{"id":498,"date":"2023-08-22T21:53:55","date_gmt":"2023-08-23T01:53:55","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=498"},"modified":"2026-01-03T16:16:38","modified_gmt":"2026-01-03T21:16:38","slug":"neoplasias","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/neoplasias\/","title":{"raw":"Neoplasias - Learning Objectives","rendered":"Neoplasias &#8211; Learning Objectives"},"content":{"raw":"<div class=\"textbox textbox--learning-objectives\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\">Learning Outcomes and Specific Learning Objectives Study Guide<\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\n<strong>Learning Outcomes:<\/strong>\r\n\r\nBy the end of this section you will be able to:\r\n\r\n<strong>Describe key aspects of Neoplasms including:<\/strong>\r\n<ol>\r\n \t<li>Benign and Malignant tumors<\/li>\r\n \t<li>Common tumors and cancers: e.g. cervical cancer, skin cancer, ovarian cancer, breast cancer, prostate cancer, and benign prostate hypertrophy<\/li>\r\n \t<li>Aspects of etiology, risk factors, pathogenesis, and treatment options<\/li>\r\n<\/ol>\r\n\r\n<hr \/>\r\n\r\n<strong>Specific Learning Objectives - Study Guide:<\/strong>\r\n\r\nBy the end of this section you will be able to:\r\n\r\n<strong><span style=\"font-size: 1em\">Describe and explain the following terms:<\/span><\/strong>\r\n<ul>\r\n \t<li><strong>Cell Type:<\/strong>\u00a0 there are over 200 different cell types in the human body, each expressing unique proteins and having unique structure that allow it to fulfill its functions and role in the human body.<\/li>\r\n \t<li><strong>Tissue Types:<\/strong>\u00a0 There are 4 categories of tissue types, each one containing different types of cells and having different physical and functional properties:\r\n<ul>\r\n \t<li><strong>Epithelial tissue<\/strong> (e.g. dermis, endothelial tissue, mucosa membranes of GI tract and respiratory tract, apical layer of serous membranes, and synovial membranes)<\/li>\r\n \t<li><strong>Connective tissue<\/strong> (areolar, adipose, reticular, dense regular, dense irregular, elastic, hyaline cartilage, elastic cartilage, fibrocartilage, bone, blood, and lymph fluid)<\/li>\r\n \t<li><strong>Muscle tissue<\/strong> (skeletal muscle, cardiac muscle, and smooth muscle)<\/li>\r\n \t<li><strong>Nervous tissue<\/strong> (neurons and neuroglial cells)<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><span style=\"font-size: 1em\"><strong>Cell Division\/Cell Multiplication\/Proliferation<\/strong> - the process of mitosis<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\"><span style=\"font-size: 1em\"><strong>Cell Cycle<\/strong>\u00a0- <\/span><\/span>the stages of cell division which most often involves an immature cell or stem cell dividing into two genetically identical cells.\u00a0 Cell Cycling includes:\r\n<ul>\r\n \t<li>G<sub>1<\/sub> phase - cell functions normally, but grows, duplicating organelles and synthesizing proteins; lasts 8+ hours<\/li>\r\n \t<li>S phase - duplication of DNA and centrioles;\u00a0 synthesis of histones; lasts 8+ hours<\/li>\r\n \t<li>G<sub>2<\/sub> phase - growth and protein synthesis; lasts 2-5hrs<\/li>\r\n \t<li>Mitosis - Prophase, Metaphase, Anaphase, Telophase<\/li>\r\n \t<li>Cytokinesis - pinching of cell membrane into two daughter cells<\/li>\r\n \t<li>G<sub>o<\/sub> phase - cells exit cell cycle and mature\/differentiate to become fully functional cells that no longer go through cell cycling.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong><span style=\"font-size: 1em\">Cell Differentiation <\/span><\/strong><\/li>\r\n \t<li><strong>DNA duplication:<\/strong> performed by DNA polymerase with assistance of DNA helicase &amp; DNA ligase as well as enzymes that check for duplication errors and induce apoptosis if the errors can not be fixed.\u00a0 DNA duplication errors may lead to mutations that give rise to non-functional enzymes that compromise the cell's ability to survive\/function.\u00a0 Mutations can also give rise to cells that are cancerous.<\/li>\r\n \t<li>\r\n<div><strong>Telomeres:<\/strong> are the end caps of chromosomes that are added by telomerase until adulthood, at which time, telomerase is inactivated, and telomeres become shorter with each round of cell division.\u00a0 Once telomeres have shortened to a certain length, the cell becomes dormant and dies.\u00a0 This is thought to help old\/worn out\/less-functional cells be eliminated.\u00a0 Additionally, each round of cell division, is susceptible to DNA errors which make cells more and more at risk for developing a mutation that makes the cell cancerous.<\/div><\/li>\r\n \t<li><strong>Telomerase re-activation:<\/strong>\u00a0 has occurred in 90% of all cancers.\u00a0 In these cancerous cells the telomeres do not shorten and apoptosis is not triggered, making these cells immortal.<\/li>\r\n<\/ul>\r\n<div>\r\n\r\nBy the end of this section you will be able to list:\r\n\r\n<strong style=\"font-size: 1em\">Cancers with Highest Incidence Rates in Canada:<\/strong>\r\n\r\n<\/div>\r\n<ul>\r\n \t<li>Skin Cancer<\/li>\r\n \t<li>Breast Cancer<\/li>\r\n \t<li>Prostate Cancer<\/li>\r\n \t<li>Lung and Bronchus<\/li>\r\n \t<li>Colon and Rectum<\/li>\r\n<\/ul>\r\n<strong>Cancers with Highest Mortality Rates in Canada:.<\/strong>\r\n<ul>\r\n \t<li>Lung and Bronchus<\/li>\r\n \t<li>Breast<\/li>\r\n \t<li>Prostate<\/li>\r\n \t<li>Colon and Rectum<\/li>\r\n \t<li>Pancreas<\/li>\r\n \t<li>Ovary<\/li>\r\n \t<li>Leukemia<\/li>\r\n<\/ul>\r\n<div>\r\n\r\nBy the end of this section you will be able to:\r\n\r\n<strong><span style=\"font-size: 1em\">Describe and explain the following terms:<\/span><\/strong>\r\n<ul>\r\n \t<li><strong style=\"font-size: 1em\">Carcinogens:<\/strong><span style=\"font-size: 1em\"> factors, chemicals, etc. that increase risk of DNA mutations that put cells more susceptible to becoming cancerous.<\/span><\/li>\r\n<\/ul>\r\n<\/div>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Cigarette smoking - increases risk of developing all cancers (not just lung cancer)<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Cancer<\/strong><span style=\"text-align: initial;font-size: 1em\"> = a group of almost 100 genetic diseases (genetic = gene mutation \u2260 not necessarily inherited).\u00a0 In cancer:<\/span>\r\n<ul>\r\n \t<li>Cell growth (mitosis) becomes uncontrolled either because:<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Cell Cycle Regulator genes<\/strong> (coding for growth factors and growth inhibiting factors) that control the rate of mitosis have been mutated <span style=\"text-decoration: underline\">or<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\"><strong>Apoptosis Regulator genes<\/strong> (controlling the rate of apoptosis) have been mutated<\/span><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">DNA mutation can be caused by:<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<div>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>Viruses<\/li>\r\n \t<li>Radiation (UV, x-ray, gamma rays)<\/li>\r\n \t<li>Chemicals (e.g. nickel, asbestos, benzene solvents, aniline dyes, rubber, formaldehyde, chemotherapy drugs)<\/li>\r\n \t<li>Spontaneous errors during normal DNA synthesis<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Rapid rates of mitosis<\/strong> during injury repair may increase the risk of errors occurring.<\/li>\r\n \t<li>Mutations in genes that are in <strong>sperm<\/strong> or <strong>oocytes<\/strong> that are then passed to offspring can mean that cancers can at times be <strong>inherited<\/strong><\/li>\r\n \t<li>The above <strong>4 factors<\/strong> (viruses, chemicals, radiation, spontaneous) are thought to be involved in mutating or changing the expression levels of specific genes, such as:\r\n<ul>\r\n \t<li>&gt;40 <strong style=\"text-align: initial;font-size: 1em\">Proto-oncogenes:\u00a0<\/strong><span style=\"text-align: initial;font-size: 1em\"> genes that stimulate cell division &amp; inhibit both cell differentiation &amp; death \u2013 when these proto-oncogenes mutate they are typically a dominant mutation and are then called Oncogenes.\u00a0 Oncogenes stimulate increased cell division, and decrease cell differentiation &amp; death<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Tumor suppressor genes (TSG):\u00a0<\/strong><span style=\"text-align: initial;font-size: 1em\"> genes that normally slow down cell division, and promote apoptosis; when these genes mutate &amp; are turned off; cells can become immortal \u2192 cancer\u00a0 (e.g.TSG p53 is essential for regulating DNA repair and cell division, it has been nicknamed the \"guardian of the genome); most cancers have a p53 mutation. BRCA1 and BRCA2 are TSGs<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Stability Genes:<\/strong><span style=\"text-align: initial;font-size: 1em\"> that normally repair DNA and other genes that control the rate of mutation.\u00a0 These genes do not have a direct impact on rate of mitosis or apoptosis.\u00a0 (FYI:\u00a0 30-50% cancers have p53 mutation)<\/span><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong style=\"font-size: 1em\">Describe Types of DNA mutations:<\/strong>\r\n<ul>\r\n \t<li><strong style=\"font-size: 1em\">Synonymous<\/strong><span style=\"font-size: 1em\"> - no change, codes for same amino acid sequence<\/span><\/li>\r\n \t<li><strong style=\"font-size: 1em\">Non-synonymous<\/strong><span style=\"font-size: 1em\"> - change, codes for different same amino acid sequence<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Insertion<\/strong><span style=\"text-align: initial;font-size: 1em\"> - results in frame shift if in coding region of DNA<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Substitution<\/strong><span style=\"text-align: initial;font-size: 1em\"> - may result in amino acid substitution if in coding region of DNA<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Deletion<\/strong><span style=\"text-align: initial;font-size: 1em\"> - results in frame shift if in coding region of DNA<\/span><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong style=\"font-size: 1em\">Describe Possible Effects of DNA mutation:<\/strong>\r\n<ul>\r\n \t<li>No effect, as mutation is in non-coding region<\/li>\r\n \t<li>No effect, on the amino acid sequence (<em>as each amino acid is coded for by 2-4 different codons, e.g. GAA and GAG both code for the amino acid Glutamine<\/em>)<\/li>\r\n \t<li>Production of Dysfunctional Protein\/Enzyme<\/li>\r\n \t<li>Increased\/decreased production of protein\/enzyme<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong style=\"font-size: 1em\">Describe Properties of Neoplasm or tumor = new growth<\/strong>\r\n<ul>\r\n \t<li>Cellular growth that no longer responds to normal genetic controls<\/li>\r\n \t<li>Cell continues to reproduce, without the need for them to reproduce<\/li>\r\n \t<li>Increase in number of cells that are immature and cell cycling<\/li>\r\n \t<li>Deprives other cells of nutrition\u2026 decreasing their function\/abilities<\/li>\r\n \t<li>Neoplasms may consist of atypical or immature cells.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>In a young healthy person, usually abnormal or cancerous cells will be recognized by the immune system and destroyed.\u00a0 However, at times, cancerous cells evade the immune system.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<div><strong>Describe Characteristics of each tumor, which depend on:<\/strong><\/div>\r\n<div>1.\u00a0 Type of cell from which the tumor arises<\/div>\r\n<div>2.\u00a0 Unique structure and growth pattern<\/div>\r\n<ul>\r\n \t<li><strong>Benign tumors:<\/strong> <span style=\"text-decoration: underline\">not<\/span> considered cancer; slow-growing;\r\n<ul>\r\n \t<li>composed of <strong>differentiated<\/strong> cells growing faster than normal;<\/li>\r\n \t<li>are often <strong>encapsulated;<\/strong> and are <strong>freely moveable<\/strong> on palpation;<\/li>\r\n \t<li><span style=\"text-decoration: underline\">don\u2019t<\/span> metastasize; and once removed usually <span style=\"text-decoration: underline\">doesn\u2019t<\/span> recur;<\/li>\r\n \t<li>any tissue damage results from <strong>compression<\/strong> on adjacent structures (e.g. blood vessels); can be fatal in the brain (due to \u2191ICP, intracranial pressure)<\/li>\r\n \t<li>have tissue name plus the suffix <strong>-oma<\/strong> (e.g., adenoma) \u2013 exceptions!\u00a0 Glioma, Lymphoma\u2026.<\/li>\r\n \t<li>effects are more often local rather than systemic<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li><strong style=\"font-size: 1em\">Malignant tumors (cancers):<\/strong><span style=\"font-size: 1em\"> invade surrounding tissues and are characterized by<\/span>\r\n<ul>\r\n \t<li>atypical, immature, undifferentiated, nonfunctional dysplastic cells<\/li>\r\n \t<li>rapid reproduction; no cell-cell contact inhibition; lack of apoptosis;<\/li>\r\n \t<li>cancerous cells having abnormal cell membranes; altered surface antigens; and not adhering to each other as normal cells do; so cancerous cells often break loose from mass and invade other tissues;\u00a0 may spread to distant sites via blood or lymph<\/li>\r\n \t<li>often having systemic effects;\u00a0 have the tissue name plus the suffix -carcinoma (e.g., adenocarcinoma); and can recur if removed<\/li>\r\n \t<li><strong>Malignant (cancerous) cells<\/strong> often have an abnormal number of chromosomes = <strong>aneuploidy<\/strong><\/li>\r\n \t<li>Abnormal shaped nuclei = <strong>pleomorphism<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<div class=\"textbox__content\">\r\n<div><strong>Describe Types of Cancers:\u00a0 <\/strong>Cancers are named by the cell type that becomes cancerous<\/div>\r\n<ol>\r\n \t<li><strong>Carcinomas:<\/strong> epithelial cancers; 90% of cancers\r\n<ul>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Adenocarcinomas:<\/strong><span style=\"text-align: initial;font-size: 1em\"> epithelial cancers in a gland<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Squamous<\/strong><span style=\"text-align: initial;font-size: 1em\"> cell carcinoma: epithelial cancers originating in the skin<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Melanomas:<\/strong><span style=\"text-align: initial;font-size: 1em\"> epithelial cancers originating in the melanocytes of the skin<\/span><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Sarcomas:<\/strong><span style=\"text-align: initial;font-size: 1em\">\u00a0 Tumors of mesenchymal tissue (e.g. bone, muscle, cartilage, blood vessels); usually malignant.<\/span>\r\n<ul>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Osteosarcoma:<\/strong><span style=\"text-align: initial;font-size: 1em\"> Cancer of the bone<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Rhabdomyosarcoma:<\/strong><span style=\"text-align: initial;font-size: 1em\"> Cancer of the striated muscle<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Chondrosarcoma:<\/strong><span style=\"text-align: initial;font-size: 1em\"> Cancer of the cartilage<\/span><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong style=\"font-size: 1em\">Glioma:<\/strong><span style=\"font-size: 1em\"> Cancers of neuroglial cells (e.g. astrocytoma, ependyoma)<\/span><\/li>\r\n \t<li><strong style=\"font-size: 1em\">Several malignant tumors have unique names:<\/strong><span style=\"font-size: 1em\"> Hodgkin\u2019s disease, Wilms\u2019 tumor, Leukemia, Lymphoma<\/span><\/li>\r\n<\/ol>\r\n<\/div>\r\n<strong>Describe Possible Effects of Cancers including:<\/strong>\r\n<ul>\r\n \t<li>Mass compresses blood vessels.<\/li>\r\n \t<li>Leads to necrosis and inflammation around tumor<\/li>\r\n \t<li>Tumor cells may secrete enzymes (e.g. collagenase) or hormones or their own growth factors.<\/li>\r\n \t<li>Break down of proteins and surrounding cells<\/li>\r\n \t<li>Systemic effects, such as altered calcium levels<\/li>\r\n \t<li>Inflammation and loss of normal cells<\/li>\r\n \t<li>Lead to progressive reduction in organ integrity and function<\/li>\r\n \t<li><strong>Angiogenesis:<\/strong> Promoted by growth factors that some tumor cells secrete that s<span style=\"font-size: 1em\">timulate the development of new capillaries in the tumor<\/span>\r\n<ul>\r\n \t<li>Some new drugs mimic human <strong>antiangiogensis<\/strong> factors to block this &amp; starve cancer!\u00a0\u00a0 - good idea!\u00a0 but\u2026<\/li>\r\n \t<li>Not as effective as hoped, as without blood vessels, chemotherapy drugs can\u2019t get to the cancer<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<div>\r\n\r\n<strong>Explain Signs &amp; Symptoms of Cancers:<\/strong>\r\n<ul>\r\n \t<li><span style=\"font-size: 1em\">Unusual bleeding or discharge<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\">Diarrhea, Constipation, Dysuria, Frequency<\/span><\/li>\r\n \t<li>Change in mole\/wart<\/li>\r\n \t<li>Sore that doesn't heal<\/li>\r\n \t<li>Unexplained weight loss<\/li>\r\n \t<li>Cachexia, Anorexia<\/li>\r\n \t<li>Anemia, persistent fatigue<\/li>\r\n \t<li>Lumps (painless or painful)<\/li>\r\n \t<li><span style=\"font-size: 1em\">Breathing\/swallowing obstructions<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\">Frequent infections<\/span><\/li>\r\n \t<li>Emotional lability<\/li>\r\n \t<li>Paraneoplastic Syndrome: associated with certain tumor types (para = alongside)\r\n<ul>\r\n \t<li>Tumor secretes hormones, or peptides, or cytokines that alter either cellular function of different tissue or alter immune responses<\/li>\r\n \t<li>Common Example:\u00a0 Tumor cells release substances that may have hormonal effects.\r\n<div>Eg. Bronchogenic carcinoma: may produce ACTH (adrenocorticotropic hormone) causing symptoms of Cushing\u2019s Syndrome (a condition in which excessive glucocorticoids (hydrocortisone or cortisol) are produced causing:<\/div>\r\n<div>a) catabolic effects leading to fragile skin, osteoporosis, delayed healing)<\/div>\r\n<div>b) Increased gluconeogenesis &amp; insulin resistance which may cause diabetes mellitus and leads to<\/div>\r\n<div>c) Retention of Na &amp; H2O \u2013 leading to hypertension, edema (puffy face &amp; torso), &amp; possibly hypokalemia<\/div>\r\n<div>d) Suppression of the immune response<\/div>\r\n<div>e) Stimulation of RBC production<\/div>\r\n<div>f) Emotional lability &amp; euphoria<\/div><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/div>\r\n<div>\r\n\r\n<strong>Explain Spread of malignant tumors:<\/strong>\r\n<ul>\r\n \t<li>Invasion of local tissue (e.g. using lytic enzymes, collagenase)<\/li>\r\n \t<li>Metastasis (spread to distant sites) via blood, lymph, peritoneal cavity fluid etc.<\/li>\r\n \t<li>Seeding<\/li>\r\n \t<li>Role of Sentinel lymph nodes<\/li>\r\n<\/ul>\r\n<\/div>\r\n<div>\r\n\r\n<strong>Explain Diagnostic Tests including:<\/strong>\r\n<ul>\r\n \t<li>Routine Screening (e.g. mammogram, Pap test, Stool test, Colonoscopy, Self-examination)<\/li>\r\n \t<li>Genetic Testing (e.g. BRAC1, BRAC2, Philadelphia chromosome)<\/li>\r\n \t<li>Imaging<\/li>\r\n \t<li>Cytological tests (e.g. biopsy analysis)<\/li>\r\n \t<li>Growth Promoter Sensitivity tests (e.g. estrogen-dependence)<\/li>\r\n \t<li>Blood tests (e.g. levels of hemoglobin, RBCs, WBCs, and tumor markers)<\/li>\r\n \t<li>Tumor markers:\u00a0 elevated levels of proteins \u2013 being produced by the cancer (usually fetal in nature \u2013 as cells have regressed), for example:\r\n<ul>\r\n \t<li>\r\n<div>CEA (carcino-embryonic antigen): colon cancer<\/div><\/li>\r\n \t<li>\r\n<div>PSA (prostate specific antigen) test: high PSA in prostate cancer<\/div><\/li>\r\n \t<li>\r\n<div>hCG (human chorionic gonadotropin) test: testicular cancer<\/div><\/li>\r\n \t<li>\r\n<div>CA125: ovarian cancer<\/div><\/li>\r\n \t<li>\r\n<div>AFP (alpha-fetoprotein): hepatocellular cancer<span style=\"font-size: 1em\">\u00a0<\/span><\/div><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<div>\r\n<div><strong>Explain Grading and Staging of Cancers, including:<\/strong><\/div>\r\n<\/div>\r\n<ol>\r\n \t<li><strong>Grading Cancer <\/strong>- based on microscopic analysis of how different they look from normal, differentiated cells:\r\n<ul>\r\n \t<li><strong>Grades I-IV:<\/strong><\/li>\r\n \t<li>\r\n<div>Grade I = well-differentiated cells similar to normal cells<\/div><\/li>\r\n \t<li>\r\n<div>Grade IV = undifferentiated cells (anaplasia); likely will be highly malignant<\/div><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>TMN Staging of Cancer:<\/strong>\r\n<ul>\r\n \t<li>Size of primary tumor (T)<\/li>\r\n \t<li>Involvement of regional lymph nodes (N)<\/li>\r\n \t<li>Spread (metastasis) of tumor (M)<\/li>\r\n \t<li><strong>Stages 0-4:<\/strong>\r\n<ul>\r\n \t<li>\r\n<div>Stage 0 \u2013 carcinoma <em>in situ<\/em><\/div><\/li>\r\n \t<li>\r\n<div>Stages I and II \u2013 cancer is limited to organ or location where it began or it may have spread to a nearby structure (localized spread)<\/div><\/li>\r\n \t<li>\r\n<div>Stage III \u2013 cancer has spread further into a surrounding structure or regional lymph nodes (regional spread)<\/div><\/li>\r\n \t<li>\r\n<div>Stage IV \u2013 the cancer has spread to a distant site in the body (metastatic spread)<\/div><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<strong>List risk factors, including:<\/strong>\r\n<ol>\r\n \t<li>high-fat diet, smoked foods \u2192 colon cancer<\/li>\r\n \t<li>estrogen \u2192 endometrial cancer<\/li>\r\n \t<li>HPV \u2192 cervical cancer<\/li>\r\n \t<li>HSVII \u2192 cervical cancer<\/li>\r\n \t<li>hepatitis virus \u2192 liver cancer<\/li>\r\n \t<li>UV \u2192 skin cancer<\/li>\r\n \t<li>gamma radiation \u2192 leukemia<\/li>\r\n \t<li>HIV \u2192 Kaposi's sarcoma<\/li>\r\n \t<li>smoke \u2192 lung cancer<\/li>\r\n \t<li>air pollution \u2192 lung cancer, bladder cancer<\/li>\r\n \t<li>age<\/li>\r\n \t<li>immediate family incidence<\/li>\r\n \t<li>genetic factors<\/li>\r\n \t<li>hormone levels<\/li>\r\n<\/ol>\r\n<strong>Define:<\/strong>\r\n<ol>\r\n \t<li><strong>procarcinogens<\/strong> = cause first unrepaired DNA mutation<\/li>\r\n \t<li><span style=\"font-size: 1em\"><strong>promoters<\/strong> = hormones and environmental chemicals that cause further DNA mutations<\/span><\/li>\r\n \t<li><strong>oncovirus<\/strong><\/li>\r\n \t<li><strong>radioresistant<\/strong><\/li>\r\n \t<li><strong>cancer-free state:<\/strong>\u00a0 generally defined as 5-year survival without recurrence<\/li>\r\n \t<li>some cancers such as childhood leukemias can be considered cured after a 10-year, cancer-free period.<\/li>\r\n \t<li><strong>remission:<\/strong>\u00a0 no clinical signs of cancer<\/li>\r\n \t<li><strong>Explain how carcinogenesis\/oncogenesis is multistage<\/strong><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Explain how the following cancer therapies work:<\/strong><\/li>\r\n<\/ol>\r\n<div><strong>Describe Treatment Options:<\/strong><\/div>\r\n<ol>\r\n \t<li><strong>Surgery<\/strong>\r\n<ul>\r\n \t<li>with or without laparoscopy<\/li>\r\n \t<li>with Radiofrequency Ablation (RFA)<\/li>\r\n \t<li>with use of CT and ultrasound imaging<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Chemotherapy<\/strong>\r\n<ul>\r\n \t<li>antimitotics, antimetabolites<\/li>\r\n \t<li>delivery via: oral, subcutaneous, intravenous, intramuscular, intralesional, intrathecally (subarachnoid), intraperitoneal, intraventricular<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Radiation Therapy<\/strong>\r\n<ul>\r\n \t<li>with use of x-rays, gamma rays (radioactive radium or cobalt, high-energy electrons\/protons)<\/li>\r\n \t<li>Cobalt machine<\/li>\r\n \t<li>Brachytherapy<\/li>\r\n \t<li>Radioactive gold salt solutions<\/li>\r\n \t<li>Oral radioactive iodine<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Immunotherapy<\/strong><\/li>\r\n \t<li><strong>Curative<\/strong> vs. <strong>Palliative<\/strong><\/li>\r\n \t<li><strong>Nutrition, Counselling, Physiotherapy, Speech Therapy, Support<\/strong><\/li>\r\n \t<li><strong>Other drugs:<\/strong>\r\n<ul>\r\n \t<li>\u00a0<strong>Hormones:<\/strong>\r\n<ul>\r\n \t<li><strong>glucocorticoids<\/strong> (prednisone): \u2193 mitosis, \u2191 RBC, \u2191 appetite, \u2193 inflammation around tumor<\/li>\r\n \t<li><strong>sex hormones:<\/strong> estrogens slow prostate cancer; estrogen-blocking agent slow estrogen-dependent breast cancer<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Antibodies:<\/strong> block receptors for growth promoters on cancer cells &amp; target cell for destruction<\/li>\r\n \t<li><strong>Radiolabeled antibodies:<\/strong> specific to cancer cells, bind them &amp; irradiate\/destroy targeted cancer cell<\/li>\r\n \t<li><strong>Biological Response Modifiers (BRMs):<\/strong> \u2191\u00a0 natural immune response (e.g. interferons , BCG, Bacillus Calmette-Guerin vaccine - normally used for tuberculosis)<\/li>\r\n \t<li><strong>Angiogenesis inhibitors:<\/strong> inhibits growth of new blood vessels which starves cancer (but also \u2193 chemo delivery)<\/li>\r\n \t<li><strong>Analgesics:<\/strong>\u00a0 however,\u00a0 be careful - narcotics *may cause nausea, constipation, drowsiness &amp; respiratory depression; tolerance occurs with long-term use, which can lead to larger &amp; more dangerous doses<\/li>\r\n \t<li><strong>Anti-emetics<\/strong><\/li>\r\n \t<li><strong>Antibiotics<\/strong><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<strong>Complementary Therapies:<\/strong>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li>\r\n<div>Massage<\/div><\/li>\r\n \t<li>\r\n<div>Meditation<\/div><\/li>\r\n \t<li>\r\n<div>Counseling<\/div><\/li>\r\n \t<li>\r\n<div>Exercise<\/div><\/li>\r\n \t<li>\r\n<div>Therapeutic touch<\/div><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<strong style=\"text-align: initial;font-size: 1em\">Explain the adverse effects of radiation &amp; chemotherapy:<\/strong>\r\n<div class=\"textbox__content\">\r\n<div><strong>The following adverse effects are<\/strong> - due to highly mitotic cells (e.g. epithelial &amp; epithelial glandular cells, endothelial cells, RBCs) being destroyed by chemotherapy\/radiation and not able to replace themselves quickly enough<\/div>\r\n<ul>\r\n \t<li><strong>Bone marrow depression<\/strong> (\u2193 #WBCs\u2014increase risk of infection; Risk of pneumonia and septicemia; \u2193 #RBCs\u2014fatigue, tissue breakdown; \u2193 #WBCs\u2014increase risk of infection; Risk of pneumonia and septicemia; \u2193 #RBCs\u2014fatigue, tissue breakdown; \u2193 #platelets\u2014excessive bleeding; \u2193 #platelets\u2014excessive bleeding)<strong>Nadir:<\/strong> is point of lowest WBC count which occurs after each chemotherapy treatment (neutropenia, leukopenia)<\/li>\r\n \t<li><strong>Vasculitis<\/strong> (blood vessel inflammation)<\/li>\r\n \t<li><strong>Alopecia<\/strong> (hair loss)<\/li>\r\n \t<li><strong>Xerostomia<\/strong> (dry mouth, reduced mucus production)<\/li>\r\n \t<li><strong>Stomatitis<\/strong> (mouth inflammation) &amp; oral fungal infections (e.g. <em>Candidiasis)<\/em><\/li>\r\n \t<li><strong>Dysphagia<\/strong> (difficulty swallowing possibly due to swollen throat)<\/li>\r\n \t<li><strong>Dyspnea<\/strong> (difficulty swallowing possibly due to swollen bronchi\/bronchioles)<\/li>\r\n \t<li><strong>Constipation, GI ulcers<\/strong>\u00a0 (reduced mucus production)<\/li>\r\n \t<li><strong>Cystitis<\/strong> - due to irritation\/cell damage by radiation\/chemotherapy and\/or UTI (due to immunosuppression)<\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Infertility<\/strong><span style=\"text-align: initial;font-size: 1em\"> - due to abdominal radiation<\/span><\/li>\r\n \t<li><strong style=\"text-align: initial;font-size: 1em\">Adhesions, obstructions<\/strong><span style=\"text-align: initial;font-size: 1em\"> - due to scarring and\/or constipation<\/span><\/li>\r\n \t<li><strong>Immunosuppresion<\/strong> - Increased risk of infections (pneumonia, septicemia) - due to bone marrow depression including neutropenia,\u00a0 and\/or malnourishment, and\/or cancer-damaged tissue.<\/li>\r\n<\/ul>\r\n<strong>Other Negative Side Effects of Chemotherapy and Radiation:<\/strong>\r\n<ul>\r\n \t<li><strong>Bleeding<\/strong> (due to thrombocytopenia or cellular damage)<\/li>\r\n \t<li><strong>Nausea<\/strong> due to chemicals, anxiety, and mucosal inflammation<\/li>\r\n \t<li><strong>Fibrosis<\/strong> (scarring)<\/li>\r\n \t<li>Change in <strong>taste<\/strong> sensation<\/li>\r\n \t<li><strong>Anorexia<\/strong><\/li>\r\n \t<li><strong>Fatigue, lethargy<\/strong><\/li>\r\n \t<li><strong>Mood depression<\/strong><\/li>\r\n \t<li><strong>Vomiting<\/strong> and\/or <strong>diarrhea<\/strong> from treatments<\/li>\r\n \t<li><strong>Sore mouth<\/strong> or <strong>loss of teeth<\/strong><\/li>\r\n \t<li><strong>Pain<\/strong> (due to cellular damage)<\/li>\r\n \t<li><strong>Malabsorption<\/strong> caused by inflammation in the digestive tract<\/li>\r\n \t<li><strong>Permanent damage to organs<\/strong> that do not regenerate (heart, kidneys, lungs, brain etc.)<\/li>\r\n<\/ul>\r\n<strong style=\"text-align: initial;font-size: 1em\">Describe risk factors, pathogenesis, signs\/symptoms, detection, prognosis, treatment of more common neoplasms in Canada:<\/strong>\r\n<div class=\"textbox__content\">\r\n<ol>\r\n \t<li><strong>Skin cancers<\/strong> (Basal Cell Carcinoma, Squamous Cell Carcinoma, Melanoma)\r\n<ul>\r\n \t<li><strong>Common Risk Factors:<\/strong> UV exposure<\/li>\r\n \t<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Moles that get larger in size, have irregular borders and colourations, bleed.<\/li>\r\n \t<li><strong>Pathogenesis:<\/strong>\u00a0 UV causes mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\r\n \t<li><strong>Diagnostic Tools<\/strong>: Visual inspection, biopsy and microscopic analysis<\/li>\r\n \t<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, chemotherapy, Radiation and other accompanying therapies - see above for list.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Lung cancer\r\n<ul>\r\n \t<li><strong>Common Risk Factors:<\/strong> exposure to inhaled carcinogens (e.g. smoking, industrial pollutants, asbestos, coal dust)<\/li>\r\n \t<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Asymptomatic, coughing, dyspnea, wheezing, hemoptysis<\/li>\r\n \t<li><strong>Pathogenesis:<\/strong>\u00a0 carcinogens causes mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\r\n \t<li><strong>Diagnostic Tools<\/strong>: Imaging (e.g. X-ray, CT scan), biopsy and microscopic analysis<\/li>\r\n \t<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, Chemotherapy, Radiation, and other accompanying therapies - see above for list.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Ovarian cancer\r\n<ul>\r\n \t<li><strong>Common Risk Factors:<\/strong> family history (genetic\/lifestyle susceptibilities), Breast Cancer 1 or 2 (BRCA1 or BRCA2) mutations, high saturated fat diet, early menarche, late menopause, nonparity,<\/li>\r\n \t<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Asymptomatic, abdominal pain, urinary frequency, as metastasis to fallopian tubes, uterus, and intrpaeritoneal organs occu, the following may occur:\u00a0 ascites, intestinal obstruction, nutritional deficiencies, cachexia, fatigue.<\/li>\r\n \t<li><strong>Pathogenesis:<\/strong>\u00a0 mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\r\n \t<li><strong>Diagnostic Tools<\/strong>: Imaging (e.g. transvaginal ultrasound, MRI), genetic testing, biopsy and microscopic analysis<\/li>\r\n \t<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, Chemotherapy, Radiation and other accompanying therapies - see above for list.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><span style=\"font-size: 1em;text-align: initial\">Brain tumor<\/span>\r\n<ul>\r\n \t<li><strong style=\"font-size: 1em\">Common Risk Factors:<\/strong><span style=\"font-size: 1em\"> for most common form, gliobastoma = biological sex (males), immunosuppresion, children and adults,\u00a0<\/span><\/li>\r\n \t<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> headaches, seizure, ataxia, weakness, increased ICP (vomiting, headache), cognitive\/behavioural changes, parestehsai, visual\/auditory\/speech disturbances.<\/li>\r\n \t<li><strong>Pathogenesis:<\/strong>\u00a0 mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\r\n \t<li><strong>Diagnostic Tools<\/strong>: Imaging, reduce ICP (e.g. corticosteroids, diuretics, craniotomy)<\/li>\r\n \t<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, Chemotherapy, Radiation and other accompanying therapies - see above for list.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Breast Cancer\r\n<ul>\r\n \t<li><strong>Common Risk Factors:<\/strong> biological sex (female), family history (genetic\/lifestyle susceptibility), age&gt;40yr, early menarche, late menopause, nulliparity, obesity (particularly in waist), high-fat diet, alcohol, exposure to toxins (e.g. pesticides), radiation, mutations in BRCA1 or BRCA2, p53<\/li>\r\n \t<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> painless firm, irregular immovable lump in breast or armpit, dimpling in breast, nipple discharge, inflammation, ulceration.\u00a0 Metatstatic signs &amp; symptoms include: shortness of breath bone pain, abdominal distention, jaundice, cognitive changes, headache<\/li>\r\n \t<li><strong>Pathogenesis:<\/strong>\u00a0 UV causes mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\r\n \t<li><strong>Diagnostic Tools<\/strong>: Imaging (e.g. mammogram=x-ray, ultrasound), biopsy and microscopic analysis<\/li>\r\n \t<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal (Mastectomy), Chemotherapy, Radiation, Hormone Therapy (estrogen or progesterone blockers, if cancer is found to be estrogen or progesterone-dependent, removal of ovaries (hysterectomy) to remove source of endogenous estrogen and progesterone, Human Epidermal Growth Factor Receptor, HER2 blockers if cancer is dependent on HEGF), and other accompanying therapies - see above for list.<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Benign Prostatic Hypertrophy\r\n<ul>\r\n \t<li><strong>Common Risk Factors:<\/strong> age, changes in hormone balance, increased androgens (testosterone), estrogen, family history (genetic\/lifestyle susceptibility)<\/li>\r\n \t<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Urinary urgency, frequency, nocturia, dysuria, hesitancy, retention, driblling; Ejaculation dysfunction<\/li>\r\n \t<li><strong>Pathogenesis:<\/strong>\u00a0 UV causes mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\r\n \t<li><strong>Diagnostic Tools<\/strong>: Urinalysis (to rule ot UTI or treat accompanying UTI), uroflowmetry, serum marker PSA test, digital rectal exam to feel for enlarged prostate, biopsy and microscopic analysis<\/li>\r\n \t<li><strong>Treatments:<\/strong> Transurethral Incision of the Prostate (TUIP) or other forms of surgery (Transurethral Resection of the Prostate, TURP or prostatectomy).<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Prostate Cancer\r\n<ul>\r\n \t<li><strong>Common Risk Factors:<\/strong> age (due to lifetime exposure to potential carcinogens, plus # of mitotic events increases chances of DNA mutations), viruses, family history (genetic\/lifestyle susceptibilities), high-fat diet, smoking, obesity<\/li>\r\n \t<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Urine retention, urgency, requency, nocturia, dysuria, hematuria, back pain.<\/li>\r\n \t<li><strong>Pathogenesis:<\/strong>\u00a0 Mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\r\n \t<li><strong>Diagnostic Tools<\/strong>: PSA test, digital rectal exam (feel for hard lumps), transrectal ultrasound and other imaging, biopsy and microscopic anallysis<\/li>\r\n \t<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, Chemotherapy, Radiation,Hormone Therapy (GnRH agonists, androgen blockers), and other accompanying therapies - see above for list.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ol>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n<\/div>\r\n&nbsp;","rendered":"<div class=\"textbox textbox--learning-objectives\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\">Learning Outcomes and Specific Learning Objectives Study Guide<\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p><strong>Learning Outcomes:<\/strong><\/p>\n<p>By the end of this section you will be able to:<\/p>\n<p><strong>Describe key aspects of Neoplasms including:<\/strong><\/p>\n<ol>\n<li>Benign and Malignant tumors<\/li>\n<li>Common tumors and cancers: e.g. cervical cancer, skin cancer, ovarian cancer, breast cancer, prostate cancer, and benign prostate hypertrophy<\/li>\n<li>Aspects of etiology, risk factors, pathogenesis, and treatment options<\/li>\n<\/ol>\n<hr \/>\n<p><strong>Specific Learning Objectives &#8211; Study Guide:<\/strong><\/p>\n<p>By the end of this section you will be able to:<\/p>\n<p><strong><span style=\"font-size: 1em\">Describe and explain the following terms:<\/span><\/strong><\/p>\n<ul>\n<li><strong>Cell Type:<\/strong>\u00a0 there are over 200 different cell types in the human body, each expressing unique proteins and having unique structure that allow it to fulfill its functions and role in the human body.<\/li>\n<li><strong>Tissue Types:<\/strong>\u00a0 There are 4 categories of tissue types, each one containing different types of cells and having different physical and functional properties:\n<ul>\n<li><strong>Epithelial tissue<\/strong> (e.g. dermis, endothelial tissue, mucosa membranes of GI tract and respiratory tract, apical layer of serous membranes, and synovial membranes)<\/li>\n<li><strong>Connective tissue<\/strong> (areolar, adipose, reticular, dense regular, dense irregular, elastic, hyaline cartilage, elastic cartilage, fibrocartilage, bone, blood, and lymph fluid)<\/li>\n<li><strong>Muscle tissue<\/strong> (skeletal muscle, cardiac muscle, and smooth muscle)<\/li>\n<li><strong>Nervous tissue<\/strong> (neurons and neuroglial cells)<\/li>\n<\/ul>\n<\/li>\n<li><span style=\"font-size: 1em\"><strong>Cell Division\/Cell Multiplication\/Proliferation<\/strong> &#8211; the process of mitosis<\/span><\/li>\n<li><span style=\"font-size: 1em\"><span style=\"font-size: 1em\"><strong>Cell Cycle<\/strong>\u00a0&#8211; <\/span><\/span>the stages of cell division which most often involves an immature cell or stem cell dividing into two genetically identical cells.\u00a0 Cell Cycling includes:\n<ul>\n<li>G<sub>1<\/sub> phase &#8211; cell functions normally, but grows, duplicating organelles and synthesizing proteins; lasts 8+ hours<\/li>\n<li>S phase &#8211; duplication of DNA and centrioles;\u00a0 synthesis of histones; lasts 8+ hours<\/li>\n<li>G<sub>2<\/sub> phase &#8211; growth and protein synthesis; lasts 2-5hrs<\/li>\n<li>Mitosis &#8211; Prophase, Metaphase, Anaphase, Telophase<\/li>\n<li>Cytokinesis &#8211; pinching of cell membrane into two daughter cells<\/li>\n<li>G<sub>o<\/sub> phase &#8211; cells exit cell cycle and mature\/differentiate to become fully functional cells that no longer go through cell cycling.<\/li>\n<\/ul>\n<\/li>\n<li><strong><span style=\"font-size: 1em\">Cell Differentiation <\/span><\/strong><\/li>\n<li><strong>DNA duplication:<\/strong> performed by DNA polymerase with assistance of DNA helicase &amp; DNA ligase as well as enzymes that check for duplication errors and induce apoptosis if the errors can not be fixed.\u00a0 DNA duplication errors may lead to mutations that give rise to non-functional enzymes that compromise the cell&#8217;s ability to survive\/function.\u00a0 Mutations can also give rise to cells that are cancerous.<\/li>\n<li>\n<div><strong>Telomeres:<\/strong> are the end caps of chromosomes that are added by telomerase until adulthood, at which time, telomerase is inactivated, and telomeres become shorter with each round of cell division.\u00a0 Once telomeres have shortened to a certain length, the cell becomes dormant and dies.\u00a0 This is thought to help old\/worn out\/less-functional cells be eliminated.\u00a0 Additionally, each round of cell division, is susceptible to DNA errors which make cells more and more at risk for developing a mutation that makes the cell cancerous.<\/div>\n<\/li>\n<li><strong>Telomerase re-activation:<\/strong>\u00a0 has occurred in 90% of all cancers.\u00a0 In these cancerous cells the telomeres do not shorten and apoptosis is not triggered, making these cells immortal.<\/li>\n<\/ul>\n<div>\n<p>By the end of this section you will be able to list:<\/p>\n<p><strong style=\"font-size: 1em\">Cancers with Highest Incidence Rates in Canada:<\/strong><\/p>\n<\/div>\n<ul>\n<li>Skin Cancer<\/li>\n<li>Breast Cancer<\/li>\n<li>Prostate Cancer<\/li>\n<li>Lung and Bronchus<\/li>\n<li>Colon and Rectum<\/li>\n<\/ul>\n<p><strong>Cancers with Highest Mortality Rates in Canada:.<\/strong><\/p>\n<ul>\n<li>Lung and Bronchus<\/li>\n<li>Breast<\/li>\n<li>Prostate<\/li>\n<li>Colon and Rectum<\/li>\n<li>Pancreas<\/li>\n<li>Ovary<\/li>\n<li>Leukemia<\/li>\n<\/ul>\n<div>\n<p>By the end of this section you will be able to:<\/p>\n<p><strong><span style=\"font-size: 1em\">Describe and explain the following terms:<\/span><\/strong><\/p>\n<ul>\n<li><strong style=\"font-size: 1em\">Carcinogens:<\/strong><span style=\"font-size: 1em\"> factors, chemicals, etc. that increase risk of DNA mutations that put cells more susceptible to becoming cancerous.<\/span><\/li>\n<\/ul>\n<\/div>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Cigarette smoking &#8211; increases risk of developing all cancers (not just lung cancer)<\/li>\n<\/ul>\n<\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Cancer<\/strong><span style=\"text-align: initial;font-size: 1em\"> = a group of almost 100 genetic diseases (genetic = gene mutation \u2260 not necessarily inherited).\u00a0 In cancer:<\/span>\n<ul>\n<li>Cell growth (mitosis) becomes uncontrolled either because:<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Cell Cycle Regulator genes<\/strong> (coding for growth factors and growth inhibiting factors) that control the rate of mitosis have been mutated <span style=\"text-decoration: underline\">or<\/span><\/li>\n<li><span style=\"font-size: 1em\"><strong>Apoptosis Regulator genes<\/strong> (controlling the rate of apoptosis) have been mutated<\/span><\/li>\n<\/ul>\n<\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">DNA mutation can be caused by:<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<div>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Viruses<\/li>\n<li>Radiation (UV, x-ray, gamma rays)<\/li>\n<li>Chemicals (e.g. nickel, asbestos, benzene solvents, aniline dyes, rubber, formaldehyde, chemotherapy drugs)<\/li>\n<li>Spontaneous errors during normal DNA synthesis<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<li><strong>Rapid rates of mitosis<\/strong> during injury repair may increase the risk of errors occurring.<\/li>\n<li>Mutations in genes that are in <strong>sperm<\/strong> or <strong>oocytes<\/strong> that are then passed to offspring can mean that cancers can at times be <strong>inherited<\/strong><\/li>\n<li>The above <strong>4 factors<\/strong> (viruses, chemicals, radiation, spontaneous) are thought to be involved in mutating or changing the expression levels of specific genes, such as:\n<ul>\n<li>&gt;40 <strong style=\"text-align: initial;font-size: 1em\">Proto-oncogenes:\u00a0<\/strong><span style=\"text-align: initial;font-size: 1em\"> genes that stimulate cell division &amp; inhibit both cell differentiation &amp; death \u2013 when these proto-oncogenes mutate they are typically a dominant mutation and are then called Oncogenes.\u00a0 Oncogenes stimulate increased cell division, and decrease cell differentiation &amp; death<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Tumor suppressor genes (TSG):\u00a0<\/strong><span style=\"text-align: initial;font-size: 1em\"> genes that normally slow down cell division, and promote apoptosis; when these genes mutate &amp; are turned off; cells can become immortal \u2192 cancer\u00a0 (e.g.TSG p53 is essential for regulating DNA repair and cell division, it has been nicknamed the &#8220;guardian of the genome); most cancers have a p53 mutation. BRCA1 and BRCA2 are TSGs<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Stability Genes:<\/strong><span style=\"text-align: initial;font-size: 1em\"> that normally repair DNA and other genes that control the rate of mutation.\u00a0 These genes do not have a direct impact on rate of mitosis or apoptosis.\u00a0 (FYI:\u00a0 30-50% cancers have p53 mutation)<\/span><\/li>\n<\/ul>\n<\/li>\n<li><strong style=\"font-size: 1em\">Describe Types of DNA mutations:<\/strong>\n<ul>\n<li><strong style=\"font-size: 1em\">Synonymous<\/strong><span style=\"font-size: 1em\"> &#8211; no change, codes for same amino acid sequence<\/span><\/li>\n<li><strong style=\"font-size: 1em\">Non-synonymous<\/strong><span style=\"font-size: 1em\"> &#8211; change, codes for different same amino acid sequence<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Insertion<\/strong><span style=\"text-align: initial;font-size: 1em\"> &#8211; results in frame shift if in coding region of DNA<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Substitution<\/strong><span style=\"text-align: initial;font-size: 1em\"> &#8211; may result in amino acid substitution if in coding region of DNA<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Deletion<\/strong><span style=\"text-align: initial;font-size: 1em\"> &#8211; results in frame shift if in coding region of DNA<\/span><\/li>\n<\/ul>\n<\/li>\n<li><strong style=\"font-size: 1em\">Describe Possible Effects of DNA mutation:<\/strong>\n<ul>\n<li>No effect, as mutation is in non-coding region<\/li>\n<li>No effect, on the amino acid sequence (<em>as each amino acid is coded for by 2-4 different codons, e.g. GAA and GAG both code for the amino acid Glutamine<\/em>)<\/li>\n<li>Production of Dysfunctional Protein\/Enzyme<\/li>\n<li>Increased\/decreased production of protein\/enzyme<\/li>\n<\/ul>\n<\/li>\n<li><strong style=\"font-size: 1em\">Describe Properties of Neoplasm or tumor = new growth<\/strong>\n<ul>\n<li>Cellular growth that no longer responds to normal genetic controls<\/li>\n<li>Cell continues to reproduce, without the need for them to reproduce<\/li>\n<li>Increase in number of cells that are immature and cell cycling<\/li>\n<li>Deprives other cells of nutrition\u2026 decreasing their function\/abilities<\/li>\n<li>Neoplasms may consist of atypical or immature cells.<\/li>\n<\/ul>\n<\/li>\n<li>In a young healthy person, usually abnormal or cancerous cells will be recognized by the immune system and destroyed.\u00a0 However, at times, cancerous cells evade the immune system.<\/li>\n<\/ul>\n<\/div>\n<div><strong>Describe Characteristics of each tumor, which depend on:<\/strong><\/div>\n<div>1.\u00a0 Type of cell from which the tumor arises<\/div>\n<div>2.\u00a0 Unique structure and growth pattern<\/div>\n<ul>\n<li><strong>Benign tumors:<\/strong> <span style=\"text-decoration: underline\">not<\/span> considered cancer; slow-growing;\n<ul>\n<li>composed of <strong>differentiated<\/strong> cells growing faster than normal;<\/li>\n<li>are often <strong>encapsulated;<\/strong> and are <strong>freely moveable<\/strong> on palpation;<\/li>\n<li><span style=\"text-decoration: underline\">don\u2019t<\/span> metastasize; and once removed usually <span style=\"text-decoration: underline\">doesn\u2019t<\/span> recur;<\/li>\n<li>any tissue damage results from <strong>compression<\/strong> on adjacent structures (e.g. blood vessels); can be fatal in the brain (due to \u2191ICP, intracranial pressure)<\/li>\n<li>have tissue name plus the suffix <strong>-oma<\/strong> (e.g., adenoma) \u2013 exceptions!\u00a0 Glioma, Lymphoma\u2026.<\/li>\n<li>effects are more often local rather than systemic<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<ul>\n<li><strong style=\"font-size: 1em\">Malignant tumors (cancers):<\/strong><span style=\"font-size: 1em\"> invade surrounding tissues and are characterized by<\/span>\n<ul>\n<li>atypical, immature, undifferentiated, nonfunctional dysplastic cells<\/li>\n<li>rapid reproduction; no cell-cell contact inhibition; lack of apoptosis;<\/li>\n<li>cancerous cells having abnormal cell membranes; altered surface antigens; and not adhering to each other as normal cells do; so cancerous cells often break loose from mass and invade other tissues;\u00a0 may spread to distant sites via blood or lymph<\/li>\n<li>often having systemic effects;\u00a0 have the tissue name plus the suffix -carcinoma (e.g., adenocarcinoma); and can recur if removed<\/li>\n<li><strong>Malignant (cancerous) cells<\/strong> often have an abnormal number of chromosomes = <strong>aneuploidy<\/strong><\/li>\n<li>Abnormal shaped nuclei = <strong>pleomorphism<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<div class=\"textbox__content\">\n<div><strong>Describe Types of Cancers:\u00a0 <\/strong>Cancers are named by the cell type that becomes cancerous<\/div>\n<ol>\n<li><strong>Carcinomas:<\/strong> epithelial cancers; 90% of cancers\n<ul>\n<li><strong style=\"text-align: initial;font-size: 1em\">Adenocarcinomas:<\/strong><span style=\"text-align: initial;font-size: 1em\"> epithelial cancers in a gland<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Squamous<\/strong><span style=\"text-align: initial;font-size: 1em\"> cell carcinoma: epithelial cancers originating in the skin<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Melanomas:<\/strong><span style=\"text-align: initial;font-size: 1em\"> epithelial cancers originating in the melanocytes of the skin<\/span><\/li>\n<\/ul>\n<\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Sarcomas:<\/strong><span style=\"text-align: initial;font-size: 1em\">\u00a0 Tumors of mesenchymal tissue (e.g. bone, muscle, cartilage, blood vessels); usually malignant.<\/span>\n<ul>\n<li><strong style=\"text-align: initial;font-size: 1em\">Osteosarcoma:<\/strong><span style=\"text-align: initial;font-size: 1em\"> Cancer of the bone<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Rhabdomyosarcoma:<\/strong><span style=\"text-align: initial;font-size: 1em\"> Cancer of the striated muscle<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Chondrosarcoma:<\/strong><span style=\"text-align: initial;font-size: 1em\"> Cancer of the cartilage<\/span><\/li>\n<\/ul>\n<\/li>\n<li><strong style=\"font-size: 1em\">Glioma:<\/strong><span style=\"font-size: 1em\"> Cancers of neuroglial cells (e.g. astrocytoma, ependyoma)<\/span><\/li>\n<li><strong style=\"font-size: 1em\">Several malignant tumors have unique names:<\/strong><span style=\"font-size: 1em\"> Hodgkin\u2019s disease, Wilms\u2019 tumor, Leukemia, Lymphoma<\/span><\/li>\n<\/ol>\n<\/div>\n<p><strong>Describe Possible Effects of Cancers including:<\/strong><\/p>\n<ul>\n<li>Mass compresses blood vessels.<\/li>\n<li>Leads to necrosis and inflammation around tumor<\/li>\n<li>Tumor cells may secrete enzymes (e.g. collagenase) or hormones or their own growth factors.<\/li>\n<li>Break down of proteins and surrounding cells<\/li>\n<li>Systemic effects, such as altered calcium levels<\/li>\n<li>Inflammation and loss of normal cells<\/li>\n<li>Lead to progressive reduction in organ integrity and function<\/li>\n<li><strong>Angiogenesis:<\/strong> Promoted by growth factors that some tumor cells secrete that s<span style=\"font-size: 1em\">timulate the development of new capillaries in the tumor<\/span>\n<ul>\n<li>Some new drugs mimic human <strong>antiangiogensis<\/strong> factors to block this &amp; starve cancer!\u00a0\u00a0 &#8211; good idea!\u00a0 but\u2026<\/li>\n<li>Not as effective as hoped, as without blood vessels, chemotherapy drugs can\u2019t get to the cancer<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<div>\n<p><strong>Explain Signs &amp; Symptoms of Cancers:<\/strong><\/p>\n<ul>\n<li><span style=\"font-size: 1em\">Unusual bleeding or discharge<\/span><\/li>\n<li><span style=\"font-size: 1em\">Diarrhea, Constipation, Dysuria, Frequency<\/span><\/li>\n<li>Change in mole\/wart<\/li>\n<li>Sore that doesn&#8217;t heal<\/li>\n<li>Unexplained weight loss<\/li>\n<li>Cachexia, Anorexia<\/li>\n<li>Anemia, persistent fatigue<\/li>\n<li>Lumps (painless or painful)<\/li>\n<li><span style=\"font-size: 1em\">Breathing\/swallowing obstructions<\/span><\/li>\n<li><span style=\"font-size: 1em\">Frequent infections<\/span><\/li>\n<li>Emotional lability<\/li>\n<li>Paraneoplastic Syndrome: associated with certain tumor types (para = alongside)\n<ul>\n<li>Tumor secretes hormones, or peptides, or cytokines that alter either cellular function of different tissue or alter immune responses<\/li>\n<li>Common Example:\u00a0 Tumor cells release substances that may have hormonal effects.\n<div>Eg. Bronchogenic carcinoma: may produce ACTH (adrenocorticotropic hormone) causing symptoms of Cushing\u2019s Syndrome (a condition in which excessive glucocorticoids (hydrocortisone or cortisol) are produced causing:<\/div>\n<div>a) catabolic effects leading to fragile skin, osteoporosis, delayed healing)<\/div>\n<div>b) Increased gluconeogenesis &amp; insulin resistance which may cause diabetes mellitus and leads to<\/div>\n<div>c) Retention of Na &amp; H2O \u2013 leading to hypertension, edema (puffy face &amp; torso), &amp; possibly hypokalemia<\/div>\n<div>d) Suppression of the immune response<\/div>\n<div>e) Stimulation of RBC production<\/div>\n<div>f) Emotional lability &amp; euphoria<\/div>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/div>\n<div>\n<p><strong>Explain Spread of malignant tumors:<\/strong><\/p>\n<ul>\n<li>Invasion of local tissue (e.g. using lytic enzymes, collagenase)<\/li>\n<li>Metastasis (spread to distant sites) via blood, lymph, peritoneal cavity fluid etc.<\/li>\n<li>Seeding<\/li>\n<li>Role of Sentinel lymph nodes<\/li>\n<\/ul>\n<\/div>\n<div>\n<p><strong>Explain Diagnostic Tests including:<\/strong><\/p>\n<ul>\n<li>Routine Screening (e.g. mammogram, Pap test, Stool test, Colonoscopy, Self-examination)<\/li>\n<li>Genetic Testing (e.g. BRAC1, BRAC2, Philadelphia chromosome)<\/li>\n<li>Imaging<\/li>\n<li>Cytological tests (e.g. biopsy analysis)<\/li>\n<li>Growth Promoter Sensitivity tests (e.g. estrogen-dependence)<\/li>\n<li>Blood tests (e.g. levels of hemoglobin, RBCs, WBCs, and tumor markers)<\/li>\n<li>Tumor markers:\u00a0 elevated levels of proteins \u2013 being produced by the cancer (usually fetal in nature \u2013 as cells have regressed), for example:\n<ul>\n<li>\n<div>CEA (carcino-embryonic antigen): colon cancer<\/div>\n<\/li>\n<li>\n<div>PSA (prostate specific antigen) test: high PSA in prostate cancer<\/div>\n<\/li>\n<li>\n<div>hCG (human chorionic gonadotropin) test: testicular cancer<\/div>\n<\/li>\n<li>\n<div>CA125: ovarian cancer<\/div>\n<\/li>\n<li>\n<div>AFP (alpha-fetoprotein): hepatocellular cancer<span style=\"font-size: 1em\">\u00a0<\/span><\/div>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<div>\n<div><strong>Explain Grading and Staging of Cancers, including:<\/strong><\/div>\n<\/div>\n<ol>\n<li><strong>Grading Cancer <\/strong>&#8211; based on microscopic analysis of how different they look from normal, differentiated cells:\n<ul>\n<li><strong>Grades I-IV:<\/strong><\/li>\n<li>\n<div>Grade I = well-differentiated cells similar to normal cells<\/div>\n<\/li>\n<li>\n<div>Grade IV = undifferentiated cells (anaplasia); likely will be highly malignant<\/div>\n<\/li>\n<\/ul>\n<\/li>\n<li><strong>TMN Staging of Cancer:<\/strong>\n<ul>\n<li>Size of primary tumor (T)<\/li>\n<li>Involvement of regional lymph nodes (N)<\/li>\n<li>Spread (metastasis) of tumor (M)<\/li>\n<li><strong>Stages 0-4:<\/strong>\n<ul>\n<li>\n<div>Stage 0 \u2013 carcinoma <em>in situ<\/em><\/div>\n<\/li>\n<li>\n<div>Stages I and II \u2013 cancer is limited to organ or location where it began or it may have spread to a nearby structure (localized spread)<\/div>\n<\/li>\n<li>\n<div>Stage III \u2013 cancer has spread further into a surrounding structure or regional lymph nodes (regional spread)<\/div>\n<\/li>\n<li>\n<div>Stage IV \u2013 the cancer has spread to a distant site in the body (metastatic spread)<\/div>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<p><strong>List risk factors, including:<\/strong><\/p>\n<ol>\n<li>high-fat diet, smoked foods \u2192 colon cancer<\/li>\n<li>estrogen \u2192 endometrial cancer<\/li>\n<li>HPV \u2192 cervical cancer<\/li>\n<li>HSVII \u2192 cervical cancer<\/li>\n<li>hepatitis virus \u2192 liver cancer<\/li>\n<li>UV \u2192 skin cancer<\/li>\n<li>gamma radiation \u2192 leukemia<\/li>\n<li>HIV \u2192 Kaposi&#8217;s sarcoma<\/li>\n<li>smoke \u2192 lung cancer<\/li>\n<li>air pollution \u2192 lung cancer, bladder cancer<\/li>\n<li>age<\/li>\n<li>immediate family incidence<\/li>\n<li>genetic factors<\/li>\n<li>hormone levels<\/li>\n<\/ol>\n<p><strong>Define:<\/strong><\/p>\n<ol>\n<li><strong>procarcinogens<\/strong> = cause first unrepaired DNA mutation<\/li>\n<li><span style=\"font-size: 1em\"><strong>promoters<\/strong> = hormones and environmental chemicals that cause further DNA mutations<\/span><\/li>\n<li><strong>oncovirus<\/strong><\/li>\n<li><strong>radioresistant<\/strong><\/li>\n<li><strong>cancer-free state:<\/strong>\u00a0 generally defined as 5-year survival without recurrence<\/li>\n<li>some cancers such as childhood leukemias can be considered cured after a 10-year, cancer-free period.<\/li>\n<li><strong>remission:<\/strong>\u00a0 no clinical signs of cancer<\/li>\n<li><strong>Explain how carcinogenesis\/oncogenesis is multistage<\/strong><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Explain how the following cancer therapies work:<\/strong><\/li>\n<\/ol>\n<div><strong>Describe Treatment Options:<\/strong><\/div>\n<ol>\n<li><strong>Surgery<\/strong>\n<ul>\n<li>with or without laparoscopy<\/li>\n<li>with Radiofrequency Ablation (RFA)<\/li>\n<li>with use of CT and ultrasound imaging<\/li>\n<\/ul>\n<\/li>\n<li><strong>Chemotherapy<\/strong>\n<ul>\n<li>antimitotics, antimetabolites<\/li>\n<li>delivery via: oral, subcutaneous, intravenous, intramuscular, intralesional, intrathecally (subarachnoid), intraperitoneal, intraventricular<\/li>\n<\/ul>\n<\/li>\n<li><strong>Radiation Therapy<\/strong>\n<ul>\n<li>with use of x-rays, gamma rays (radioactive radium or cobalt, high-energy electrons\/protons)<\/li>\n<li>Cobalt machine<\/li>\n<li>Brachytherapy<\/li>\n<li>Radioactive gold salt solutions<\/li>\n<li>Oral radioactive iodine<\/li>\n<\/ul>\n<\/li>\n<li><strong>Immunotherapy<\/strong><\/li>\n<li><strong>Curative<\/strong> vs. <strong>Palliative<\/strong><\/li>\n<li><strong>Nutrition, Counselling, Physiotherapy, Speech Therapy, Support<\/strong><\/li>\n<li><strong>Other drugs:<\/strong>\n<ul>\n<li>\u00a0<strong>Hormones:<\/strong>\n<ul>\n<li><strong>glucocorticoids<\/strong> (prednisone): \u2193 mitosis, \u2191 RBC, \u2191 appetite, \u2193 inflammation around tumor<\/li>\n<li><strong>sex hormones:<\/strong> estrogens slow prostate cancer; estrogen-blocking agent slow estrogen-dependent breast cancer<\/li>\n<\/ul>\n<\/li>\n<li><strong>Antibodies:<\/strong> block receptors for growth promoters on cancer cells &amp; target cell for destruction<\/li>\n<li><strong>Radiolabeled antibodies:<\/strong> specific to cancer cells, bind them &amp; irradiate\/destroy targeted cancer cell<\/li>\n<li><strong>Biological Response Modifiers (BRMs):<\/strong> \u2191\u00a0 natural immune response (e.g. interferons , BCG, Bacillus Calmette-Guerin vaccine &#8211; normally used for tuberculosis)<\/li>\n<li><strong>Angiogenesis inhibitors:<\/strong> inhibits growth of new blood vessels which starves cancer (but also \u2193 chemo delivery)<\/li>\n<li><strong>Analgesics:<\/strong>\u00a0 however,\u00a0 be careful &#8211; narcotics *may cause nausea, constipation, drowsiness &amp; respiratory depression; tolerance occurs with long-term use, which can lead to larger &amp; more dangerous doses<\/li>\n<li><strong>Anti-emetics<\/strong><\/li>\n<li><strong>Antibiotics<\/strong><\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<p><strong>Complementary Therapies:<\/strong><\/p>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>\n<div>Massage<\/div>\n<\/li>\n<li>\n<div>Meditation<\/div>\n<\/li>\n<li>\n<div>Counseling<\/div>\n<\/li>\n<li>\n<div>Exercise<\/div>\n<\/li>\n<li>\n<div>Therapeutic touch<\/div>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p><strong style=\"text-align: initial;font-size: 1em\">Explain the adverse effects of radiation &amp; chemotherapy:<\/strong><\/p>\n<div class=\"textbox__content\">\n<div><strong>The following adverse effects are<\/strong> &#8211; due to highly mitotic cells (e.g. epithelial &amp; epithelial glandular cells, endothelial cells, RBCs) being destroyed by chemotherapy\/radiation and not able to replace themselves quickly enough<\/div>\n<ul>\n<li><strong>Bone marrow depression<\/strong> (\u2193 #WBCs\u2014increase risk of infection; Risk of pneumonia and septicemia; \u2193 #RBCs\u2014fatigue, tissue breakdown; \u2193 #WBCs\u2014increase risk of infection; Risk of pneumonia and septicemia; \u2193 #RBCs\u2014fatigue, tissue breakdown; \u2193 #platelets\u2014excessive bleeding; \u2193 #platelets\u2014excessive bleeding)<strong>Nadir:<\/strong> is point of lowest WBC count which occurs after each chemotherapy treatment (neutropenia, leukopenia)<\/li>\n<li><strong>Vasculitis<\/strong> (blood vessel inflammation)<\/li>\n<li><strong>Alopecia<\/strong> (hair loss)<\/li>\n<li><strong>Xerostomia<\/strong> (dry mouth, reduced mucus production)<\/li>\n<li><strong>Stomatitis<\/strong> (mouth inflammation) &amp; oral fungal infections (e.g. <em>Candidiasis)<\/em><\/li>\n<li><strong>Dysphagia<\/strong> (difficulty swallowing possibly due to swollen throat)<\/li>\n<li><strong>Dyspnea<\/strong> (difficulty swallowing possibly due to swollen bronchi\/bronchioles)<\/li>\n<li><strong>Constipation, GI ulcers<\/strong>\u00a0 (reduced mucus production)<\/li>\n<li><strong>Cystitis<\/strong> &#8211; due to irritation\/cell damage by radiation\/chemotherapy and\/or UTI (due to immunosuppression)<\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Infertility<\/strong><span style=\"text-align: initial;font-size: 1em\"> &#8211; due to abdominal radiation<\/span><\/li>\n<li><strong style=\"text-align: initial;font-size: 1em\">Adhesions, obstructions<\/strong><span style=\"text-align: initial;font-size: 1em\"> &#8211; due to scarring and\/or constipation<\/span><\/li>\n<li><strong>Immunosuppresion<\/strong> &#8211; Increased risk of infections (pneumonia, septicemia) &#8211; due to bone marrow depression including neutropenia,\u00a0 and\/or malnourishment, and\/or cancer-damaged tissue.<\/li>\n<\/ul>\n<p><strong>Other Negative Side Effects of Chemotherapy and Radiation:<\/strong><\/p>\n<ul>\n<li><strong>Bleeding<\/strong> (due to thrombocytopenia or cellular damage)<\/li>\n<li><strong>Nausea<\/strong> due to chemicals, anxiety, and mucosal inflammation<\/li>\n<li><strong>Fibrosis<\/strong> (scarring)<\/li>\n<li>Change in <strong>taste<\/strong> sensation<\/li>\n<li><strong>Anorexia<\/strong><\/li>\n<li><strong>Fatigue, lethargy<\/strong><\/li>\n<li><strong>Mood depression<\/strong><\/li>\n<li><strong>Vomiting<\/strong> and\/or <strong>diarrhea<\/strong> from treatments<\/li>\n<li><strong>Sore mouth<\/strong> or <strong>loss of teeth<\/strong><\/li>\n<li><strong>Pain<\/strong> (due to cellular damage)<\/li>\n<li><strong>Malabsorption<\/strong> caused by inflammation in the digestive tract<\/li>\n<li><strong>Permanent damage to organs<\/strong> that do not regenerate (heart, kidneys, lungs, brain etc.)<\/li>\n<\/ul>\n<p><strong style=\"text-align: initial;font-size: 1em\">Describe risk factors, pathogenesis, signs\/symptoms, detection, prognosis, treatment of more common neoplasms in Canada:<\/strong><\/p>\n<div class=\"textbox__content\">\n<ol>\n<li><strong>Skin cancers<\/strong> (Basal Cell Carcinoma, Squamous Cell Carcinoma, Melanoma)\n<ul>\n<li><strong>Common Risk Factors:<\/strong> UV exposure<\/li>\n<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Moles that get larger in size, have irregular borders and colourations, bleed.<\/li>\n<li><strong>Pathogenesis:<\/strong>\u00a0 UV causes mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\n<li><strong>Diagnostic Tools<\/strong>: Visual inspection, biopsy and microscopic analysis<\/li>\n<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, chemotherapy, Radiation and other accompanying therapies &#8211; see above for list.<\/li>\n<\/ul>\n<\/li>\n<li>Lung cancer\n<ul>\n<li><strong>Common Risk Factors:<\/strong> exposure to inhaled carcinogens (e.g. smoking, industrial pollutants, asbestos, coal dust)<\/li>\n<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Asymptomatic, coughing, dyspnea, wheezing, hemoptysis<\/li>\n<li><strong>Pathogenesis:<\/strong>\u00a0 carcinogens causes mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\n<li><strong>Diagnostic Tools<\/strong>: Imaging (e.g. X-ray, CT scan), biopsy and microscopic analysis<\/li>\n<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, Chemotherapy, Radiation, and other accompanying therapies &#8211; see above for list.<\/li>\n<\/ul>\n<\/li>\n<li>Ovarian cancer\n<ul>\n<li><strong>Common Risk Factors:<\/strong> family history (genetic\/lifestyle susceptibilities), Breast Cancer 1 or 2 (BRCA1 or BRCA2) mutations, high saturated fat diet, early menarche, late menopause, nonparity,<\/li>\n<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Asymptomatic, abdominal pain, urinary frequency, as metastasis to fallopian tubes, uterus, and intrpaeritoneal organs occu, the following may occur:\u00a0 ascites, intestinal obstruction, nutritional deficiencies, cachexia, fatigue.<\/li>\n<li><strong>Pathogenesis:<\/strong>\u00a0 mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\n<li><strong>Diagnostic Tools<\/strong>: Imaging (e.g. transvaginal ultrasound, MRI), genetic testing, biopsy and microscopic analysis<\/li>\n<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, Chemotherapy, Radiation and other accompanying therapies &#8211; see above for list.<\/li>\n<\/ul>\n<\/li>\n<li><span style=\"font-size: 1em;text-align: initial\">Brain tumor<\/span>\n<ul>\n<li><strong style=\"font-size: 1em\">Common Risk Factors:<\/strong><span style=\"font-size: 1em\"> for most common form, gliobastoma = biological sex (males), immunosuppresion, children and adults,\u00a0<\/span><\/li>\n<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> headaches, seizure, ataxia, weakness, increased ICP (vomiting, headache), cognitive\/behavioural changes, parestehsai, visual\/auditory\/speech disturbances.<\/li>\n<li><strong>Pathogenesis:<\/strong>\u00a0 mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\n<li><strong>Diagnostic Tools<\/strong>: Imaging, reduce ICP (e.g. corticosteroids, diuretics, craniotomy)<\/li>\n<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, Chemotherapy, Radiation and other accompanying therapies &#8211; see above for list.<\/li>\n<\/ul>\n<\/li>\n<li>Breast Cancer\n<ul>\n<li><strong>Common Risk Factors:<\/strong> biological sex (female), family history (genetic\/lifestyle susceptibility), age&gt;40yr, early menarche, late menopause, nulliparity, obesity (particularly in waist), high-fat diet, alcohol, exposure to toxins (e.g. pesticides), radiation, mutations in BRCA1 or BRCA2, p53<\/li>\n<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> painless firm, irregular immovable lump in breast or armpit, dimpling in breast, nipple discharge, inflammation, ulceration.\u00a0 Metatstatic signs &amp; symptoms include: shortness of breath bone pain, abdominal distention, jaundice, cognitive changes, headache<\/li>\n<li><strong>Pathogenesis:<\/strong>\u00a0 UV causes mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\n<li><strong>Diagnostic Tools<\/strong>: Imaging (e.g. mammogram=x-ray, ultrasound), biopsy and microscopic analysis<\/li>\n<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal (Mastectomy), Chemotherapy, Radiation, Hormone Therapy (estrogen or progesterone blockers, if cancer is found to be estrogen or progesterone-dependent, removal of ovaries (hysterectomy) to remove source of endogenous estrogen and progesterone, Human Epidermal Growth Factor Receptor, HER2 blockers if cancer is dependent on HEGF), and other accompanying therapies &#8211; see above for list.<\/li>\n<\/ul>\n<\/li>\n<li>Benign Prostatic Hypertrophy\n<ul>\n<li><strong>Common Risk Factors:<\/strong> age, changes in hormone balance, increased androgens (testosterone), estrogen, family history (genetic\/lifestyle susceptibility)<\/li>\n<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Urinary urgency, frequency, nocturia, dysuria, hesitancy, retention, driblling; Ejaculation dysfunction<\/li>\n<li><strong>Pathogenesis:<\/strong>\u00a0 UV causes mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\n<li><strong>Diagnostic Tools<\/strong>: Urinalysis (to rule ot UTI or treat accompanying UTI), uroflowmetry, serum marker PSA test, digital rectal exam to feel for enlarged prostate, biopsy and microscopic analysis<\/li>\n<li><strong>Treatments:<\/strong> Transurethral Incision of the Prostate (TUIP) or other forms of surgery (Transurethral Resection of the Prostate, TURP or prostatectomy).<\/li>\n<\/ul>\n<\/li>\n<li>Prostate Cancer\n<ul>\n<li><strong>Common Risk Factors:<\/strong> age (due to lifetime exposure to potential carcinogens, plus # of mitotic events increases chances of DNA mutations), viruses, family history (genetic\/lifestyle susceptibilities), high-fat diet, smoking, obesity<\/li>\n<li><strong>Signs<\/strong> &amp; <strong>Symptoms:<\/strong> Urine retention, urgency, requency, nocturia, dysuria, hematuria, back pain.<\/li>\n<li><strong>Pathogenesis:<\/strong>\u00a0 Mutations in genes responsible for regulating appropriate levels of cell cycling and\/or apoptosis.\u00a0 Mutated cells become undifferentiated and immortal, continuing to cell cycle producing non-functional cycling daughter cells that accumulate and spread through the body.<\/li>\n<li><strong>Diagnostic Tools<\/strong>: PSA test, digital rectal exam (feel for hard lumps), transrectal ultrasound and other imaging, biopsy and microscopic anallysis<\/li>\n<li><strong>Treatments:<\/strong> Depends on the extent of metastasis: Surgical removal, Chemotherapy, Radiation,Hormone Therapy (GnRH agonists, androgen blockers), and other accompanying therapies &#8211; see above for list.<\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<p>&nbsp;<\/p>\n","protected":false},"author":1370,"menu_order":2,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[48],"contributor":[60],"license":[57],"class_list":["post-498","chapter","type-chapter","status-web-only","hentry","chapter-type-standard","contributor-zoe-soon","license-cc-by-nc-sa"],"part":35,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/498","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":25,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/498\/revisions"}],"predecessor-version":[{"id":4383,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/498\/revisions\/4383"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/35"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/498\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=498"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=498"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=498"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=498"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}