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| The risk of developing cancer increases or decreases with age. |
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| Cancer is caused by an accumulation of.. |
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| a tissue overgrowth that is independent |
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| Not all tumors or neoplasms are cancerous. |
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| Cancer refers to what type of tumor? |
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| This can cause life threatening symptoms if they enlarge in critical locations |
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| These are not called cancers |
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| Well encapsulated and well differentiated, retains some normla tissue structure, and doesn't invade the capsule or spread to regional lymph nodes or distant locations. |
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| benign tumor of fat cells |
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| False, they can progress to cancer. |
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| Some benign cancers can't progress to cancer. |
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| rapid growth rate and specific alterations, loss of differentiation, absence of normal tissue organizations, lack of a capsule, invades blood vessels, lymphatics, surrounds structures, anaplasia and spreads. |
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| Cancers in epithelial tissue |
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| Cancer from ductal or glandular epithelium |
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| Malignant tumor from breast glandular tissue |
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| Cancer of CT have the suffix |
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| Cancers of lympatic tissue |
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| Cancers of blood forming cells |
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| Preinvasive epithelial tumors of glandular or squamous cell origin |
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| Found in cervix, skin, oral cavity, esophagus, and bronchus |
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| Is an important component of diagnosis and treatment planning |
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| Cancer confined to the organ or origin |
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| Cancer that is locally invasive |
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| Cancer that has spread to regional structures such as lymph nodes |
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| Cancer that has spread to distant sites such as liver cancer spreading to lung. |
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| Cancer cell's independence from normal cellular controls |
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| Loss of Differentiation and is recognized by a marked increase in nuclear size and ongoing proliferation such as mitotic figures. |
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| process of developing specialized functions and organizations |
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| varies in size and shape such as anaplastic cells |
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| pluripotent cells, precursor cells, or stem cells |
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| substances produces by cancer cells that are found on tumor plasma membranes or in the blood, spinalfluid, or urine |
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| Clonal proliferation or Clonal expansion |
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| Cell that accumulates faster than its nonmutant neighbors |
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| Cancers that secret growth factors that stimulate their own growth |
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| Activating mutation in an intracellular signaling protein that stimulates cell growth even when growth factors are missing. |
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| Self destruct mechanism and is disabled in advanced cancers |
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| Mutations resisting apoptosis |
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| new blood vessel growth, small cancers lack ability to do this, but advanced cancers secrete factors to stimulate new blood vessel growth |
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| Germ cells and some stem cells |
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| the only cells that are usually immortal |
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| specialized, multicopy repeat DNA sequence that protects and maintains the ends of the chromosomes |
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| specialized enzyme that maintains telomerase to shorten telomeres after each cell division cycles |
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| Germ cells and some stem cells |
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| Where telomerase primarily are |
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| In cancer cells this restores and maintains the telomeres which has the chromosomes divide over and over again |
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| mutant genes that in their normal nonmitant state direct synthesis of proteins that positively regulate (accelerate) proliferation |
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| Encode proteins that in their normal state negatively regulate (put the brakes on ) proliferation |
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| A genetic event that activates oncogenes and alters one or a few nucleotides base pairs |
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| Chromosome translocations |
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| Genetic lesion that can activate oncogenes by either cause excess and inappropriate productions or a proliferation factor. |
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| Chromosome amplifications |
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Genetic abnormality turning oncogenes on from the duplications or a small piece of chromosome overnad over again so instead of two normal copies of a gene there are tens or even hundred of copies
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| a tumor supressor gene that strongly inhibits the cell division cycle |
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| loss of a chromosome region in a tumor |
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| Gene expression that can be regulated in a hertible manner that doesn't require mutations or changes in DNA sequence and shuts of whole regions of chromosomes. |
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| Genes that are responsible for the maintenance of genomic integrity |
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| encode proteins that are involved in repairing damaged DNA, an errors in DNA replications, mutations due to UV or ionizing radiations, and mutations from chemicals and drugs |
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| Results in high rate of chromosome loss, as well as loss of heterozygosity and chromosome amplification which can accelerate the loss of tumor supressor genes and overexpression of oncogenes |
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| agents causing mutations in somatic tissues |
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| prerequisite for metastasis and first step in the metastic process |
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| Cancers cells are characterized by |
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| These are the primary basis of carcinogenesis |
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| activate growth promotion pathways, block antigrowth signals, prevent apoptosis, turn on telomerase, angiogensis, and allow tissue incasion and distant metastasis |
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| five or six distinct mutations |
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| It takes ____ or ____ mutations in different signaling pathways to produce cancer |
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| encode for growth factors, growth factor receptors, signal transducers, and nuclear growth-promoting proteins |
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| What human cervical cancer is caused by |
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| Immunodepressant drugs or HIV infections |
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| Contributes to the development of cancer by stimulating increased proliferation and angiogensis |
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| chronic hepatitis and colitis |
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| Two examples of chronice inflammation that increases the risk of cancer |
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| Where cancers metastasize through |
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| first regionally then distantly |
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| how does metastasis spread first |
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| Most cells aren't capable of successful metastasis, but when are it often protends a poor prognosis |
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| invasion, survival in circulation, attachment, growth, angiogensis at a favorable distant site. |
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| Steps of successful metastasis |
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