Download - Molecular Basis of Cancer
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CANCER PATHOGENESISFacilitator: Bethy S. Hernowo,
dr., SpPA (K), PhD. Akhmad Mustafa, dr. (Urology)
Dedi Farokka, dr. (General Surgery)Farry, dr. (Orthopaedic and
Traumatology)Erwin Wijatmiko, dr. (Neurosurgery)
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• Neoplasia: New growth• Neoplasma: abnormal mass of tissue the
growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after the cessation of the stimuli which evoked the change.
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• Neoplasm BenignMalignant
Benign microscopic and gross characteristics are considered to be relatively innocent, implying that it will remain localized, it cannot spread to other sites, and is amenable to local surgical removal
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GENE DEFECTS IN TUMOR DEVELOPMENT
• Balanced translocations• Deletions• Amplifications• Lost/Gain a whole chromosome
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Translocations
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Deletions
• Deletions: loss of parts of a chromosome• Can results in inactivation of tumor supressor
gene• Most common seen in nonhematopoietic solid
tumors
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Gene Amplification
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NONLETHAL GENETIC DAMAGE
Four classes of normal regulatory genes:• growth-promoting proto-oncogenes• growth-inhibiting tumor suppressor genes• genes that regulate programmed cell death
(i.e., apoptosis)• genes involved in DNA repair
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Proto-Oncogenes
• Proto-oncogenes: normal cellular genes whose products promote cell proliferation
• Oncogenes: mutant versions of proto-oncogenes that function autonomously without a requirement for normal growth-promoting signals
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Tumor Supressor Gene
• Tumor suppressor genes encode proteins that inhibit cellular proliferation by regulating the cell cycle
• Both copies of the gene must be lost for tumor development, leading to loss of heterozygosity at the gene locus
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Genes that Regulate Programmed Cell Death
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Genes Involved in DNA Repair
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