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29 Cards in this Set
- Front
- Back
- 3rd side (hint)
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side 1: what is differentiation? Side 2: for benign neoplasm?
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refers to the degree to which neoplastic cells morphologically, functionally, and behaviorally resemble the cell of origin
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usually composed of cells that resemble the cell of origin in appearance and function (ie adrenal neoplasms are more likely to produce corticosteroids than malignant neoplasms)
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side 1: what is pleomorphism? Side 2: for malignant neoplasms?
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variation in the size and shape of cells and nuclei is a characteristic of neoplastic, usually malignant cells
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can be well differentiated, but may range from poorly differentiated (bearing some resemblance to the cell of origin) to anaplastic
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side 1: what is anaplasia? Side 2: what is the prognosis for patients with anaplastic neoplasms?
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a characteristic of cancerous cells; it implies a lack of differentiation and marks a cell as malignant. Function of cells tends to correlated with morphologic differentiation and anaplastic cells rarely produce a product, such as protein, that the original cell did
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less hopeful than with other tumor types
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side 1: what is the term for an anaplastic tumor of epithelial origin? Side 2: what is the term for an anaplastic tumor of mesenchymal origin?
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undifferentiated carcinoma
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undifferentiated sarcoma
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what is the term for an anaplastic tumor of unknown origin?
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undifferentiated malignancy
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what happens to function in poorly differentiated tumor cells?
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loss of function
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side 1:how do benign tumors behave? Side 2: how do malignant tumors behave?
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expand without invasion and tend to compress adjacent structures
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invasive and many eventually metastasize
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what are the cytologic characteristics of malignant cells?
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unequal cell size (anisocytosis), unequal nuclear size (anisokaryosis), hyperchromatic nuclei: abnormal DNA content, abnormal nuclear/cytoplasmic ratio approx 1:2 instead of 1:4-1:6, enlarged an multiple nucleoli, irregular clumping of chromatin, high mitotic index, abnormal mitoses, tumor giant cells
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side 1: how are most tumore cells believed to arise? Side 2: what is an alternative theory?
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from alterations of the stem cell that gives rise to the cell type typical for the tumor (ie stem cells in the skin may be the source of squamous cell carcinoma)
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de-differentiation of mature cells types into tumor cells
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side 1:what does a cell cycle consist of? Side 2: what occurs in tumor cells?
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G1 > S (DNA synthesis) > G2 > M (mitosis) with alternate routes to G0 and removal from cell proliferation or continued participation in the cell cycle (tightly regulated in normal cells). Note there are checkpoints between G1 & S and between G2 & M
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these controls are lost (central feature of neoplastic transformation)
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what is a characteristic features of cell cycle control in tumor growth?
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lack of normal control of the cell cycle at the major check points where cells assess the integrity of the genome before going through mitosis, leading to uncontrolled proliferation
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how are normal cell populations regulated?
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through the balance of creation and loss of cells from the population
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how is proliferation regulated?
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balance of growth stimulating factors (growth factors, extracellular matrix components, cytokines) and growth inhibiting factors (growth inhibiting factors, cytokines, extracellular matrix factors)
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how does differentiation affect growth of cell population?
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some cell populations mature into a post-mitotic state (neutrophils for example)
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what is apoptosis?
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programmed cell death is a normal activity for many tissues such as the epithelium lining the gut (triggered by extensive cell damage, especially damage to the genome where apoptosis is mediate by the tumor suppressor gene p53 or by molecular signaling via the Fas and TNF receptors), tmor cells frequently undergo apoptosis for a variety of reasons and this is one of the major limits to tumor volume expansion and overall growth
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side 1:what is the potential for tumor cell growth? Side 2: how does this affect diagnostics?
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transformed cell = 10u diameter > 30 doublings = 1gm (10^9 cells) mass (limit of ability to detect neoplasm) > 10 more doublings = 1kg mass (10^12 cells)= lethal
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by the time we detect a neoplasm, it has completed most of its life span
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side 1: what is the tumor volume doubling time without therapy in mice? In humans?
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1-5d
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1-5m
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the potential for unlimited growth is a hallmark of what?
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neoplasia
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side 1: what are telomeres? Side 2: how do tumor cells maintain telomeres?
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structures at the end of chromosomes composed of several thousand 6 base pair repeats; each time a cell duplicated a chromosome during mitosis several hundred base pairs are lost (due to the way DNA replicates) an after all of the telomere DNA is used up the chromosome become unstable and can stick to one another and disrupt normal cell proliferation as well as homeostasis leading to cell death
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some turn on enzyme telomerase that replaces the telomeres and allows unlimited replication; detection of telomerase is one way to identify malignant cells
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what modulates the ability of tumore masses to grow?
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various host responses, local environmental factors (hypoxia, nutrient deficiency), and tumor cell factors (dependence on growth factors). May also develop insensitivity to factors that would normally inhibit growth
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how is apoptosis affected by some tumors?
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tumors able toe expand because of the resistance to apoptosis (lymphomas)
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genomic instabilty is a characteristic of what?
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tumor cells; abnormal DNA content (aneuploidy) is a very common characteristic of tumor cells
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what limits the growth of a tumor?
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genetic abnormalities, host defenses, hypoxia, induced apoptosis (in some more than 80% of cells die)
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how do tumors evolve?
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initiation, promotion, progression
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side 1: what is initiation in terms of tumor evolution? Side 2: what is promotion in terms of tumor evolution?
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a change, usually permanent, produced in a cell by sufficient single exposure to a carcinogen that can't produce neoplasia alone; the change is fixed by replication at or just following exposure to the carcinogen ( a two step process)
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enhancement of tumor development by exposure of initiated cells to noncarcinogenic (by themselves) substances or environments; promoters often stimulate cellular proliferation (Ie saccharin, cyclamates, hormones)
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side 1: what duration of exposure is required for initiation? Side 2: for promotions?
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minutes to a few days
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much longer exposure periods (weeks to months)
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side 1: how does initation and promotion affect tumors? Side 2: what is a complete carcinogen?
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tumors develop only when the promoter is applies after initiation
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one that can both initiate and promote if given in sufficient dosages over sufficient periods of time
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side 1: what is progression? Side 2: what is monoclonality?
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a multistage process whereby more abnormal characteristics are acquired as a malignant phenotype is approached, this is related to a 'multi-hit' theory in chemical carcinogenesis (more than one mutation required to develop malignant phenotype)
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most neoplasms are believed to arise from a single cell (clonal origin)
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side 1: what is tumor heterogeneity? Side 2: how is this impacted by clonal selection?
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sequential appearance of subpopulations of cells that differe with respect to several phenotypic attributes such as invasiveness, rate of growth, metastatic ability, karyotype, hormonal responseiveness, an ability to resist anticancer drugs
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even arising from a clonal expansion, a transformed cell eventually gives rise to a heterogeneous mass of cells (tumor heterogeneity) due to genetic instability, mutation, selection, an continued clonal expansion of subclones
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