Download SDL 3- Neoplasia 1 Tumor: any swelling Neoplasia: mass of cells

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