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SS: Cancer Test 2 Study Guide

by: Elle Humes

SS: Cancer Test 2 Study Guide

Elle Humes
Virginia Tech

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About this Document

An organized summary of foundational knowledge about cells, the hallmarks of cancer and some tricks for remembering facts.
SS: Cancer
Dr. Walker
Study Guide
cancer, Hallmarks, Cell, division
50 ?




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This 4 page Study Guide was uploaded by Elle Humes on Sunday October 9, 2016. The Study Guide belongs to at Virginia Polytechnic Institute and State University taught by Dr. Walker in Fall 2016. Since its upload, it has received 72 views. For similar materials see SS: Cancer in BIOL at Virginia Polytechnic Institute and State University.


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Date Created: 10/09/16
Cancer Test 2 Study Guide Foundational Knowledge  Normal, Somatic Cells  Depend on contact inhibition = must be attached to a surface to grow and stop growing  when a monolayer of cells is formed  Exhibit controlled growth, and are mortal (cells die after hitting a plateau of growth  called senescence) RSV   RSV is a cancer promoting virus, discovered originally in one chicken  Gave researchers a way to manipulate and study cancer  RSV is a mutated form of AVL o It accidentally picked up a cellular gene, c­src o Since this gene isn’t important to the virus it accumulated mutations o These mutations promoted sarcoma in chickens o The cancer promoting gene is called v­src  Other Cancer Research  Invention of tissue culture greatly advanced cancer research (less need for live animals)  Oncogenes o Research question: can mutations create an Oncogene in cells in the absence of  viruses? 1. Treat cells with alkylation agent (promote mutations)  2. Isolate DNA 3. Add DNA to normal cells in culture 4. Select for transformed cells, if they occur 5. Inject transformed cells into animal and observe tumor formation 6. Identify the mutant gene that was injected  o Yes. There are some genes that acquire mutations that promote cancer. This is a  Proto­oncogene  Oncogene change This test mostly focuses on the “Hallmarks of Cancer” which tell us that cancer cells…  Reproduce without Growth Factors  Proto­oncogene  Oncogene can occur in cells if one of these four processes happens o Gene Amplification (more copies of the gene = more protein)  Even though this is normal protein, it causes problems by being  overactive o Chromosome Translocation (changes regulatory region of gene) o Point Mutation (changes in amino acids  change protein folding  change  protein function) o Chromosome Translocation (mixes coding regions to create a new protein gene  product) o Red colored processes are Gene Amplification Events while Green colored  processes change Protein Structure  Gene Amplification Events leads to too much protein  Protein Structure Events lead to different proteins  The oncogene “tells” the cell to divide constantly, regardless of signals from the  surrounding tissue  Examples o N­myc cancer is caused by gene amplification, where the prognosis of the patient correlates with the number of copies of the amplified gene o Ras oncogene is caused by a point mutation, and is mutated in 30% of human  cancers o C­src is a proto­oncogene, V­src is an oncogene  Gain of Function mutation, normally turns “on” growth factor pathway, now pathway  always on Ignore growth inhibitory factors  Tumor suppressor info  Retinoblastoma (Rb) Tumor Suppressor is the best studied gene o Retinoblastomas (cancer) can occur in one eye or both eyes o Bilateral is hereditary and occurs early in life o Unilateral is sporadic and requires “2 hits” or two mutations to develop  o We can see that both copies of Rb must be inactivated to promote cancer because  1/3 of bilateral Rb cases have cancer again later in life  Linear relationship of age and Rb cancer shows that bilateral sufferers  probably inherit one bad copy of Rb and only one mutation happened  Unilateral incidence increases non­linearly, showing two mutations  Tumor Suppressor are inactivated due to one of these processes o Deletion o Point Mutation o Insertions or Translocations o Promoter methylation (adding a ­CH group) 3  o The blue colored are mutations, while the orange is epigenetic control o Epigenetic markers are maintained over generations, passed down  Loss of Function mutation, normally turns “off” growth factor pathway to prevent  reproduction, since it can no longer work the growth factor pathway has no “brakes”  Survive with major DNA damage  Differentiation and Reproduction are “opposite” outcomes o Differentiation is triggered when a cell leaves the cell cycle  o Differentiating cells show  no growth factors  activated Rb  activated  checkpoint inhibitors   p53  o More of this protein was found in cells with DNA damage (because DNA damage activates this protein through phosphorylation)  o This protein is often mutated in cancerous cells o p53 is activated by DNA damage, and it either halts the cell cycle, or triggers  apoptosis based on the level of damage o If the protein is mutated, then it may not be able to do its job, so the cell cycle  loses a “quality control” step  cells are more likely to pass on mutations and  survive when they should have died   Telomeres and Telomerase are very important here o Telomerase extends telomeres  o When telomeres become too short, apoptosis is triggered o Telomerase gene is a proto­oncogene because it contributes to cells living longer.  The removal of telomerase decreases the risk of cancer Have no limits on reproduction  Thrive in new environments – hypoxic environments, etc.   NO SENESCENCE  Make ATP by Glycolysis  Cancer cells often exhibit the Warburg Effect o Stop using oxidative phosphorylation and start using glycolysis as the primary  ATP production o Cells uptake much more glucose (there must be a mutation that allows them to do  this, such as a cell that expresses more glucose receptors)   Leading Idea – allows the cell to divert carbon to other pathways o Allows cells to get ATP and create more organic molecules (which they must  have to sustain their fast growth) Recruit Blood Vessels  “Angiogenesis” o Angio – blood o Genesis – origin/formation   Tumors can survive hypoxic environments, but not anoxic environments  all eukaryotic  cells need some level of oxygen to survive   As the tumor grows, the middle becomes increasingly hypoxic, so the tumor must recruit  blood vessels to bring in more O2 and to take out waste products Metastasize  There is a difference between invasiveness and metastasis o Invasiveness – ability of cells to leave the primary tumor; become “unstuck,”  often see and EMT to allow this hallmark  o Metastasis – ability of cells to create a colony at a new location  Micrometastases  ~16 cells or less, very small  Macrometastases  New tumors   Carcinomas activate the wound healing process o Release signals that: recruit fibroblasts and macrophages, change stroma  behavior, trigger angiogenesis o This also triggers movement of epithelial cells, which leads to invasiveness   Cancer cells release enzymes, which breaks down the extracellular matrix, allows for  invasion  Intravasation – Cancer cells literally “squeeze” between the blood vessel epithelial cells  to enter the blood stream o These cells are supposed to be epithelial cells, so this isn’t normal, but… o Behaving like mesenchymal cells allows them to crawl around the body o EMT is essential for invasiveness   Most invasive cells don’t become macrometastases because they cannot survive/thrive in  the new “hostile” environment. The traveling cells have to be able to… o Use anchorage­independent growth (divide despite being free floating) o Survive without the stroma o Survive physical damage in the blood stream Avoid the Immune System  Cannot include, because it will be covered on Monday 10/10/16 Don’t get tripped up on these facts  Only one copy of a proto­oncogene has to be mutated to an oncogene to promote cancer,  but two (both) copies of tumor suppressor gene must be inactivated to promote cancer  (which makes tumor suppressor mutations recessive) o One Oncogene  o Two Tumor  EMT – Epithelial to Mesenchymal Transition  MET – Mesenchymal to Epithelial Transition  Carcinomas can contain up to 90% normal cells   “activated” cells have changed behavior 


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