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Neoplasia
Stack #164015
| Question | Answer |
|---|---|
| refers to a "new growth" of abnormal tissue (usually derived from a single cell precursor) that serves no physiologic function and, for the most part, is independent of normal restraints on orderly growth | Neoplasia |
| retinoblastoma, neurofibromatosis, multiple endocrine neoplasia syndrome | Genetically influnced neoplasm |
| of human neoplasia is due, in part, to environmental factors. | 75 - 90 percent |
| tissues most directly exposed to the environment | skin, respiratory tract, gastrointestinal tract |
| in the majority of cases, neoplastic transformation involves | somatic mutations of cellular DNA |
| It appears, therefore, that neoplasia is, in essence, is what type of disease | genetic but influenced by environment |
| "Tumors" are denoted by the suffix | "-oma" |
| usually indicates a neoplastic process | oma |
| "-oma" usually indicates a neoplastic process but occasionally may be applied to a non-neoplastic mass, identify three examples | hematoma, granuloma, xanthoma |
| An unmodified suffix generally denotes what type of neoplasm? | a benign neoplasm |
| referring to epithelial malignancies | carcinoma |
| referring to mesenchymal/connective tissue malignancies | sarcoma |
| malignant neoplasm of melanocytes | melanoma |
| malignant neoplasm of lymphoid tissue | lymphoma |
| malignant neoplasms of supporting tissue of the CNS | glioma |
| malignant tumors arising from early, partially differentiated embryonal tissue | blastoma |
| a neoplasm which contains cells from more than one embryonic germ cell layer and may be benign or malignant. | teratoma |
| a non-neoplastic "tumor" that represents abnormal overgrowth or differentiation of cells native to the tissue of origin | hamartoma |
| refers to the presence of normal tissue in an abnormal location | choristoma (also termed ectopic or heterotopic tissue) |
| the basic terms indicating neoplasia are modified by prefixes that generally denote what three things? | the cell of origin, gross appearance and/or microscopic architectural growth patterns. |
| squamous,adeno,transitional,fibro,leiomyo,rhabdomyo,lipo,chondro,osteo,hemangio,lymphangio | PREFIXES INDICATING CELL OR TISSUE OF ORIGIN |
| squamous | squamous epithelium |
| adeno | glandular epithelium |
| transitional | transitional epithelium |
| fibro | fibrous connective tissue |
| leiomyo | smooth muscle |
| rhabdomyo | skeletal muscle |
| lipo | adipose tissue |
| chondro | cartilage |
| osteo | bone |
| These include scirrhous, medullary , colloid cystic, | PREFIXES INDICATING GROSS FEATURES |
| hard due to excessive production of tumor stroma | scirrhous |
| soft resembling marrow,due to scant production of tumor stroma | medullary |
| gelatinous, mucinous | colloid |
| fluid or gas filled spaces | cystic |
| These include follicular, cyst, papillary, villous, tubular, cribriform | PREFIXES INDICATING ARCHITECTURAL GROWTH PATTERN |
| forming follicles | follicular |
| forming small cystic spaces | cyst |
| forming "nipple-like" projections | papillary |
| forming shaggy, "finger-like" projections | villous |
| forming cylindrical tubules | tubular |
| pierced by small holes | cribriform |
| The distinction between benign and malignant tumors is based on their | microscopic appearance and clinical behavior. |
| Type of neoplastic cells,characterized by cellular and nuclear pleomorphism | malignant |
| nuclear pleomorphism is due to alterations | in the cell cytoskeleton |
| This refers to the extent to which neoplastic cells resemble their cell of origin histologically | CELLULAR DIFFERENTIATION |
| complete lack of differentiation | anaplasia |
| These type of neoplasms grow by expansion and tend to compress the surrounding tissue into a "capsule" that separates the tumor from normal tissue. | Benign |
| This refers to spread of a neoplasm to points that are not contiguous with the primary lesion. | METASTASIS |
| In general, metastases occur via: | LYMPHATIC DISSEMINATION, HEMATOGENOUS DISSEMINATION,TRANSCOELOMIC SEEDING,TRAUMATIC SEEDING |
| This is the most common route of metastasis | LYMPHATIC DISSEMINATION |
| Type of dissemination that follows the natural lymphatic drainage of the site of malignancy | LYMPHATIC DISSEMINATION |
| Regional lymph nodes may be enlarged due to | metastatic tumor or to immune reaction to the presence of tumor products. |
| TYPE OF DISSEMINATION - This is characteristic of connective tissue neoplasms (sarcomas). | HEMATOGENOUS |
| Carcinomas, however, are also spread by a hematogenous route since there are | vascular-lymphatic anastomoses. |
| Invasion and metastases are more likely to occur via the arterial/venoous system | venous |
| Invasion and metastases are more likely to occur via the venous system, why? | due to its thin walled structure. |
| This may occur with malignancies that involve coelomic (peritoneal, pleural) surfaces. | TRANSCOELOMIC SEEDING |
| peritoneal, pleural | coelomic |
| Excessive manipulation or cutting into malignant tumors may detach and carry small portions of the tumor to other sites. | TRAUMATIC SEEDING |
| small tumors that may cause sudden death by interfering with vital functions would be loacated where? | brainstem, conduction system of heart |
| Type of neoplasms, more prone to infarction, necrosis, hemorrhage, ulceration, and infection. | Malignant |
| Metastic or Benign stimulate excessive production of connective tissue (desmoplasia). | Malignant |
| excessive production of connective tissue | desmoplasia |
| hormones or hormone-like substances that can have systemic effects are known as | paraneoplastic syndromes |
| hypercalcemia, Cushing's syndrome, Syndrome of Inappropriate ADH Secretion, polycythemia are examples of what? | paraneoplastic syndromes |
| two or more different chemicals may act synergistically to induce cell transformation | co-carcinogenesis |
| Most of the known carcinogens are metabolized by cytochrome | P-450-dependent mono-oxygenases |
| Where are most carcinogens metabolized | in the liver |
| Does carcinogenic changes occur in stages or all at once? | in stages |
| Cell contact with what can produce permanent changes in the genetic make-up of a cell? | chemical initiators |
| Initiators react with what to cause strand breaks? | DNA |
| What causes alterationof methylation to hinder DNA repair. | strand breaks |
| The DNA changes, during iniation must not be so severe as to prevent the cell from being able to | replicate. |
| During iniation, why can't the DNA be prevented from replicating? | Initiators do not stimulate cell division, and initiated cells do not have growth autonomy nor do they have unique, readily identifiable genotype or phenotype markers. |
| Part of iniation these can induce neoplastic transformation in a previously initiated cell but cannot cause neoplastic transformation in and of themselves in a non-initiated cell. | Chemical promoters |
| Instead of altering the DNA, chemical promoters action seems to induce clonal proliferation of initiated cells by | altering the regulation of mitosis and the differentiation and maturation pathways. |
| Part of iniation when ultimately the cells are no longer dependent on the promoters for proliferation. | CONVERSION |
| Once the neoplastic cells become autonomous, continued genetic mutation confers new attributes to subclones of the neoplastic cells | PROGRESSION |
| The ability of ionizing radiation to induce neoplastic transformation, however, appears to correlate best with its ability to | induce genetic mutation within the cell. |
| carcinoma of the uterine cervix, hepatocellular carcinoma, Burkitt's lymphoma | DNA and RNA viruses associated with human neoplasia |
| Through the process of __________and __________, viruses may directly rearrange the structure or alter the expression of the host cell genome. | transduction and insertional mutagenesis |
| loss of contact inhibition, anchorage independent growth, immortal, develop invasive properties, metastatic potential, transplantability | FEATURES OF MALIGNANT CELLS |
| Their growth is no longer inhibited by the presence of neighboring cells | loss of contact inhibition |
| they do not require attachment to a hard surface to proliferate | anchorage independent growth |
| less cohesive | loss of surface cellular adhesion molecules |
| cell lines can be kept alive indefinitely | immortal |
| When injected into other animals, these cells will produce neoplasms | transplantability |
| naturally occurring cellular genetic segments were termed | proto-oncogenes |
| Type of oncogene found to be similar in sequence to normal proto-oncogene sequences and may have arisen through simple somatic mutation of the proto-oncogenes. | cellular oncogenes |
| STRUCTURAL CHANGES & REGULATORY CHANGES | MECHANISMS OF ONCOGENE ACTIVATION |
| can lead to synthesis of a protein that has aberrant structure and function. This can occur through point mutations, insertions/deletions, or translocations. | STRUCTURAL CHANGES |
| , mutations affect the amount of protein product rather than the structure. This can occur through translocation or gene amplification. | REGULATORY CHANGES |
| Oncogenes may code for large amounts of growth factors to which the cell can respond, this is known as | autocrine stimulation |
| Oncogenes may impart growth autonomy by | deregulating genes that encode growth factors. |
| most neoplasms arise from ___________ "spontaneous" somatic mutations of cellular DNA | multiple |
| retinoblastoma, Wilms' tumor | tumors related to heritable factors. |
| the expression of these genes (particularly the growth suppressor genes) serves to protect the cell from the events leading to neoplastic transformation, they are referred to as | tumor suppressor genes |
| The _________products of the tumor suppressor genes modulate the activity of proto-oncogenes, oncogenes, or their protein products. | protein |
| tumor suppressor gene on the short arm of chromosome 17 becomes much more active after DNA damage. | p53 |
| How does p53 tumor suppressor work? | It codes for a protein that binds to damaged DNA and inhibits cell mitosis until the damaged DNA can be repaired |
| and inactivation of the p53 gene are seen in what human malignancies | astrocytoma of the brain and carcinoma of the colon |
| Defects in the DNA repair genes may also predispose to malignant transformation and have been associated with various cancer syndromes such as | xeroderma pigmentosum. |
| the autosomal dominant neoplasia syndromes (multiple endocrine neoplasia syndromes, familial polyposis coli, Von Recklingshausen disease, etc) appear to be the result of inheriting at least one | mutated gene allele |
| This refers to the proportion of cells within a tumor population that are in the proliferating pool. | GROWTH FRACTION |
| Most cancer drugs act primarily on dividing cells, therefore those tumors which have a _______________ are most vulnerable. | high growth fraction |
| Without this, neoplastic growth will stop at approximately one millimeter diameter due to the limited diffusion capacity of oxygen and solutes. | vascularization |
| The neovasculature, of maloignant tumors, tends to be abnormal due to the loss of | endothelial junctions |
| _________ in the tumor environment also significantly impairs the biologic effect of radiation therapy and some forms of chemotherapy which is oxygen dependent | Hypoxia |
| a greater degree of tumor angiogenesis is correlated with a more ___________ behavior and ____________ prognosis. | agressive, poorer |
| These cells are more likely to have characteristics that enable them to spread | Dedifferentiated |
| This refers to antigens that are found on neoplastic cells and not on normal cells. | TUMOR SPECIFIC ANTIGENS |
| These are antigens found in normal cells but which are present in higher concentration in tumor cells. | TUMOR ASSOCIATED ANTIGENS |
| This refers to a microscopic pathologic determination of tumor aggressiveness based on the degree of differentiation of the neoplastic cells and the number of mitoses as an estimate of the rate of growth | GRADING |
| Grading is based on what two things | microscopic pathologic dteremination of degree of differentaiation of neoplastic cells and the number of mitoses |
| This refers to a clinical and pathologic determination of tumor aggressiveness based on the size of the neoplasm, the presence or absence of regional lymph node involvement, and the presence or absence of distant metastases. | STAGING |
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