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SDL 3- Neoplasia 1 Tumor: any swelling Neoplasia: mass of cells that have uncoordinated growth that is not shut off by absence of stimuli -no purpose to the organism -uncoordinated with normal tissues Parenchyma: cells are neoplastic cells proper, well differentiated, organized and proliferate slowly (can be poorly differentiated, unorganized, rapidly divide) Stroma: host is induced to supply stroma for the tumor; mediated by angiogenic factors that are synthesized by the parenchyma and stimulate the proliferation of stromal cells (fibroblasts, vascular) -CT and vessels supplied by the host to nourish and support neoplastic cells -somatic mutations within genes distinguishing cells growth and survival Hyperplasia: increased number of normal cells Metaplasia: larger than normal because changes in differentiation Dysplasia: normal maturation of the cells is interrupted -usually immature stem cells with corresponding decrease in number/location of mature cells Carcinoma in situ: cancer separated from the underlying connective tissue by a basement membrane -intraepithelial noninvasive carcinoma -if left untreated will turn into invasive cancer -from metaplasia to dysplasia to carcinoma in situ to invasive carcinoma Benign tumors: only grow locally, does not grow in an aggressive manner -can compress adjacent normal tissues (if in a critical location it can be deadly) -stroma of normal tissue is all that remains after compression and forms a capsule around tumor -fibrous capsule (some are not: papilloma, polyp, hepatic adenoma) -well-differentiated -Lipoma: subcutaneous fat -Leiomyoma: smooth muscle of uterus -Ependymoma: third ventricle of brain -Myxoma: left atrium -may secrete hormones (fewer per cell than normal tissues but if the tumor gets too large toxic doses of hormones can be seen) -adrenal medulla: epinephrine -pituitary gland: growth hormone Malignant tumors -uncontrolled growth, invade surrounding tissues, spread to distant organs (metastasis) -invasion: direct migration and penetration into neighboring tissues -metastasis: cancer cells to penetrate into lymph and blood vessels -dedifferentiation Neoplasms are named according to the tissue or organ they originate from and whether benign/malignant -benign: -oma -fibroma, lipoma, chondroma, osteoma, adenoma, teratoma (all 3 germ layers), hamartoma (localized, disordered differentiation during embryonic development, choristoma (collection of normal cells at an abnormal location) -malignant: carcinoma (epithelial cancers) Sarcoma (mesechymal origin) -emia: hematopoetic system -chondrosarcoma, fibrosarcoma, osteogenic sarcoma, transitional cell carcinoma SDL 3- Neoplasia 1 Gross features -form nodules or lumps that are palpable, solid, round or oval lesions -usually firmer than the surrounding tissue “scirrhous” -epithelial cancers with little stroma are soft “medullary carcinoma” Polyp: club shaped soft and fleshy from mucosa surface by a stalk -sessile polyp: lacks a stalk Papilloma: outgrowth from an epithelial surface with long thin branches Ulcer: area of tissue erosion, can happen in gut due to bacteria Linitis plastic: proliferation of the CT resulting in wall thickening so that the stomach is constricted and rigid like a leather bottle Leukemia: lymphoid or myeloid cells arising in bone marrow (WBC count increase) Stroma -benign tumors tend to have sharply defined edges, malignant have branches reaching into their surroundings -may benign tumors have no capsule at all, some malignant tumors have a capsule that tumor breaks -this makes benign tumors easy to cut out in surgery -blood vessels can arise from angiogenesis or from preexisting microcirculation -tumors have less blood supply than normal tissue -tumors react poorly to vasoactive agents making them be leaky -VEGF is a potent vascular endothelial GF that increases angiogenesis and increases vascular permeability VEGF-A is the mediator of tumor angiogenesis -renders microvessels hyperpermeable to plasma and plasma proteins with 50,000 times the potency of histamine -tumors are missing lymphatics -tissue pressure is positive and is elevated in the center of tumors (blood flow to the center of tumor is impaired= typical necrosis of malignant tumors) -can have chemotactic messages: macrophages, NKT cells, T lymphocytes -tumors cannot grow much beyond the size of a pinhead unless supplied blood vessels -Angiogenic index: numbers of cessels/mm2 -benign tumors are sparsely vascularized and tend to grow slowly -malignant tumors are highly vascularized and fast-growing Parenchyma -benign tumors resemble their parent tissue; malignant tumors depart from tissue morphology -anaplasia: lack of differentiated features, correlates with aggressiveness -cytoplasmic basophilia: due to increased amounts of RNA and thus more active protein synthesis -many free ribosomes in cancer cells, which means that the cell is not producing proteins for export (is busy making more of itself) -nucleoli increase in size and number is explained by increased amounts of RNA -glycogenic content is high (anaerobic glycolysis is typical in tumor cells) -pleomorphism: shapes of the cell and its nucleus are irregular -abnormal nuclei -mitoses: numerous and may be abnormal -cell-specific organelles: disoriented or lost -new-types of organelles: ribosome-lamella complex of the hairy-cell leukemia, Auer rod of acute myelogenous leukemia -Mucus secretion: irregular (can not be produced at all) SDL 3- Neoplasia 1 Tumor cells: look less differentiated, similar to stem cells, increased nuclear-cytoplasmic ratio, anaplasia and cellular atypism refer to lack of differentiation, degree of dedifferentiation (anaplasia, atypism) correlates with the degree of aggressiveness of the tumor Fast growth: cytoplasmic basophilia, nucleoli increase in size and number, abundant mitoses Secondary changes in tumors -ulceration -necrosis: impaired blood flow to tumor -calcification: usually develops in dead cells or necrotic masses (good to use mammography) -torsion: accident that occurs with pedunculated tumors, veins twisted stalk are compressed first and arteries still pump blood (red infarct) -it is believed that tumors arise in stem cells located in the basal layer (difficult to id) -only long-term residents in various tissues (target for mutations) -most cancers are monoclonal: from 1 cell -neoplastic plasma cells in multiple myeloma produce a single immunoglobulin unique to an individual patient -G6PD has different enzymes that can be turned on or off with female X chromosomes -tumors initially remain small, proliferation offset by apoptosis -take months or years to generate the proper genetic conditions necessary to tip the balance and activate angiogenesis switch -malignant tumors go from bad to worse -under constant evolutionary pressures some cells are eliminated because of biological disadvantage, others succeed due to less demanding growth factors, more invasive, more metastatic -most tumors first have a benign stage, some can occur without -tumors have a doubling time after it attains 1 cm3; 1 kg tumor is max compatible with life -grow exponentially