Biology And Biomedical Sciences BIOL 2960 Lecture Notes - Lecture 41: Pie Chart, Tumor Suppressor Gene, Operational Taxonomic Unit
14 Aug 2018
School
Department
Bio2960 Spring 2018
Study Guide 15: Cancer (Lectures 38-39) and Microbiome (Lectures 40-41)
Foundational Vocabulary:
At the end of this unit, you should be able to define and/or use the following terms and concepts:
o Cancer:
! Cancer genetics: carcinogenesis &
mutagenesis
! Tumors are clonal, “transformed” cells
(Note: this is different than
“transformed” cells in cloning)
! Cancer mutations:
• Oncogene: proto-oncogene, cell
cycle “accelerator”, overactivity,
types of mutations
• Tumor suppressor genes: cell
cycle “brake”, underactivity, genetic
mutation, epigenetic inactivation
! Hallmarks of cancer: no apoptosis
(programmed cell death), blood supply,
telomere maintenance, proliferative
signaling (ex. growth factor), evading
growth suppressors, metastasis
! Four Mutations that Transform Cultured
Cells:
1. Ras: small G-protein, GTPase activity,
growth factor signaling, kinase cascade
2. Retinoblastoma (Rb): G1 cyclin/cdk
(cyclin-dependent kinase) complex
target, transcriptional repressor,
inactivation by phosphorylation
3. p53: “guardian of the genome,” DNA
damage checkpoint, activates p21
(cyclin/Cdk inhibitor) transcription
4. Telomerase: prevents telomere
shortening
! Results of sequencing projects: classifying
tumors by shared mutations (rather than
organ of origin), DNA repair genes
(Brca1/2), “driver” vs. “passenger”
mutations
o Microbiome:
! Methods used to identify microbes in a
microbial community: microscopy;
culturing microbes; culture-independent
methods, metagenomics:
! Targeted metagenomics (similar to 2960
lab): PCR, 16S rRNA, conserved and
variable regions, universal primers,
operational taxonomic unit (OTU)
! Shotgun metagenomics: sequencing
whole genomes of all microbes within a
community
! Microbial communities in humans: skin,
mouth, nose, parts of the gastrointestinal
(GI) tract (i.e. stomach, small intestine,
colon/”gut”/large intestine), mutualistic
! Composition of microbe community in
human “gut”: Bacteriodetes, Firmicutes
! Methods used to study the roles of
microbiomes: Germ-free (gnotobiotic)
mouse model, microbial transplantation
When you’re done studying for this unit, you should be able to:
26. Appreciate that uncontrolled cell division is a pre-requisite for cancer.
26.1. Explain why genes involved in cancer can categorized as accelerators and brakes of the cell
cycle.
26.1.1. Know which category (accelerator or brakes) describe proto-oncogenes and tumor
suppressor genes.
26.1.2. When given details or observations relating to cell division, categorize a new gene as a
tumor suppressor gene or proto-oncogene.
26.2. In order for proto-oncogenes and tumor suppressor genes to contribute to cancer, contrast the
(1) the associated types of changes that occur (point mutation, amplification, epigenetic
silencing etc.), (2) the result of those changes to protein activity (overactivity or underactivity),
and (3) the number of copies of the gene that must be mutated (i.e. both copies or just one).
26.3. Outline some of the ways that oncogenes and tumor suppressor genes have been discovered.
26.4. Explain why two breast cancer tumors might respond to the same treatment differently.
26.5. Know the four genes, which when mutated are sufficient to cause cancer (i.e. Ras, Rb, p53,
and telomerase). For each gene,
26.5.1. Predict whether activity would be increased or decreased in cancer
Document Summary
Study guide 15: cancer (lectures 38-39) and microbiome (lectures 40-41) At the end of this unit, you should be able to define and/or use the following terms and concepts: cancer, telomerase: prevents telomere. Tumors are clonal, transformed cells (note: this is different than. Cancer mutations: oncogene: proto-oncogene, cell cycle accelerator , overactivity, types of mutations, tumor suppressor genes: cell cycle brake , underactivity, genetic mutation, epigenetic inactivation. Hallmarks of cancer: no apoptosis (programmed cell death), blood supply, telomere maintenance, proliferative signaling (ex. growth factor), evading growth suppressors, metastasis. Cells: ras: small g-protein, gtpase activity, growth factor signaling, kinase cascade, retinoblastoma (rb): g1 cyclin/cdk (cyclin-dependent kinase) complex target, transcriptional repressor, inactivation by phosphorylation, p53: guardian of the genome, dna damage checkpoint, activates p21 (cyclin/cdk inhibitor) transcription. Results of sequencing projects: classifying tumors by shared mutations (rather than organ of origin), dna repair genes (brca1/2), driver vs. passenger mutations: microbiome:
