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16 Cards in this Set
- Front
- Back
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What is a characteristic of malignant tumors
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metastatic
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Gain-of-function mutations in which gene typifies colorectal carcinomas
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K-ras
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To promote metastasis, the basal lamina is digested by
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plasmin
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What promotes angiogenesis?
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VEGF
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In females, all the cells in a tumor have the same inactive X chromosome. The reason for this is that
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all of the cells in a tumor are derived from a single progenitor cell.
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Name a couple of tumor-suppressor genes
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APC
RB |
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an example of a proto-oncogene is
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myc
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Germ-line mutations in which of the following genes has (have) been implicated in hereditary cancers?
a. APC b. BRCA1 c. RB d. a and c e. all of the above |
APC
BRCA1 RB |
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Hereditary cancers typically possess loss-of-heterozygosity in
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tumor-suppressor genes
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Name the six fundamental properties of malignant tumors. Which of these properties are amenable to study in a cell culture model of cancer?
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Malignant tumors exhibit (1) self-sufficiency in growth signals; (2) insensitivity to antigrowth signals; (3) evasion of apoptosis; (4) limitless replicative potential; (5) sustained angiogenesis; and (6) tissue invasion and metastasis. The first four properties are amenable to study in a cell-culture model because they are autonomous properties of cancer cells. In contrast, sustained angiogenesis and tissue invasion and metastasis involve the interaction of cancer cells with other tissues and may be better studied in vivo.
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Leukemias are different from most other classes of cancers. Which of the fundamental properties of cancer cells are likely to be lacking in leukemias and why?
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Leukemias are derived from blood cells or their precursors and proliferate as individual cells in the blood rather than as solid tumors. Because they already exist in the circulation, leukemias do not need to promote angiogenesis and likewise do not need to escape their tissue of origin and metastasize although some leukemias may do so.
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What is the multi-hit model of cancer? What data support this model?
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The multi-hit model proposes that multiple, successive mutations are required to produce a cancer cell. Many lines of evidence support this model, including the fact that tumor cells are clonally derived and possess the same genetic alterations. The increased incidence of cancer with age also supports the model. Finally, the cooperative effect of oncogenes in producing tumors in mice supports the model.
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Nearly all malignant tumors possess a loss-of-function mutation in one or more cell-cycle checkpoints. However, a loss of checkpoints is not a requisite characteristic of cancer cells per se. Explain this paradox.
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Because multiple mutations are required to produce the cancer phenotype, a loss of checkpoint function will greatly increase the likelihood that cancer-promoting mutations will develop. It is possible that these mutations could occur by chance, even with all checkpoint pathways intact. However, cancer would be a much less frequent event than it is if mutations in checkpoint genes never occurred.
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What are the differences and similarities between the transforming genes of retroviruses and those of DNA tumor viruses?
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The oncoproteins encoded by transducing retroviruses are derived from normal cell proteins, whereas those encoded by DNA viruses are required for viral replication. Indeed, the presence of oncogenes in transducing retroviruses renders these viruses defective (unable to replicate). Both types of viruses express oncoproteins from integrated genomes.
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Describe gain-of-function and loss-of-function mutations with respect to cancer.
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A gain-of-function mutation converts a proto-oncogene into an oncogene. Such mutations are dominant. A loss-of-function mutation occurs in tumor-suppressor genes, abrogating their function in preventing cancer. Such mutations are recessive and require alteration of both alleles.
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How can DNA microarrays be used to detect gene amplifications in cancer cells?
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Using genomic DNA from cancer cells as probes and DNA microarrays containing fragments of normal genomic DNA, it is possible to tell the difference between amplified DNA and normal DNA. Amplified DNA genes give stronger signals than control spots.
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