Gcd 3022 1st edition Lecture 37Outline of Last Lecture I. Genetic basis of cancera. Characteristicsb. StatisticsII. Viruses that cause cancera. Efficiency of causing cancerb. Acutely transforming virusesc. Rous sarcoma virusIII. Oncogenesa. Development b. Patterns of expressionc. Conversion of proto-oncogenesi. Missense mutationii. Gene amplificationiii. Chromosomal locationsiv. Viral integrationIV. Tumor-suppressor genesa. Inactivation of tumor-suppressor genesi. Mutation in gene itselfii. DNA methylationiii. Aneuploidyb. Genome maintenancei. Checkpoint proteinsii. Cyclins and cyclin-dependent kinasesiii. DNA repair enzymesc. p53 genei. Functionsii. Apoptosisd. Retinoblastomai. Two typesii. Two-hit modelV. Multiple genetic changesa. Development pattern of cancersb. Colorectal cancer studyc. Genetic changes leading to cancerVI. Inherited forms of cancersThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.a. Predisposition for developing cancerb. Loss of heterozygosityOutline of Current LectureI. Locus heterogeneityII. Formation of cancera. Proto-oncogenesb. Transformationc. Causes of cancerd. Accumulation of mutationse. Missense mutationf. RetinoblastomaIII. Stages of cancer progression IV. Patterns of inheritancea. Inherited cancersb. Haploinsufficiencyc. ConcordanceCurrent LectureI. Locus heterogeneity: a situation where people with the same phenotype have different genotypes. II. Formation of cancera. Proto-oncogenes: not usually involved in inherited forms of cancer because mutations that occur in these genes are gain-of-function mutations which would be exhibited in thedevelopment of the embryo and could result in fatality. Most inherited forms of cancer typically contain mutations in tumor-suppressor genes, not proto-oncogenes. b. Transformation: can refer to the process of introducing DNA into prokaryotic cells by chemical or physical means or the process that results in conversion of a normal cell intoa cancer cell. c. Causes of cancer: mutation to tumor-suppressor gene (loss of function mutation), reduced function of tumor-suppressor gene, point mutations, increase in the copy number of the proto-oncogene, or a change in the relationship between a coding region and regulatory elements of the proto-oncogene.d. Accumulation of mutations: cancer cells are more likely than normal cells to accumulate mutations over time because they are allowed to divide despite potential errors in DNA synthesis. e. Missense mutation: the missense mutation in ras that contributes to cancer decreases the GTPase activity of ras so that it is always in the “on” position, leading to constitutive downstream signaling. f. Retinoblastoma: a tumor in the retina, can be inherited and form early in life or develop spontaneously later in life. Both types of retinoblastoma require two mutations to occurto the same cell (“two-hit model”). People with the inherited disease already have one mutation, which is why they develop the condition earlier in life. III. Stages of cancer progression: begins a normal cell that acquires at least one mutation that converts it to a tumor cell. This cell divides to form a benign growth. Additional genetic changes may occur to these cells that result in an invasive tumor called a malignant tumor. The cells can then metastasize to other parts of the body. Cancer is considered clonal because the growth originates from one cell.IV. Patterns of inheritancea. Inherited cancers: usually occur from the mutation of a tumor-suppressor gene (loss-of-function) mutation and follow the “two-hit model”. These tumor-suppressor genes are responsible for allowing cell division under appropriate conditions. b. Haploinsufficiency: the phenomenon where half of the normal amount of gene product is not sufficient to produce a wild-type phenotype. This type of mutation can play a role in how tumor suppressor genes contribute to cancer because it is a loss-of-function mutation. c. Concordance: the degree to which identical twins and fraternal twins share the same trait. A high rate of concordance would be indicated by the finding that identical twins share the same traits and fraternal twins are no more similar than other siblings. If fraternal and identical twins show the same degree of concordance it is more likely that the trait is not determined solely by
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