BIOL 1140 1st Edition Lecture 15Outline of Last LectureI. History of our cellsII. All life starts with a fertilized eggIII. Take home message of the dayIV. TissuesV. Epithelial TissuesVI. The basement membraneVII. Connective TissueVIII. Fibrous Connective TissueIX. Specialized Connective Tissue, special function X. Muscle TissueXI. Nervous TissueXII. Organs and organ systemsXIII. Body cavitiesXIV. Tissue membranesXV. The skin as an organ system XVI. Epidermis and dermisOutline of Current LectureI. Accessory structures of dermisII. Multicellular organisms and homeostasisIII. Negative FeedbackIV. Cancer in the cell cycle V. Tumor suppressor genesVI. OncogenesVII. Normal cellsVIII. Tumors IX. Cancer cells lose control X. Cancer can affect DNA repair systemsXI. BRCA1 and BRCA2XII. Cancer is heterogeneousXIII. SummaryXIV. AccomplishmentsCurrent LectureThese 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.I. Accessory Structures of Dermisa. Hairi. Shafii. Follicleb. Smooth musclei. Attached to hair follicle, raises hair to upright positionc. Oil glands/ sebaceous glandsi. Secretion moistens and sofens skinII. Multicellular organisms must maintain homeostasisa. Maintenance of relative constancy of the conditions of the internal environmentb. Negative feedback control system: deviations from normal are detected and counteractedc. Components of a negative feedback control systemi. Controlled variableii. Sensoriii. Control centeriv. Effector III. Negative Feedback helps maintain core body temperaturea. Controlled variable: body tempb. Sensors: temp sensors in skin and internal organsc. Control center: hypothalamus (CNS)d. Effectors:i. Blood vesselsii. Sweat glandsiii. Skeletal musclesiv. Skin hair (somewhat)IV. Cancer involves changes in the cell cyclea. Study of two classes of genes has established a relationship between cancer, regulation of cell growth and division, and the cell cyclei. Tumor suppressor genes decrease cell divisionii. Oncogenes increase cell divisionV. Tumor Suppressor Genesa. Genes encoding proteins that suppress cell division and regulate the cell cycleb. Deletion or inactivation of these products cause cells to divide continuouslyVI. Oncogenesa. Proto-oncogenesi. Genes that initiate or maintain cell divisionii. May become cancer genes (oncogenes) by mutationb. Oncogenesi. Genes that induce or continue uncontrolled cell proliferationVII. Normal Cellsa. Have regulatory mechanisms that maintain an appropriate rate of cell divisioni. Internal clockii. Hormonesiii. Inhibitory signals from nearby cellsb. Remain (mostly) in one location throughout their lifespanVIII. Tumors - benign or cancerousa. Hyperplasiai. Substantial increase in the rate of cell divisionb. Tumori. Also known as neoplasmii. Discrete mass of cells resulting from hyperplasiac. Benign tumorsi. Noncancerousii. Remain in one locationiii. Single, well-defined massiv. May be surrounded by connective tissueIX. Cancerous cells lose control over cell cycle/functionsa. Dysplasiai. Abnormal change in cell structureii. Considered a precancerous stateb. Cancerous tumorsi. Abnormal cell structureii. Loss of regulation of cell cyclec. Tumor suppressors and/or proto-oncogenes are mutatedd. Malignant tumori. Tumor invades normal tissue and compromises organ functionii. Tumor may undergo metastasis1. Spread of the cancer to another organ or body region2. Secondary, malignant tumors at other locations may developX. Cancer can affect DNA repair systemsa. Many basic properties of cancer result from the inability of cancer cells to repair damage to DNAi. High rates of mutation, chromosomal abnormalities, and genomic instabilityb. DNA repair genes are now recognized as a class of cancer-related genes along with tumor suppressor genes and proto-oncogenesXI. BRCA1 and BRCA2 are DNA repair genesa. BRCAA1 protein, found only in the nucleus, is activated when DNA Is damagedi. Stops DNA replicationii. Helps to identify DNA damage and initiate repairb. Mutant forms are unable to repair DNAi. Mutations accumulate; cells become cancerousii. Remember: 2 billion nucleotides are copied per cell division at a rate of 5-10 per secondXII. Cancer is Heterogeneousa. Not all cancers are caused by the same genetic or environmental factorsb. BRCA1 and BRCA2 mutations both cause cancerc. 1-200 women are hetero for the BRCA1 allele and 82% of these women will develop breast cancer (due to a 2nd BRCA1 mutation)XIII. Summary of diffusible signalsa. Single diffusible factors can induce entire organsb. Diffusible factors can regulate proliferation and differentiation of target cellsc. Diffusible factors typically interact with others to form a positive or negative feedback loopXIV. Accomplishmentsa. Gurdon: cloned gut nucleus into from oocyte, beginning of cloning in 1962b. Yamanaka: generated with the 4 Yamanaka factors iPS cells (induced pluripotent stem cells)c. iPS cells are the fastest growing research in stem cell