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19 Cards in this Set
- Front
- Back
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Abnormal cell growth and division |
Abnormal proliferation |
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Defects in normal restraints that prevent cells from spreading |
Metastasis |
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Result from unregulated cell growth forming a multicellular mass that can be removed by surgery, causing no serious harm |
Benign tumors |
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Are difficult to treat and may become life threatening |
Malignant tumors |
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All cancer cells in primary and secondary tumors are |
Clonal |
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Shows reciprocal translocations between chromosome 8 and chromosomes 2, 14, or 22 |
Burkitt’s lymphoma |
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Occurs early in development and occurs at random |
X-chromosome inactivation |
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Tumor cells that proliferate give rise to cancer stem cells that have the capacity for self-renewal |
Cancer stem cell hypothesis |
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The high level of genomic instability in cancer cells is known as |
Mutator phenotype. |
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A number of inherited cancers are caused by |
Defects in genes that control DNA repair |
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The study of factors that affect gene expression but do not alter the nucleotide sequence of the DNA |
Epigenetics |
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The process of transmitting growth signals from external environments to the nucleus is called |
Signal transduction |
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Checkpoints monitor cell size and determine whether DNA has been damaged |
G1/Scheckpoint |
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Is where physiological conditions are checked (once G1/S are passed) prior to mitosis |
G2/M checkpoint |
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The formation of the spindle-fiber system and the attachment of spindle fibers to the kinetochores associated with the centromeres are monitored |
Mcheckpoint |
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Genes whose products promote cell growth and division |
Proto-oncogenes |
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Is a mutated or aberrantly expressed proto-oncogene, a gain-of-function alteration |
Oncogene |
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Are mutated in more than 30 percent of human tumors and encode signal transduction molecules that are associated with the cell membrane and regulate cell growth and division |
RAS genes |
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Mutated in more than 50 percent of all cancers |
p53 tumor-suppressor gene |
