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1. How do cells become transformed into a clonal population of cancer cells?

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a. Cancer cells divide rapidly and continuously, resulting in tumors that crowd out normal cells i. Somatic cells, never gonna be sperms or eggs (fyi) b. Mutations in certain genes of it

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2. How do defects in cell cycle control lead to cancer?

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a. Mutations in the cell check points. b. Various checkpoints serve as monitors as the status of DNA repair, replication, and spindle apparatus formation, etc

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How do mutations in tumor suppressor genes and proto-oncogenes contribute to cancer?

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a. Tumor Suppressor Genes - b. Mutations in these genes lose the ability to inhibit proliferation. i. Proteins involved in inhibiting progression of the cell cycle (e.g. RB). ii. Proteins involved in the repair of DNA damage (e.g. p53). iii. Proteins that promote apoptosis (e.g. p53). c. Proto-oncogenes i. Dominant oncogenes -- Mutant proto-oncogenes that promote proliferation without the signal

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Tumor Suppressor Genes -

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...

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Mutations in these genes lose the ability to inhibit proliferation.

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i. Proteins involved in inhibiting progression of the cell cycle (e.g. RB). ii. Proteins involved in the repair of DNA damage (e.g. p53). iii. Proteins that promote apoptosis (e.g. p53).

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Proto-oncogenes

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i. Dominant oncogenes -- Mutant proto-oncogenes that promote proliferation without the signal

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Understand the G1

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S cell cycle control checkpoint. a. G1—S Checkpoint i. Deals with CDK, if the RB and the E3F are phosphorylated, it'll make the RB no longer bound to E2F. E2F will become a transcription factor required for DNA replication.

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Xerogerma Pigmentsum

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i. Mutation in a general exicision repair gene; prone to UV-induced mutations

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Chronic Myeloid Leukemia (CMS)

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i. Bone marrow cell cancer, between chromosome 22 and 9 1. Result in Philadelphia chromosome

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Burkitt Lymphoma

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i. B lymphocyte cancer 1. Myc transcribed at all times (transcription

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Helicobacterpylori (bacteria

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i. Ulcers and stomach cancer

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Human Papilloma Virus (HPV)

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i. Causes cervical cancer

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Hepatitis B and C viruses

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Understand what the Hardy-Weinberg equilibrium is and the forces that disturb this equilibrium.

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b. Assumes that the population is: i. large (i.e. no genetic drift) ii. randomly mating iii. no new mutation iv. no migration v. no natural selection

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Genetic Drift

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a. Sampling error, founder effect, genetic bottleneck

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Mutation

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a. Germinal Mutation i. Raw source of evolution

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Migration

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a. Movement of alleles into and out of a population

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Mating

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a. Inbreeding and positive assortative mating lead to decreased heterozygosity. b. Outbreeding and negative assortative mating lead to increased heterozygosity.

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Inbreeding and positive assortative mating lead

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decreased heterozygosity

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Outbreeding and negative assortative mating lead to

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increased heterozygosity

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How are new genes acquired?

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1. Mating and/or migration

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Learn about hominid evolution

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...

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Understand the evolutionary relationships of the concestors that I discussed during the evolutionary pilgrimage lecture.

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...

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Ch15 Q 2. * What is the difference between a map-based approach to sequencing a whole genome and a whole-genome shotgun approach?

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Answer: The map-based approach first assembles large clones into contigs on the basis of genetic and physical maps and then selects clones for sequencing. The whole-genome shotgun approach breaks the genome into short sequences—typically, from 600 to 700 bp—and then, with the use of powerful computers, assembles them into contigs on the basis of sequence overlap.

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Ch15 Q3. What is a single-nucleotide polymorphism (SNP)? How are SNPs used in genomic studies?

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...

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Ch15 Q 7. What is a microarray? How can it be used to obtain information about gene function?

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...

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Ch 16 Q1. In some cancer cells, a specific gene has become duplicated many times. Is this gene likely to be an oncogene or a tumor-suppressor gene? Explain your reasoning.

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The gene is likely to be an oncogene. Oncogenes stimulate cell proliferation and act in a dominant manner. Therefore, extra copies of an oncogene will result in cell proliferation and cancer. Tumor-suppressor genes, on the other hand, suppress cell proliferation and act in a recessive manner; a single copy of a tumor-suppressor gene is sufficient to prevent cell proliferation. Therefore, extra copies of the tumor-suppressor gene will not lead to cancer.

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Ch16 Q 1 * What types of evidence indicate that cancer arises from genetic changes?

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Many types of cancer are associated with exposure to radiation and other environmental mutagens. Some types of cancer tend to run in families, and a few cancers are linked to chromosomal abnormalities. Finally, the discovery of oncogenes and specific mutations that cause proto-oncogenes to become oncogenes or that inactivate tumor-suppressor genes proved that cancer has a genetic basis.

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Ch16 Q 5. * What is the difference between an oncogene and a tumor-suppressor gene? Give some examples of the functions of proto-oncogenes and tumor suppressers in normal cells.

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Oncogenes stimulate cell division, whereas tumor-suppressor genes put the brakes on cell growth. Proto-oncogenes are normal cellular genes that function in cell growth and in the regulation of the cell cycle. Some examples are erbA, erbB, myc, src, and ras. Tumor-suppressor genes inhibit cell-cycle progression; examples are RB and p53, which encode transcription factors.

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Ch16 Q 6. * How do cyclins and CDKs differ? How do they interact in controlling the cell cycle?

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The CDKs, or cyclin-dependent kinases, have enzymatic activity and phosphorylate multiple substrate molecules when activated by binding to the appropriate cyclin. Cyclins are regulators of CDKs and have no enzymatic activity of their own. Each cyclin molecule binds to a single CDK molecule. Whereas CDK levels remain relatively stable, cyclin levels oscillate in the course of the cell cycle.

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Ch 16 Q9. * What role do telomeres and telomerase play in cancer progression?

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DNA polymerases are unable to replicate the ends of linear DNA molecules. Therefore, the ends of eukaryotic chromosomes shorten with every round of DNA replication, unless telomerase uses its RNA component to add back telomeric DNA sequences, which it does in reproductive cells. Normally, somatic cells do not express telomerase; their telomeres progressively shorten with each cell division until vital genes are lost and the cells undergo apoptosis. Transformed cells (cancerous cells) induce the expression of the telomerase gene, thus leading to cell proliferation.

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ch 16 Q 10. * Explain how chromosome deletions, inversions, and translocations can cause cancer.

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Deletions can cause the loss of one or more tumor-suppressor genes. Inversions and translocations can inactivate tumor-suppressor genes if the chromosomal breakpoints are within tumor-suppressor genes. Alternatively, a translocation can place a proto-oncogene in a new location, where it is activated by different regulatory sequences, causing the overexpression or unregulated expression of the proto-oncogene. Finally, inversions and translocations can also bring parts of two different genes together, causing the synthesis of a novel protein that is oncogenic.

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ch 16 Q13. * How do viruses contribute to cancer?

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Retroviruses have strong promoters. After its integration into a host genome, a retrovirus promoter can drive the overexpression of a cellular proto-oncogene. Alternatively, the integration of a retrovirus can inactivate a tumor-suppressor gene. A few retroviruses carry oncogenes that are altered versions of host proto-oncogenes. Other viruses, such as the human papilloma virus, produce proteins that affect the cell cycle.

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