred to as a neoplasm new growth
- 3. Benign vs. Malignant Tumors Benign Malignant Grow slowly Grow rapidly Well-defined capsule Not encapsulated Not invasive Invasive Well differentiated Poorly differentiated Low mitotic index High mitotic index Do not metastasize Can spread distantly (metastasis) Mitotic index = rate of growth
- 4. Classification and Nomenclature Benign tumors Named according to the tissues from which they arise, and include the suffix -oma Lipoma Hemangioma Leiomyoma Chondroma
- 5. Classification and Nomenclature Malignant tumors Named according to the tissues from which they arise Malignant epithelial tumors are referred to as carcinomas Adenocarcinoma (from glandular epithelium) Malignant CT tumors are referred to as sarcomas Rhabdomyosarcomas (from skeletal muscle)
- 6. Classification and Nomenclature Cancers of lymphatic tissue are lymphomas Cancers of blood-forming cells are leukemias Carcinoma in situ (CIS) Epithelial malignant tumors that have not broken through BM or invaded the surrounding stroma
- 8. Stages of Cancer Spread Stage 1: Confined to organ of origin Stage 2: Locally invasive Stage 3: Spread to lymph nodes Stage 4: Spread to distant sites CIS special case
- 9. Tumor Staging by TNM System TUMOR NODES METASTASIS
- 10. Tumor Markers Tumor cell markers (biologic markers) are substances produced by cancer cells or that are found on plasma cell membranes, in the blood, CSF, or urine Hormones (Epi in blood, adrenal medullary tumor) Enzymes Genes Antigens (PSA in blood, prostate cancer) Antibodies
- 12. Viruses and Cancer Implicated Hepatitis B and C viruses Epstein-Barr virus (EBV) Kaposis sarcoma herpesvirus (KSHV) Human papillomavirus (HPV) Human T cell leukemialymphoma virus (HTLV)
- 13. Bacterial Cause of Cancer Helicobacter pylori Chronic infections are associated with: Peptic ulcer disease Stomach carcinoma Mucosa-associated lymphoid tissue lymphomas
- 14. Inflammation and Cancer Chronic inflammation is an important factor in development of cancer Cytokine release from inflammatory cells Free radicals Mutation promotion Decreased response to DNA damage
- 15. Tumor Spread Direct invasion of contiguous organs Known as local spread Metastases to distant organs Lymphatics and blood Metastases by way of implantation
- 16. Local Spread Invasion Cellular multiplication Mitotic rate vs. cellular death rate Mechanical pressure Release of lytic enzymes Decreased cell-to-cell adhesion Increased motility Intravasation Extravasation
- 17. Three-Step Theory of Invasion Tumor cell attachment Fibronectin and laminin Degradation or dissolution of the matrix Enzymes Locomotion into the matrix Invadopodia (pseudopodia)
- 18. HeLa cell a cell type in an immortal cell line used in research one of the oldest, most commonly used human cell lines derived from cervical cancer cells taken from Henrietta Lacks patient eventually died of her cancer on October 4, 1951 cell line was found to be remarkably durable cells propagated by George Otto Gey first human cell line to prove successful in vitro, which was a scientific achievement for the benefit of science neither Lacks nor her family gave Gey permission (at that time, permission was neither required nor sought) HeLa cells were used by Jonas Salk to test the first polio vaccine in the 1950s
- 19. Concept Check 1. Neoplasia a. abnormal proliferating cells w/ higher degree of autonomy 2. Anaplasia b. lack of differentiation, primitive cells 3. Autonomy c. cancer cells independence from normal cell controls 4. Tumor markers d. substances produced by cancer cells
- 20. 5. Which characterizes cancer cells? A. Poorly differentiated B. Metastasis C. Infiltrative growth D. Poor cell cohesiveness E. All of the above 6. Which is/are not malignant? A. Glioma B. Adenocarcinoma C. Rhabdomyoma D. Leukemia E. A and C
- 21. 7. Metastasis is: A. Alteration in normal cell growth B. Growth of benign or or malignant cells C. Mutational D. Ability to establish a secondary neoplasm at a new site 8. CIS is: A. Preinvasive B. Glandular or epithelial lesion C. Teratoma D. Carcinoma that has broken through BM E. Both a and b are correct
- 23. Environmental Risk Factors Increased Decreased Tobacco * Exercise Radiation * Proper Diet Ionizing UV Alcohol Sexual Behavior Diet Obesity Occupational Hazards Electromagnetic Fields ?
- 24. Environmental Risk Factors Tobacco Multipotent carcinogenic mixture Linked to cancers of the lung, lower urinary tract, aerodigestive tract, liver, kidney, pancreas, cervix Linked to myeloid leukemia
- 25. Environmental Risk Factors Ionizing radiation Emission from x-rays, radioisotopes, and other radioactive sources Exposure causes cell death, gene mutations, and chromosome aberrations Bystander effects Poor gene repair Changes in gap junction intercellular communication
- 26. Environmental Risk Factors Ultraviolet radiation Causes basal cell carcinoma, squamous cell carcinoma, and melanoma Principal source is sunlight Ultraviolet A (UVA) and ultraviolet B (UVB) Promotes skin inflammation and release of free radicals
- 27. Environmental Risk Factors Alcohol consumption Risk factor for oral cavity, pharynx, hypopharynx, larynx, esophagus, and liver cancers Cigarette/alcohol combination increases a persons risk
- 28. Environmental Risk Factors Sexual reproductive behavior Carcinogenic types of human papilloma virus High-risk HPV
- 29. Environmental Risk Factors Physical activity Reduces cancer risk Decreases insulin and insulin-like growth factors Decreases obesity Decreases inflammatory mediators and free radicals Increased gut motility
- 30. Environmental Risk Factors Occupational hazards Substantial number of occupational carcinogenic agents Asbestos Dyes, rubber, paint, explosives, rubber cement, heavy metals, air pollution, etc. Radon
- 31. Environmental Risk Factors Electromagnetic fields Carcinogenic? Are they, or arent they?
- 32. Environmental Risk Factors Diet Xenobiotics Toxic, mutagenic, and carcinogenic chemicals in food Activated by phase I activation enzymes Defense mechanisms Phase II detoxification enzymes Examples Compounds produced in the cooking of fat, meat, or proteins Alkaloids or mold by-products
- 33. Environmental Risk Factors Obesity Correlates with the body mass index (BMI) Adipose tissue is active endocrine and metabolic tissue
- 34. Environmental Risk Factors Obesity In response to endocrine and metabolic signaling, adipose tissue releases free fatty acids Increased free fatty acids gives rise to insulin resistance and causes chronic hyperinsulinemia Correlates with colon, breast, pancreatic, and endometrial cancers
- 35. Clinical Manifestations of Cancer Pain Little or no pain is associated with early stages of malignancy Influenced by fear, anxiety, sleep loss, fatigue, and overall physical deterioration Mechanisms Pressure, obstruction, invasion of sensitive structures, stretching of visceral surfaces, tissue destruction, and inflammation
- 36. Clinical Manifestations of Cancer Fatigue Subjective clinical manifestation Tiredness, weakness, lack of energy, exhaustion, lethargy, inability to concentrate, depression, sleepiness, boredom, and lack of motivation Suggested causes Sleep disturbance, biochemical changes (cytokines), secondary to disease and treatment, psychosocial factors, level of activity, nutritional status, and environmental factors
- 37. Clinical Manifestations of Cancer Syndrome of cachexia (Gr. bad condition) Most severe form of malnutrition Present in 80% of cancer patients at death Includes: Anorexia, early satiety, weight loss, anemia, asthenia, taste alterations, and altered protein, lipid, and CHO metabolism
- 38. Cachexia
- 39. Clinical Manifestations of Cancer Anemia A decrease of hemoglobin in the blood Mechanisms Chronic bleeding resulting in iron deficiency, severe malnutrition, medical therapies, or malignancy in blood- forming organs
- 40. Clinical Manifestations of Cancer Leukopenia and thrombocytopenia Direct tumor invasion to the bone marrow causes leukopenia and thrombocytopenia Chemotherapy drugs are toxic to the bone marrow Infection Risk increases when the absolute neutrophil and lymphocyte counts fall
- 41. Cancer Treatment Chemotherapy Use of nonselective cytotoxic drugs that target vital cellular machinery or metabolic pathways critical to both malignant and normal cell growth and replication Goal Eliminate enough tumor cells so bodys defense can eradicate any remaining cells
- 42. Cancer Treatment Chemotherapy Compartments 1: cells undergoing mitosis and cytokinesis 2: cells capable of entering the cell cycle in G1 phase 3: cells not dividing or have irreversibly left cell cycle Cells in compartment 3 will die a natural death
- 43. Chemotherapy
- 44. Cancer Treatment Ionizing radiation Eradicate cancer without excessive toxicity Avoid damage to normal structures Ionizing radiation damages the cancer cells DNA Surgery Biopsy and lymph node sampling Sentinel nodes Debulking surgery remove most of tumor Palliative surgery relief of symptoms Hormone therapy Receptor activation or blockage Interferes with cellular growth and signaling
- 45. Cancer Treatment Immunotherapy Theoretically, antitumor responses can selectively eliminate cancer cells while sparing normal cells Immune memory is long lived Numerous immunologic mechanisms are capable of rejecting different types of cancer Biologic response modifiers (BRMs)
- 46. Cancer Treatment Other forms of immunotherapy Interferon administration Antigens Effector cell lymphokines Monoclonal antibodies
- 47. Side Effects of Cancer Treatment Gastrointestinal tract Bone marrow Hair and skin Reproductive tract
- 48. Concept Check 1. Likely cause for fatigue in cancer patients: A. Biochemical changes due to treatment B. Muscle loss C. Pychologic factors D. All of the above 2. The pain experience with cancer: A. Affects the patient only in the early stages B. Occurs in bone metastasis C. Due to tissue necrosis D. Both b and c are correct
Editor's Notes
- #5: Fats, glial cells, uterine SMC, cartilage
- #11: Adrenal medulla tumor - pheochromocytoma
- #12: Currently accepted that multiple mutations are nec. for cancer to dev. A number of cell control paths must be altered: 1. cancer cells proliferate in absence of growth factors 2. antigrowth signals (contact inhibition) inactivated in cancer 3. & 4. apoptosis = self destruction path (like excessive growth) is disabled excess growth takes place 5. Angiogenesis new blood vessel growth 6. VEGF (vascular endothel. GF) is inactivated will fight cancer growth and spread
- #19: The cells were later commercialized, although never patented in their original form. Then, as now, there was no requirement to inform a patient, or their relatives, about such matters because discarded material, or material obtained during surgery, diagnosis or therapy, was the property of the physician and/or medical institution. This issue and Mrs. Lacks' situation was brought up in the Supreme Court of California case of Moore v. Regents of the University of California. The court ruled that a person's discarded tissue and cells are not their property and can be commercialized.(As stated in The Immortal Life of Henrietta Lacks by Rebecca Skloot) Initially, the cell line was said to be named after a "Helen Lane" or "Helen Larson", in order to preserve Lacks' anonymity. Despite this attempt, her real name was used by the press within a few years of her death. These cells are treated as cancer cells, as they are descended from a biopsy taken from a visible lesion on the cervix as part of Mrs. Lacks' diagnosis of cancer. A debate still continues on the classification of the cells.[citation needed] HeLa cells are termed "immortal" in that they can divide an unlimited number of times in a laboratory cell culture plate as long as fundamental cell survival conditions are met (i.e. being maintained and sustained in a suitable environment). There are many strains of HeLa cells as they continue to evolve by being grown in cell cultures, but all HeLa cells are descended from the same tumor cells removed from Mrs. Lacks. It has been estimated that the total number of HeLa cells that have been propagated in cell culture far exceeds the total number of cells that were in Henrietta Lacks' body.[5] Since that time HeLa cells have been used for "research into cancer, AIDS, the effects of radiation and toxic substances, gene mapping, and countless other scientific pursuits".[6] According to author Rebecca Skloot, by 2009, "more than 60,000 scientific articles had been published about research done on HeLa, and that number was increasing steadily at a rate of more than 300 papers each month."[7] Rebecca Skloot author of The Immortal Life of Henrietta Lacks 2009 http://www.jhu.edu/jhumag/0400web/01.html
- #20: 1. A 2.B 3.C 4.D
- #21: 5. E 6. E (a and c)
- #22: 7. D new growth at new site 8. e
- #32: EMR or EMF http://quwave.com/EMF-Pollution.html?gclid=CIyygLqm76kCFRYf3wodghjoYw
- #33: Xeno = foreigner, stranger; bios = life
- #49: 1. D 2. D