CSF: Intro to Neoplasia
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Biscutigem on April 16, 2012
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47 terms
Terms | Definitions |
|---|---|
 What is neoplasia? | New growth from uncontrolled or autonomous proliferation due to genetic mutations. - results in a mass or neoplasm - neoplasm = benign or malignant depending on clinical behavior or aggressiveness |
| What is a tumor? | - originally a result of swelling due to inflammation - also may be a benign or malignant neuplasm that produces a swelling |
| Characteristics of benign neoplasms/tumors | - Slow growing neoplasms that stay put - Do not invade surrounding tissues - Do not metastasize (travel to other organs) |
| Characteristics of cancer/malignant neoplasms | - Do invade surrounding tissues - Do metastasiize (travel to other organs) |
| What is metaplasia? | - Non-neoplastic change in type of tissue at a site of injury or irritation; a form of reaction to injury - assoc. w/ chronic irritations and explains cancers arising from cells not normally found in those sites - ex. squamous epithelium replaces glandular epithelium = squamous metaplasia |
| What is dysplasia? | - Neoplastic mutations which result in abnormal features in some but not all original or metaplastic cells sothet there is a mix of abnormal and normal cells |
| What is carcinoma-in-situ? | Neoplastic mutations which result in replacement of all the normal epithelial cells w/ abnormal cells w/out invasion of basement membrane |
| What is carcinoma? | Invasion through the basement membrane and or metastases |
| Lung Cancer: ex. of metaplasia | - smoking changes ciliated columnar epithelium to benign squamous epithelium (non-neoplastic change) --> dysplasia (neoplastic change) -->carcinoma-in-situ --> invasive squamous cell carcinoma (among most common types of lung cancer) |
| Cervical Cancer: ex. of metaplasia | - chronic HPV infection changes endocervical epithelium to squamous epithelium --> dysplasia --> carcinoma-in-situ --> invasive squamous cell carcinoma (most common type of cervical cancer) |
| Esophageal Cnacer: ex. of metaplasia | - chronic reflux of gastric acid into distal esophagus changes squamous lining into gastric glandular epithelium --> dysplasia --> adenocarcinoma-in-situ --invasive adenocarcinoma (most common type of esophageal cancer in US) |
| What is the significance of accumulation of mutations? | - neoplastic cells often have genetic instability allowing for additional mutations altering the tumor and often making it more aggressive; i.e progression from dysplasia to metaplaisia - a larger population of tumor cells increases the tumor's chance of surviving and accumulating additional mutations = allow mutational experimentation despite loss of many cells that develop unsuccessful mutations |
| What is differentiation? | The degree to which neoplastic cells resemble normal cells and structure (morphologically and functionally) |
| What are the grades/degrees of differentiation? | - Low grade (well differetiated): look the same or nearly the same as tissue of origin - Intermediate grade (moderately differentiated: some resemblance to tissue of origin - High grade (poorly differentiated or anaplastic): little or no similarity to origin of tissue **Grade/degree of anaplasia relates well to aggressiveness of the tumor |
| Grades or degrees of benign vs. malignant tumors | - Benign tumors are almost always well differentiated, not aggressive, and very rarely graded - Malignant tumors - behavior predicted by grade; the uglier/ less lke its tissue of origin the WORSE it behaves |
| What is the grade/degree of anaplasia or lack of differentiation determined by? | - Cellular and nuclear pleomorphism (varied size and shape) - Hyperchromatic staining or hyperchromasia (increased nuclear DNA) - Increased nuclear/cytoplasmic ratio (usually from larger nuclei) - Prominent nucleolus or nucleoli - Increased mitotic activity - Disorganized growth: failure to produce structures ( glands or keratin) |
| What are some characteristics of growth for neoplasms? | - Benign usually grow slow while malignant grow more rapidly - growth is measured byt doubling time - time required for tumor to double in size - the higher the grade, the faster the growth and the shorter the doubling time |
| How does cell cycle relate to doubling times in a tumor? | - Cell cycle is usually NOT shorter - cancer grows faster b/c cells produced exceeds cells lost; fewer cells are lost to permanet terminal maturation (non-replicating stage) or apoptosis - therefore, there are more cells capable of re-entering the cell replicative cycle |
| What does the stage of a neoplasm refer to? | - Stage = extent of spread - low stage = tumor limited to site of origin; good prognosis - high stage = spread to other organs; poor prognosis - TNM cancer staging system: * T = size or local extent of primary tumor * N = number and distribution of lymph node metastases * M = presence and extent of distant metastases |
| What is invasion and what are its steps? | - progressive inflitration and destruction of surrounding tissues (usually malignant tumors) 1) Less cell-to-cell adhesion 2) Binding of malignant cells to ECM by activation of adhesion molecules 3) Migration of tumor cells int degraded zone of ECM |
| What causes less cell-to-cell adhesion | - Due to down regulation of: * Epithelial (E) cadhedrin = fewer bridges btwn cells which anchor cells to catenins - catenins - membrane attacment sides under the plasma membrane; unbound or free catenins also induce cellular proliferation |
| What are some adhesion molecules that are activated by malignant cells? | - Immunoglobulin supergene family (expression correlates w/ aggressiveness) * ICAM (intercellular adhesion molecule) * VCAM (vascular cell adhesion molecule) - Integrins *bind to basement membrane and/or matrix proteins as laminin or fibronectins * transmembrane molecules for signal conduction; increase and initiate BM penetration by secreting proteolytic enzymes = matrix degradation |
| What are some cells/enzymes activated by integrins? | - Proteinases * Serine proteinase - activates plasmin * Collagenases (metalloproteins) #Type IV collagen of BM and Type I collagen of stroma * Cystein proteinase (cathepsin B) - Activates fibroblasts resulting in: * Desmoplastic rxn * Type I collagenase production = penetration of fibrous stroma by tumor cells |
| What allows tumor cells to migrate into ECM? | - Autocrine motile factor (AMF) causes pseudopodia of tumor cells rich in receptors for laminin and fibrinectin |
| What is metastasis and how is it spread? | - separate sites of tumor which are discontinuous with primary neoplasm b/ tumor cells were separted and traveled to other sites via: * direct seeding of body cavities or surfaces * spread through lymphatic or blood (hematogenous) vessels - not all organs (ex. spleen) are equally susceptible to metastases |
| What are the steps in formation of metastases | - invasion of blood/lymphatic vessels by malignant cells - cells transported by embolization or mechanical means - lodging and growth in new location (lung, liver, bone, etc) requiring angiogenesis to support new growth |
| What are the most important angiongenic factors and how are they produced? | - vascular endothelial growth factor (VEGF) and basic fibroblast growth factor or (bFGF) *Produced by either: #tumor cells directly or benign stromal cells in response to signals from tumor cells **Suppression of normal anti-angiogenic factors (ex. thrombospondin-1) must occur for angiogenesis to take place. |
| What is the Walburg Effect? | - altered glycolysis: most tumor cells * don't use mitochondria for glycolysis (20 ATPs from 1 glucose) * but use direct aerobic glycolysis (2 ATPs from 1 glucose) therefore tumor cells take up more glucose than most normal cells - Use Walburg effect by CT/PET scans to detect increased uptake of radioactive labelled glucose (fludeoxyglucose, 18Fm to detect tumor, particularly metastases) |
| What are the components of neoplasms? | 1) parenchyma or neoplastic cells: proliferating malignant cells of the neoplasm; nomenclature usually based on parenchymal component 2) Stroma: benign supporting framework of CT and blood vessels (adequate blood supply is critical to tumor growth); derived from non-neoplastic cells |
| How are neoplasms classified? | ** based on histogenesis (cell of origin) of parenchymal component and behavior (benign or malignant - most benign neoplasms = suffix "-oma" - most malignancies = suffix "-carcinoma" or "-sarcoma" - exceptions: some malignancies by convention end with "oma" = lymphoma, mesothelioma, melanoma, seminoma |
| What are Epithelial Neoplasms? | - carcinomas: malignancies of epithelial cells (cells w/ BMs) typically spread by lymphatic channels - may be carcinoma in-situ or invasive carcinoma - may be ectodermal (skin and brain), mesodermal (kidney and endometrium, or endodermal (gut) origin |
| What are some tumors of non-glandular epithelium? | - Stratified squamous epithelium *Benign: squamous papilloma * Malignant: squamous cell carinoma - Basal cells of skin * Malignant: basal cell carcinoma - Transitional epithelium * Benign: Transitional papilloma * Malignant: Transitional cell carcinoma |
| What are neoplasms of glandualr/ductal epithelium? | Benign: Adenoma or Papilloma Malignant: Adenocarcinoma or Papillary adenocarcinoma |
| What are mesenchymal neoplasms? | - arise from stromal or supporting tissues (CT, muscles, bld vessels) - generally nambed for mature tissue they most closely resemble but some malignancies are sufficiently undifferentiated making subclassification difficult - benign: end w/ "-oma" - malignant: end w/ "-sarcoma" - typically spread by blood (hematogenously) |
| What are some CT neoplasms [benign (B) or malignant (M)]? | - Fibrocytes: fibroma (B); fibrosarcoma (M) - Adipocytes: lipoma (B); liposarcoma (M) - Chondrocytes: chondroma (B); chondrosarcoma (M) - Osteocytes (bone): osteoma (B); Osteosarcoma (M) |
| What are some muscle neoplasms? | - Smooth muscles: Leiomyoma (B); Leiomysarcoma (M) - Skeletal muscles: Rhabdomyoma (B); Rabdomyosarcoma (M) |
| What are some endothelial cell neoplasms? | - Blood vessels: hemangioma (B); angiosarcoma (M) - Lymph vessels: lymphangioma (B); lymphangiosarcoma (M) |
| What are mesothelial cell neoplasms called? | - Benign/malignant mesothelioma |
| What are some neoplasms of the Nervous system (derived from neuroectoderm)? | - Support/glial cells * Astrocytes: astrocytoma (M) - lower grades; glioblastoma (M) - high grade * oligodendrioglia: oligodendroglioma (M) * Nerve sheath: benign/malignant schwannoma - Nerve cells: Neuroma/ganglioma (B); Neuroblastoma/medulloblastoma (M) - Retina: Retinoblastoma (M) - Melanocytes in skin (neural crest origin): nevus (benign mole); melanoma (malignant mole) |
| What are germ cell neoplasms? | - arise from pleuripotent stem cells; can differentiate into cell lines of >1 dermal (ecto-, meso-. and/or endodermal) origin and thus contain one or more types of mature tissues |
| What are some examples of germ cell neoplasms? | - Germ cells w/out differentiation: Seminoma (M) in males; Dysgerminoma (M) in females - Placenta: hydatidiform mole (B); choriocarcinoma (M) - mature tissues (mix of brain, gut, skin and/or lung): mature teratoma (B); immature teratoma (M) |
| Hematopoietic malignancies: What are leukemias? | - malignant neoplasms of the myeloid or lymphoid hematopoietic stem cells (granulocytes, lymphocytes, monocytes, RBCs and/or megakaryocytes) - diffusely replae bone marrow and often spill over into peripheral bld |
| What is the difference between acute and chronic leukemias? | - Acute: composed of very immature cells (blasts) and rapidly progressive (ex. acute lymphoblastic/myeloblastic leukemia) - Chronic: more mature and clinical cours is usually indolent or prolonged (ex. chronic lymphocytic/myelogenous leukemia) |
| Hematopoietic malignancies: What are lymphomas? | - malignancies of lymphocytes that form solid tissue masses and usually DO NOT spill over into peripheral blood although frequently invlolve bone marrow - Divided into two main groups: Hodgkin's and Non-Hodgkin's lymphoma |
| What is Hodgkin's Lymphoma? | - always malignant and accounts for 20% of lymphomas - primarily involves lymph nodes - has Reed-Sternberg (RS) cells = giant usually multinucleated cells w/ large red nucleoli of lymphocytic origin (owl-eyed) -histologic changes in lymph nodes mostly due to non-neoplastic host response (benign, small lymphs, eosinophils, plasmacytes) - usually depression of T-cell fxn (cellular immunity) |
| What is Non-Hodgkin's lymphoma? | - Malignancies of lymphocytes w/ NO Reed-Sternberg cells - 80% of lymphomas - most involve lymph nodes but 1/3 of cases have primary sites in other tissues (ex. oropharynx, gut, bone marrow, or skin) - morphological features of malignant cells recapitulate (repeat) various stages of normal lymphocyte transformation (small to giant lymphs) - usually furthur characterised by immunologic methods into: * B cell (80%) - cause depression of humoral immunity * T cell (20% of non-Hodgkin) - cause depression of cellular and humoral immunity |
| Hematopoietic Malignancies: What is multiple myeloma? | - Malignant proliferation of plasma cells (transformed B cells) - usually remains in the bone marro and causes lytic lesions (holes) in the bones - plasma cells secrete monoclonal immunoglobulin (M-protein); usually IgG or IgA - Sometimes produces Bence-Jones proteins: component of monoclonal kappa or lamda light chain which is small enough to pass into urine - Amyloidosis of AL type - assoc. w/ myelomas that produce Bence-Jones proteins - Most pts die of infection b/c of 1) depression of humoral immunity = infection 2) renal failure b/c proteins plug up renal tubules and/or amyloidosis |
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