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121 Cards in this Set
- Front
- Back
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What study demonstrated transdifferentiation |
2010 Stanford Culture Study with mouse cells Epithelial --> Neuron |
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Where do HESC's come from? |
The inner mass of the blastocyst |
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Chimera Test |
Label cells from inner mast of blostocyst in cell A, implant cells from A to blastocyst of a mouse Let cells grow and see is cell A fully differentiated |
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STAP Cells |
Stimulus triggered acquisition of pluripotency Took cells and put them in acid bath to shock them into pluripotency Probably just fraud |
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What animal has limb regeneration? |
Red Spotted Newt |
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What are the ways to generate Stem Cells? |
Somatic Cell Nuclear Transfer (SCNT) Parthenogenesis Induced Pluripotent Stem Cells (IPSC's) |
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When was the first successful SCNT and by who? |
1960 John Gurdon Got a nobel prize in 2012 |
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What was the first SCNT experiment |
Replaced frog egg nucleus with epithelial cell nucleus and successfully generated a tadpole
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Who made Dolly the Sheep? |
Ivan Wilmut |
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How did they make Dolly the Sheep? |
SCNT |
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What animal was used in the first successful parthenogenesis experiment? |
Gave eggs a osmotic shock and produced full sea urchins Did this with star fish too |
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When was the first Parthenogenesis experiment and by who? |
1913 Sea Urchin Eggs by Loeb
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How do we get stem cells from human differentiated cells? |
Shock them to a parthenotes then viola human parthenogenic stem cells aka hPSC's |
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How does International Stem Cell Corp (ISCO) make stem cells? |
Make the human eggs parthenotes by shocking them into a diploid zygotic state Claim that 200-300 human eggs could produce HPSC's as a perfect match for the entire globe |
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Whats the problem with the way ISCO makes stem cells? |
Since eggs get socked into a diploid state, all the alleles are identical and thus inbreeding problems |
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What happened Nov. 30th, 2007 |
Shinya Yamanake and James Thomson published papers the same day about successful iPSC work with human cells |
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Who/When got the nobel prize in 2012 for iPSC's? |
Shinya Yamanaka 2012 |
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Why aren't iPSC's a viable option yet? |
iPSC's form benign teratoma (tumor) or teratocarcinoma (maligant tumor) |
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What happens if an iPSC isn't fully differentiation in-vitro prior to transfusion? |
Teratocarcinoma forms = Malignant tumor |
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How do human skin cells differentiate? |
They differentiate upway with stem cells being at the bottom. Figured this out by labeling with 3H-Thyminine and then visualizing |
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What companies store cord blood for future transplant? |
ViaCell and ViaCord |
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Who used C. elegans for differentiation/apoptosis experiments and why? |
Robert Horvitz of MIT |
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How do proteins pass through the nuclear pore? |
Diffusion |
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How do histones pass through the nuclear pore? |
if <20,000 diffusion without ATP, otherwise you need ATP |
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What forms the karyoskeleton? |
Lamins - Intermediate filaments |
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How do we know that nucleoplasmin can enter the nucleus |
Tag the nucleoplasmin and inject it into cell. Do gel electrophoresis and you'll see the proteins inside the nucleus Once cooled to 4 degrees, you can add ATP and it'll move into nucleus |
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What is lamin |
fibrous intermediate filaments, providing structure and regulation in the cell nucleus. |
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Where are lamins found? |
lamins form the nuclear lamina on the interior of the nuclear envelope. |
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What do lamins do? |
They're involved in the breakdown and reformation of the nuclear envelope during mitosis, as well as the positioning of nuclear pores. |
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How does the Mitotic Promoting Factor (MPF) interact with nuclear lamins? |
tetramers --> dimers MPF Causes nuclear envelope to disappear |
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when/how/why does the nuclear envelope breakdown? |
During prophase 1, increase in concentration of MPF phosphorylates tetrameric lamins causing dimerization and subsequent breakdown This allows for DNA to do it's **** for cell division |
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How is lamin involved in the cell cycle? |
Phosphorylation of Lamin A, B, and C causes nuclear envelope breakdown triggering mitosis |
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Who defined the cell cycle and when? |
Howard and Pelc 1953 |
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G0 phase |
Resting state of the cell cycle Neurons are arrested in G0 |
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How does a cell go from G0 phase to G1 Phase? |
Each cell has a specific set of growth factors that need to be introduced in an exact order |
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What are late response genes? |
Genes which can only be activated following the synthesis of early response gene products Thus protein synthesis inhibitors also inhibit late response genes |
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Whats the effect of amino acid deprivation on the cell cycle? |
Stall in G1 |
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Whats the effect of microtubule inhibitors on the cell cycle? |
Stall in Mitosis |
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Whats the effect of DNA synthesis inhibitors on the cell cycle? |
Stall in S phase |
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What experiment suggested the presence of MPF |
Fuse mitotic cell with G1 cell and you'll see a premature condensing of chromosomes Chromosomes aren't suppose to condense until G2 |
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What is the restriction point? |
Point where you can't return to G0 and are committed to cell cycle |
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What are cyclins |
Regulate cell cycle and are present during all phases No cyclin = no cell cycle High cyclin promotes division, then drops, once it builds up again --> division |
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Who discovered cyclin |
Ruderman and Hunt with SDS Gel electrophoresis of sea urchin eggs |
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Cyclin B |
Mitotic Cyclin |
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Cyclin A |
S phase cyclin |
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Cyclin D |
G1 Cyclin |
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Describe the cell free cyclin B experiment |
Add ATP, Frog egg cytoplasm with MPF activity, and sperm nuclei Results in 2 nuclei + Chromatids |
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Results of Cyclin B synthesis/degradation |
Only Cyclin B is required for cell cycling |
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Who discovered tumor suppressor genes |
Columbia Professor Ruth Sager |
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How were tumor suppressor genes discovered? |
Bind normal and cancer cell and eventually the cell becomes cancerous probably because there was a tumor suppressor gene lost |
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Which checkpoint has tumor suppressor genes? |
G1 checkpoint |
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Why is p53 known as the guardian of the genome |
>50% of cancers have p53 defects It stalls cells to allow for reperation of damage or apoptosis depending on severity |
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BRCA 1 and 2 |
If genes are defective theres a 60% chance of breast cancer |
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BRCA gene lawsuit |
Myriad Genetics (company) tried to patent the BRCA test but the supreme court decided (4/2013) you can't patent a product of nature |
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Indirect carcinogen effect |
Non carcinogens get modified in the liver by p450 to something carcinogenic |
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What disease is the product of defective caretaker genes |
Xeroderma Pigmentosa |
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What is xeroderma pigmentosa |
Severe childhood disease where you're extra sensitive to UV light |
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What are the traditional approaches to treating cancer? |
1) Radiation 3) Ablation/Surgery 4) Chemotherapy |
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Types of radiation therapy |
1) Focused beam aka External Beam Radiation Therapy (EBRT) 2) Non-focused beam aka all other radiation therapies |
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What's cyberknife? |
A form of focused beam radiation good for brain tumors |
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What is brachytherapy? |
Non-focused beam radiation therapy that uses implanted radioactive seeds for point radiation Commonly used for prostate cancer |
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What ablation/surgery treatment did VanBuskirks CPSI-Biotech invent? |
Cryoblast cell freezing therapy |
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What are the chemotherapy drugs? |
Taxol, Taxotere, and 5-FU |
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Which chemotherapy drugs effect microtubule polymerization |
Taxol and taxotere effect all actively dividing cells |
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Fluorouracil aka 5-FU |
Chemo that effects DNA Synthesis |
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What are new era approaches? |
Combination treatment of new drugs + traditional therapies |
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Bispecific Antibodies |
Synthetic antibodies that look like normal antibodies except they have 2 different FAB region |
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Conjugated antibodies |
Non binding region is heavy chain and in conjugated ones they are attached to a "bomb" some other drug |
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How does herceptin work? |
Binds to HER2 receptor on cell surface |
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What does the HER2 receptor do |
signals cell growth Thus too many receptors can lead to misregulation of growth and cancer |
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What is kadcyla |
New Era cancer approach Conjugated Herceptin + DM1 toxin that effects microtubules |
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How is angiogenesis inhibition an effective cancer treatment |
If tumor is >2mm, there needs to be angiogenesis otherwise the cell will suffer from hypoxia |
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How do we treat basal cell carcinoma? |
Erivedge which shrinks the tumors by targeting smoothened receptor in hedgehog pathway |
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What drug is an angiogenesis inhibitor? |
Avastin |
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What is R-CHOP? |
Acronym representing 5 different drugs New Era + traditional drugs as a combination therapy |
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What's a super expensive yet highly effective Leukemia drug? |
Imatinib aka Glivec |
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What estrogen agonist treats breast cancer? |
Tamoxifen |
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First HPV vaccine? |
Gardasil |
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How does helix Biopharmaceuticals modify a tumors microenvironment as an effect cancer treatment? |
Alkalizing the microenvrionment by conjugating urease to a monoclonal antibody Used for non-small cell lung cancer |
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How does Provenge work? |
Immunomodulator that trains your immune system to kill cancer Aka Denderon Gives you 4 more months of life for 100,000 |
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What's the fundamental difference between apoptosis and necrosis? |
Necrosis is pathological cell death Apoptosis is programmed cell death |
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How does apoptosis relate to having webbed feet? |
Improper apoptosis of webbing material during digit differentiation |
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What's the SC40 Large T Antigen |
Proto-oncogone that inactivates tumor suppressor genes |
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What are the 4 unique features of Necrosis |
Swelling membrane, no inflammatory response, it's a messy process that produces a lot of waste, and requires no ATP |
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What are the 3 unique features of apoptosis? |
It is gene activated, ATP dependent, has condensing DNA, and apoptotic bodies |
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What are apoptotic bodies? |
Aka Apobodies Small vesicles produced by apoptotic cell in an effort to prevent leakage of potentially toxic apoptotic products |
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What does it mean that apoptosis is a tidy event while necrosis is a messy event? |
Apoptosis is considered tidy because it has associated apobodies that clean up whatever it leaks out. Necrosis is messy because there are no apobodies |
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How does the inflammatory response vary between apoptotic and necrotic events? |
Apoptosis shows litter inflammatory activity, while necrosis has none |
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How can you differentiate apoptosis vs necrosis on a Gel Electrophoresis |
Apoptosis generates non-random "latter sequence" Necrosis generates random smear sequence |
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What is responsible for the latter sequence seen in Gel electrophoresis is apoptotic cells? |
Since apoptosis is a regulated sequence, distinct portions of the cell are broken down at any point instead of just random breakdown seen in necrosis |
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What people investigated apoptosis? |
Started with Rita Levi Montalcini then John Kerr |
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Who was Rita Levi Montalcini and what/how did she discover? |
She was an embryologist who observed cell death in mouse brains with a microscope Observed the importance of NGF as a survival factor of nerve cells |
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Who won the nobel prize for nerve growth factor? |
Rita Levi Montalcini |
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Who is John Kerr and why is he important? |
He tied off the liver and then observed cell death |
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What is "shrinking necrosis" and who observed this? |
John Kerr saw apoptosis around the periphery of the cell and called it "shrinking necrosis" |
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Complementation analysis of what cells led to more cancer understanding? |
Budding Yeast and Fission Yeast |
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How do we know cancer cells are not substrate dependent unlike normal cells? |
They can grow in soft agar, they secrete proteases, have little/none ECM, and don't secrete fibronectin |
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What are the consequences of contact inhibition? |
It means that normal cells can only grow in monolayers Thus cancer cells can be observed growing in multilayers since it doesn't express contact inhibition |
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How many time can a cell divide and why? |
A cell can divide 25-50 times and then enters apoptosis due to shortening telomeres |
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What are the external causes of cancer? (Excluding genes) |
Viruses UV Light Chemical Mutagens Ionizing Radiation |
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What genes cause cancer? |
Cell Cycle Genes Defective Tumor Suppressor Genes Defective Caretake Genes |
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What cell defects cause cancer? (Excluding genes) |
Defects in apoptosis Defects in growth factor pathways Overproduction of Nuclear Transcription Factors Cancer Stem Cells Chomosomal Translocation DNA Amplification Telomeres
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What viruses cause cancer? |
Rou Sarcoma Virus (Retrovirus) HPV Epstein-Barr |
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How does the Rou Sarcoma virus cause cancer? |
Inhibits SV40 gene which inhibits tumor suppressor genes --> inhibits apoptosis |
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What cancer presents as genital warts? |
HPV virus |
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What virus causes Burkitt's and Hodgkin's Lymphoma? |
Epstein-Barr |
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How does UV light cause cancer? |
Irradiation causes 2 unlinked thymines to form dimer residues which keeps transcription factors from writing correctly |
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Example of chemical mutagens? |
Tobacco smoke and Ethylmethane sulfonate (EMS) |
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How does misregulation of cell cycle genes lead to cancer? |
Cyclin D is required for transit into G1 Cyclin D1 defects leads to breast cancer |
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Overproduction of ___ leads to apoptosis defects |
BCL-2 gene |
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How do growth factor pathways contribute to cancer? |
Overproduction of Her-2 promotes cancerous cell growth If RAS D is constitutively turned on, cells keep dividing |
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How do we identify cancer stem cells? |
CD133+ Cancer stem cells have a specific set of cell-surface receptors |
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How can ionizing radiation contribute to cancer relapse? |
Ionizing radiation can potentially make a cancer cell into a cancer stem cell |
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What cancer is caused by chromosomal translocation? |
Burkitts lymphoma |
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Over production of what 3 transcription factors can cause cancer? |
C-Fos, C-Jun, and C-MYC |
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Who did the first oncogene work? |
Robert Weinberg |
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What were the 3T3 cell line experiments |
1) Inject bladder cancer DNA in 3T3 cells and viola cancer Genes cause non-species specific cancer 2) Take Ha-Ras oncogene and add it to rat embryo fibroblast and theres no cancer until you put it in soft agar Microenvironment is important
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Which cells are most suceptible to cancer and why? |
Epithelial cells since they get the most environmental exposure |
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What did the Myc and Ras V12 mouse mutant experiment teach us? |
Found that myc and ras v12 both increased the likelihood of cancer but when both mutations were found together the sum of their effect was stronger than separately |
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What is the warburg effect |
Tumor cells can run solely on glycolysis |
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Why would cancer cells utilize glycolysis rather than oxidative phosphorylation? |
Since tumor cells are multilayered and dense, they're in a oxygen free environment where there is not much oxidative phosphorylation |
