front 1 Neoplasm | back 1 A new abnormal growth or tumor |
front 2 Oncology | back 2 Study of neoplasms (tumors) or cancer |
front 3 Tumor parenchyma | back 3 The clonal neoplastic cancer cells of a tumor |
front 4 Tumor stroma | back 4 Supportive tissue including connective tissue, blood vessels, and immune cells. Growth and evolution of the tumor dependent on the stroma. |
front 5 Benign tumor | back 5 Localized, encapsulated, slow growing tumor that does not metastasize. Usually differentiated cells that reproduce at a higher rate than normal and can cause tissue damage (result of compression of adjacent structures). |
front 6 Malignant tumor | back 6 Invasive, rapidly, growing tumor capable of metastasis and tissue destruction. Undifferentiated (Look nothing like normal healthy cells) and nonfunctional. |
front 7 Key difference benign vs malignant | back 7 Benign stays localized while malignant invades and spreads |
front 8 Typical benign naming rule | back 8 Cell type plus suffix -oma |
front 9 Carcinoma | back 9 Malignant tumor arising from epithelial tissue (Most common) |
front 10 Sarcoma | back 10 Malignant tumor arising from mesenchymal/connective tissue |
front 11 Adenocarcinoma | back 11 Malignant epithelial tumor forming glandular structures |
front 12 Teratoma | back 12 Tumor containing tissues from multiple germ layers: Ectoderm (nervous tissue and epithelial tissue), Mesoderm (muscle, connective tissue), and endoderm (digestive system and internal organs) (More rare) |
front 13 Malignant tumor characteristics | back 13 Rapid growth, abnormal mitosis, lack of differentiation, invasion, metastasis, angiogenesis |
front 14 Angiogenesis | back 14 Formation of new blood vessels to supply tumor growth |
front 15 Loss of contact inhibition | back 15 Cancer cells continue growing despite touching neighboring cells |
front 16 Common cancer warning signs | back 16 Unusual bleeding, persistent lump, chronic cough, unexplained weight loss, change in bowel or bladder habits, nonhealing sore, change in mole |
front 17 Where cancer can arise: Epithelia | back 17 High occurrence (80% of cancer deaths); Carcinoma. Highest risk of exposure and high replacement rate (highly mitotic) |
front 18 Where cancer can arise: Connective | back 18 Sarcomas (1% of tumors in clinics). Bone, cartilage, fat, muscle, blood vessels, or other connective/supportive tissues |
front 19 Where cancer can arise: Blood forming (hematopoietic) tissues | back 19 Leukemia (starts in marrow and produces abnormal blood cells that enter the blood) and lymphoma (begin in cells of the immune system) (17% of cancer related deaths) |
front 20 Where cancer can arise: Central and Peripheral Nervous System | back 20 Spinal cord and outlying nervous tissues. Neuroectodermal tumors (2.5% of cancer related deaths) |
front 21 Local tumor effects | back 21 Pain, obstruction, tissue necrosis, bleeding, infection |
front 22 Tumor obstruction effect | back 22 Compression of ducts vessels or airway impairing organ function |
front 23 Systemic cancer effect cachexia | back 23 Severe weight loss and muscle wasting due to cancer metabolism |
front 24 Systemic cancer anemia | back 24 Blood loss or nutritional deficiency reduces hemoglobin |
front 25 Systemic cancer Severe fatigue | back 25 Caused by inflammatory changes, cachexia, anemia, stress of treatment schedule, and psychological factors |
front 26 Effusion | back 26 Fluid buildup in body cavities due to inflammation |
front 27 Systemic cancer Infections | back 27 Occur frequently as resistance declines |
front 28 Systemic cancer Bleeding | back 28 Tumor cells may erode the blood vessels |
front 29 Paraneoplastic syndrome | back 29 Systemic hormonal or neurologic effects caused by tumor secretions |
front 30 Diagnostic tests | back 30 Routine screening, self-examination, blood tests, tumor markers, and genomic tumor assessment |
front 31 Cancer screening and self-examination | back 31 Purpose is early detection and monitoring recurrence |
front 32 Blood tests | back 32 Measure blood cell levels during treatment. May detect tumor markers. |
front 33 Tumor markers | back 33 Substances, enzymes, antigens, or hormones produced by cancer cells detectable in blood |
front 34 Genomic tumor assessment | back 34 Testing tumor DNA mutations to guide treatment |
front 35 Imaging for cancer diagnosis | back 35 Xray, CT, MRI, ultrasound used to visualize tumor location |
front 36 Biopsy | back 36 Removal of tissue sample for histologic confirmation of cancer |
front 37 Histology vs cytology | back 37 Histology examines tissue structure while cytology examines individual cells |
front 38 Most reliable cancer confirmation | back 38 Biopsy with histologic examination |
front 39 How do cells invade and spread? | back 39 1. Altered cell adhesion (cadherins) 2. Change in interaction with stroma (loses anchors/integrins) 3. Altered synthesis of enzymes that break down basement membrane and stroma (Metallopeptidases); factors produced that help cells spread (scatter factor) |
front 40 Invasion ability | back 40 Cancer cells break through basement membrane and then spread into surrounding tissue and lymphatic/vasculature channels. Malignant cells. |
front 41 Metastasis | back 41 Spread of cancer cells to distant sites through lymph blood or body cavities |
front 42 Primary tumor | back 42 Original site where cancer begins |
front 43 Secondary tumor | back 43 Metastatic growth at distant location |
front 44 Common metastasis route lymphatic | back 44 Spread through lymph nodes common for carcinomas |
front 45 Common metastasis route blood | back 45 Spread through veins to lung liver brain or bone |
front 46 Coelomic spread | back 46 Cancer spread through body cavity fluid such as ovarian cancer |
front 47 Role of cadherins in cancer | back 47 Reduced adhesion allows tumor cells to detach and migrate |
front 48 Role of integrins in cancer | back 48 Altered interaction with stroma allows invasion and movement |
front 49 Matrix metalloproteinases | back 49 Enzymes that break down basement membrane to allow tumor spread |
front 50 Carcinogenesis | back 50 Process of normal cells transforming into cancer cells |
front 51 Initiation stage | back 51 First irreversible DNA mutation caused by carcinogen |
front 52 Promotion stage | back 52 Hormones and environmental chemicals that cause further DNA changes that increase proliferation and reduce differentiation |
front 53 Proto-oncogene | back 53 Normal gene regulating growth that can mutate into cancer promoting oncogene |
front 54 Oncogene | back 54 Mutated gene increasing cell growth and division. Cell growth and survival increase; accelerates cell division; gas pedal. Gain of function mutation- increase activity or expression level of a gene product |
front 55 Tumor suppressor gene | back 55 Gene that normally inhibits cell division or promotes apoptosis; brakes that protect cells from carcinogenesis. Loss of function mutation- gene product has lost partial or total activity or expression. |
front 56 Loss of tumor suppressor function | back 56 Removes cell growth control and promotes cancer |
front 57 Cancer risk factors genetic | back 57 Inherited mutations affecting growth regulation |
front 58 Cancer risk factors viral | back 58 Oncoviruses that alter host DNA such as HPV or hepatitis B |
front 59 Cancer risk factors radiation | back 59 UV rays, x rays, gamma radiation, cumulative exposure |
front 60 Cancer risk factors chemicals | back 60 Asbestos, solvents, heavy metals, formaldehyde |
front 61 Cancer risk factors lifestyle | back 61 Smoking, alcohol, diet, obesity, inactivity |
front 62 Cancer prevention avoid tobacco | back 62 Eliminates major carcinogen exposure |
front 63 Cancer prevention diet | back 63 High fiber fruits vegetables antioxidants reduce DNA damage |
front 64 Cancer prevention vaccination | back 64 HPV and hepatitis B vaccines reduce cancer risk |
front 65 Host defense tumor suppressor genes | back 65 Normal mechanisms that block carcinogenesis |
front 66 Host defense immune system | back 66 Cell mediated immunity recognizes and destroys tumor cells |
front 67 Cancer staging | back 67 Purpose is determine prognosis and treatment planning |
front 68 In situ cancer | back 68 Cells remain in original layer and have not invaded |
front 69 Invasive cancer | back 69 Cancer has penetrated basement membrane and spread locally |
front 70 TNM staging | back 70 T describes tumor size N lymph node involvement M metastasis |
front 71 Stage IV cancer | back 71 Most advanced cancer with distant metastasis |
front 72 Cancer treatment options | back 72 Surgery, radiation, chemotherapy, immunotherapy, or combination therapy |
front 73 Surgery for cancer | back 73 Removal of tumor and surrounding tissue |
front 74 Radiation therapy | back 74 Uses ionizing radiation to damage DNA of rapidly dividing cancer cells |
front 75 Radiation side effects | back 75 Bone marrow suppression, infection, fatigue, hair loss, infertility |
front 76 Chemotherapy | back 76 Antineoplastic drugs that interfere with DNA replication or protein synthesis |
front 77 Chemotherapy side effects | back 77 Bone marrow suppression, nausea, epithelial damage, hair loss, organ toxicity |
front 78 Hormone blocking therapy | back 78 Drugs that block growth signals to hormone sensitive tumors |
front 79 Biological response modifiers (BRMs) | back 79 Drugs that enhance immune response against cancer |
front 80 Angiogenesis inhibitors | back 80 Drugs that prevent tumor blood vessel formation |
front 81 Cancer nutrition issue | back 81 Many patients develop malnutrition due to treatment effects |
front 82 Cancer metabolic demand | back 82 Tumors often have high glucose requirements |
front 83 Remission | back 83 Period with no clinical signs of cancer |
front 84 Five year survival | back 84 Common benchmark used to define cancer free status |