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Lecture 18

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Department
Biology
Course
Biology 1002B
Professor
Denis Maxwell
Semester
Winter

Description
Lecture 18: Cancer Not winning the war against cancer as proven with death rates  In Canada, men are at higher risk to get cancer than women o 40% for women will develop cancer o 45% for men will develop cancer  28% of men can be expected to die from cancer  Top 4 o Prostate cancer o Breast cancer o Lung cancer o Colorectal cancer  Cancer is the leading cause of premature death in Canada o 25% of Canadian can expect to die of cancer o Rates among youth are rising Heritability estimates from twin studies  Fairly low – more environmental factors Embryogenesis rapidly dividing cells  Cyclin/CDK(inase) complexes regulate cycling o Diagram in textbook o Biochemical control o CDK – cyclic dependent kinase o Kinase – add phosphate groups (phosphorylate – turn on or off, posttranslational regulation) o CDK only activate when bind to cyclin o CDK releases G1 checkpoint o Cyclin degraded and made again in next cell cycle (cyclin – cyclically made) o CDK there all the time but not always activate o Repeat for next checkpoint  Different cyclins and different CDK at each checkpoint Expression of proto-oncogenes promotes cell cycling: e.g. EGFR  Unactivated oncogenes – proto-oncogenes before oncogenes  There is no such thing as a cancer gene o Oncogenes are not cancer genes o It is an embryoic gene o Need these genes to function as an embryo  EGFR – epidermal growth factor o Protein that stimulates growth o Receptor that recognizes outside of cell o Gene product will stimulate cell division when you are an embryo o Proto-oncogenes when deregulated show uncontrolled growth  EGF Pathways o Genes that promote cell cycling turn on when get the signal that EGF is present o DNA binding proteins, intermediates o All of these can be oncogenes if deregulated Expression of tumor suppressor genes slows cell cycling e.g. p53  “TP53” is a master tumour suppressor genes, coding a transcription factor whose activity can result in o Increased DNA repair o Cell cycle arrest by blocking cyclin/CDK o Apoptosis  TP53 – stops cells from passing G1 checkpoint if there is too much DNA damage o Tumor suppressor gene o If mutated or missing – uncontrolled growth  Shut down of cell division o Didn’t evolve to supress tumours o Have natural functions during embryology Sporadic cancer requires new loss of function mutations in both alleles  BRCA/BRCA1  If born with two normal alleles from both parents  Lifetime may suffer mutation  Sporatic breast cancer when both defective alleles o But slow process  Usually inherit a defect allele and only one good allele o Predisposition to breast cancer o Good allele higher chance to be mutated o Reasons why cancer seems to be more common in families due to inheriting a tumour supressing gene Encodgenes and tumor suppressor gene and oncomirs are stupid names Inappropriate expression of miRNA can promote cycling e.g. oncomirs  miRNA regulate cell cycling  Tumours may be expressing a different collection of RNA  miRNA expression profiles classify human cancers  Particular distribution of miRNA is very diagnostic for particular kinds of tumours  Each of the tumour lanes has a characteristic particular banding pattern Cancer is deregulation  Uncontrolled growth can arise from upsetting the balance between the activity of gene products that promote cell cycling vs those products that suppress cell cycling  Possible ways to activate oncogenes, knock out tumour suppressor genes (make list) Cancer is Progressive  Death rates are high because there is a lot of old people in this area  Accumulative to make it into a high risk  Rare for a single mutation to give rise to a tumour  Single mutation would predispose that cell to suffer from another mutation Cancer may begin as alterations to gene expression in stem cells…  All tissues have stem cells  Stem cells is at least pleuripotent o Its descendant can differentiate into a wide range of tissues o One of their daughter cells becomes a progenitor and specialize o Other daughter stays as stem cell o Asymmetrical fate of daughter cells  Differentiated, progenitor and stem cells can go back to be a stem cell that is out of control o Out of control stem cell can be a cancer cell  In many tumours, the bad cells are stem cells o Can’t kill a tumour unless you kill the stem cell Some tumor cell nuclei can be re-programmed  Mouse embryos cloned from brain tumors with no tumor supressor  Brain tumor cell  enucleated egg cell  Take nucleus out of cell and put it into an egg cell that has its nucleus removed o Baby gets born and that is pretty fine  If cancer is caused by mutated gene, how can you make a baby then o It can drive perfectly normal development of a mouse  Maybe cancer isn’t so genetically control o Maybe it is epigenetically control o Change expression of the nucleus and make it behave normally  Maybe the initial stages of cancer is epigenetically o Suppressor genes turned off by methylation first o Maybe bullying increases risk of cancer o Maybe anything that affects epigenetic changes that will cause a mutation and lead to risk of cancer Is cancer contagious?  Human papillomavirus  DNA virus  Many different strains cause increased growth (warts) in different tissues in both men and women  Some strains are oncogenic; particularly strong association of strains 16 and 18  Total HPV prevalence, 27% women 1914 to 59)  Total incidence of high risk type 16 and 18 are 2.3%  New HPV infections over the course of first year at university vs “risk factors” o Number of new partners o Frequency of condom use by partner o Number of previous partners of sex partners How might HPV cause cancer? Lecture 18: Cancer 1. Four most common types of cancer in Canada  Prostate cancer  Breast cancer  Lung cancer  Colorectal cancer 2. Likely factors contributing to cancer incidence in Canada  majority of the population is older (more likely to get cancer) 3. Role of cyclin/CDK complexes in cell cycle regulation  Biochemical control  CDK – cyclic dependent kinase o Kinase adds phosphate groups (phosphorylate) to turn on/off gene (posttranslational regulation) o Only active when bind to cyclin (production cycles with cell cycle) o Releases G1 checkpoint (before cells replicate DNA) o Degraded and made again in next cycle
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