Cancer Cell Self Sufficiency in Growth Signals
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1 Name Date Cancer Cell Self Sufficiency in Growth Signals Part 1: Introduction Read the introduction. Draw a flower in the box when finished with this step. RAS Diagram Use the space below the diagram to describe what s going on. Part 2: Learn Read How Cancer Cells Beat the System. Draw a bee in the box when finished. Write down 3 things you think everyone should remember about this hallmark Growth Factor Pathway Diagram Use the space below the diagram to describe the diagram. Mnemonic Device Come up with your own mnemonic device for Cancer Makes Growth Signals (ex Chopping Musty Garlic Stinks ) Part 3: Flashcards Go through the flashcard set. Draw a cell during telophase in the box when done. Part 4: Quiz Time! Take the 10 question quiz. Draw a smiley face in the box when you re done.
2 Part 5: Word Search! U S L P Q W A T U M O R S T U D W W T T J I X U F N S Y G P A R E A J B I C U U F E E D B A C K E B L V X C X G Y I J Z N H B S X M S L Z M R E L Z E R U S P R L M S E G H B B B U M Z F B N P X P P P U I E C Z V E A F Q N H I Q V Q T N E B W Y N I N V Y L G G B P H U F Y R O N D L Z H H N W D M G F F G Z M M V M O R U W D O C I D W O P G H P Q U D R I T F O H B Z R H B E Y V I A G R F H T H P S L L X M E H R I P B I D G P H C G E U F T I U Y Y T H G T E L O Q G U J P R T C D S V T O L F K L O N B K D V B N C V Y I U X T B M X M Z W R D S N O J G E S I V A E F P Z W C A N R N E U D V L P V M I A C Y X A N N T Z A W G N Y L P T R A S F D F T U R I U R O O B G C C R I W S I N Q F E C M U T A T I O N U E N N S U O L X V Q O P P L K N V K W Z X A V J E N F G M N K Y M A W W C Q R E M W N H B D WORD BANK DIVISION FEEDBACK HERCEPTIN INDEPENDENCE INHIBITOR MUTATION RAS RECEPTOR TUMORS TRANSDUCTION 2
3 Saul, Ivan, Giakhoue, Robert Insensitivity to Antigrowth Signals 1. Read the introduction. 2. Read Anti-growth Signals. 3. How do anti-growth signals normally work? 4. Which molecules inhibit what in normal cells? In cancerous cells? a. b. 5. Examine the diagram 6. Label this diagram: a b c d 7. Explain how the retinoblastoma can be inactivated. 8. Read Evidence. 9. Read Treatment.
4 10. Describe how chemotherapy and chemoprevention differ. 11. Go through slideshow 12. Go through the flashcard deck. Complete the crossword!!!!!! Across 3. RBp is short for Protein 6. The human produces a protein known as E7, which binds to and inactivates Retinoblastoma. 10. The presence of this blocks advancement of the cell cycle. 11. to Antigrowth Signals 14. Cancer cells have that change the way their proteins function. 15. When DNA is, normal cells do not divide. 16. Inhibition prevents cells from dividing when they get too crowded. 17. Tumor genes prevent cells from dividing when they have problems. Down 1. Some inhibitors are located in the matrix. 2. A primary function of Retinoblastoma is to bind to and inactivate E2F. 4. signals prevent healthy cells from dividing out of control. 5. How many stages does the cell cycle have? 7. What number hallmark of cancer is Insensitivity to Antigrowth Signals? 8. Cells that divide without stopping are considered to be 9. Regulatory protein that starts with a c 12. A mass of cells that has the potential to become cancerous. 13. Cyclin Dependent Kinases
5 Name: Period: Date: Module 1000: Evading Apoptosis :) Instructions: 1. Work in pairs (share a computer). 2. You can t really log in so just do this paper. 3. Go to Ezra Torio s Webpage on qwizcards.berkeley.net Tutorial 2: Slideshow Watch the Evading Apoptosis Google slideshow Look at Two Main Pathways for Apoptosis. Which pathway do you think seems more likely to be evaded and why? Tutorial 1: Description of Apoptosis in Cancer Read: Description of Apoptosis in Cancer Summarize: What are the key differences between intrinsic and extrinsic pathways? Create a key to the diagram below What is the consequence of cancer cells evading apoptosis? Key Terms: Term Caspase Death Signal P53 BCL-2 BAX Cytochrome C Definition I II a b c d e f g h
6 i j k l m n Who first linked oncogenes to the evasion of apoptosis? Name two ways that cancer cells can evade apoptosis Tutorial 4: Quiz Use your knowledge gained from the description, slideshow, and flashcards to complete the quiz Name a catalyst that induces apoptosis Name an enzyme that performs cell death Compare E6 and BCL-2 Checking Understanding: Your highly intelligent talking monkey asks you about how apoptosis is related to cancer. In the space below, provide an explanation using the information gained from the webpage! What are some possible treatments that include apoptosis? Tutorial 3: Interactive Flashcards Use the flashcards until you feel comfortable answering each one According to the mice study, what is the effect of inactivating the p53 gene? What is the link between apoptosis and cancer treatments? Define the functions of the following: Sensors: Effectors:
7 Name: Date: Period: Hallmark of Cancer: Limitless Replicative Potential Work in pairs (share a computer). 1. Answer all questions for full credit. 2. Go to Noah Dilworth s AP Biology Limitless Replicative Potential Qwizcards page. 3. Do the best you can!! Introduction: Limitless Replicative Potential 1. Read the introduction, and fill in the blanks. a. Cancer cells can beyond the limits of a regular cell. This is why they are often referred to as, meaning they are not bound to the limit after a given number of divisions. This is what allows to increase in almost indefinitely. Part 1: Description of Limitless Replicative Potential 1. Read the description, and write a one paragraph summary. 2. Answer the questions about Limitless Replicative Potential. Paragraph: What is the role of telomeres in the chromosome? What is the Hayflick Limit? What is the end replication problem? What is the role of telomerase in cancer cells? What is some evidence to support this? Part 2: TEST YOUR MIGHT! 1. Review the slideshow presentation. 2. Quiz yourself with all 20 flashcards. 3. Give us your score as a comment Part 3: Final Summary 1. Did you actually read it? I hope so because now that you ve read all there is to know about Limitless Replicative Potentia l, you are going to right a 5 paragraph essay about what you have learned. Just kidding, but you will tell us three of your favorite facts from everything that you just learned
8 Name: Period: Date: Sustained Angiogenesis as a Hallmark of Cancer 1. Work in pairs (share a computer). 2. So that you can get credit, turn in this paper! 3. Go to Colleen Burns AP Biology Sustained Angiogenesis Qwizcards page. 4. Start exploring the page! Why is sustained angiogenesis important to the development of cancer cells? How can angiogenesis be influenced to create an excessive number of blood cells? Introduction: Sustained Angiogenesis 1. Read the introduction, and fill in the blanks. a. Angiogenesis is the of blood vessels and capillaries to bring nutrients and oxygen to cells. Normally, angiogenesis occurs during. When tumors form, they develop the ability to angiogenic genes and initiate the growth of new and so that they can grow and expand. This process involves the of growth factors that stimulate cells to move towards tumors. The formation of vessels and capillaries provides tumors with and essential to growth and development. Part 1: Description of Angiogenesis 1. Read the description, and write a one paragraph summary of what you have read. 2. Answer the questions about angiogenesis. Summary Paragraph: What is the role of VEGF in angiogenesis? What kinds of studies have been conducted to learn more about sustained angiogenesis? Part 2: Interacting with Angiogenesis 1. Review the slideshow presentation. 2. Quiz yourself with 10 flashcards. 3. Test your knowledge with the interactive diagrams and multiple choice questions. 4. Leave us a comment at the bottom of the page! :) Part 3: Final Summary 1. Now that you have read all of the information about sustained angiogenesis, it s time to write a final piece about what you have learned. In bullet points, write out three interesting facts that you learned from the webpage.
9 Sustained Angiogenesis Crossword ACROSS 4) The process of developing or being developed 8) Physiological process through which new blood vessels form from pre-existing vessels 10) Group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body 14) Development of organs within an animal 15) Interior lining of blood vessels DOWN 1) A tubular structure carrying blood through the tissues and organs 2) Deficiency in the amount of oxygen reaching the tissues 3) A substance that provides nourishment essential for growth and the maintenance of life 5) Chemical element with symbol O and atomic number 8 6) Outline the outer surfaces of organs and blood vessels 7) Continuing for an extended period or without interruption 9) Any of the fine branching blood vessels that form a network between the arterioles and venules 12) Activated in a pericyte cell 13) Vascular endothelial growth factor
10 Name Date Period Tissue Invasion and Metastasis Work in pairs Getting to the website Go to Click on Aidan, Camila, Emily and then start by reading the introduction Introduction: An Into to Metastasis Read the introduction, check the box when completed. Answer the following questions: 1. What is Metastasis? 5. Explain the evidence that supports the theory that Metastasis did not occur randomly. 500 Word Summary 1. The formation of new tumors ultimately leads to what percent of cancer deaths? 2. Explain the difference between a benign and a malignant tumor? I II a b 3. Why is it important to distinguish between these two tumor types? c d e Review slideshow if needed Complete the flashcard Deck Complete the Multiple Choice Review 4. What is the EMT process? Why is it important? Reflection: What is the most important piece about metastasis? Why is it a hallmark of cancer?
11 Name: Period: Date: 1. Read the introduction 2. Read the description of the cancer hallmark 3. Why do cancer cells have an accelerated metabolism? 4. How many ATPs per glucose do cancer cells make? 5. Review the slide show 7. Finish the interactive quiz 8. What does the P53 gene do in normal cells? 9. What does the P53 gene do in cancerous cells? 10. How do chemotherapeutic drugs inhibit the energy pathways in cancerous cells? 6. Review all of the flashcards 11. Letter Molecule/Process A B C D E
12 Name: _ Date: Evading the Immune System 1. List the three immune hallmarks that cells develop as they form a tumor: A. B. C. 2. The Three E s: In, the immune system manages to destroy such cells before they can spread or cause significant harm. is when the immune system doesn t eliminate the tumor right away, but is able to contain it. To grow into a full-blown cancer, the cells will have the immune system s defenses. 3. Briefly summarize what immunosurveillance is. Explain the role of immunogenicity in it. 4. Immunosuppression works by the system. Tumors release factors and molecules to transform naive T-cells into. In a healthy environment cells help shut down activated T-cells at the end of an immune response. However, in a cancerous microenvironment, cells are used to autoimmune responses. 5. Choose two types of immunotherapy. Briefly describe each. A. : B. : 6. Write down one thing that surprised/interested you from the presentation and interactive webpage.
13 Name: Date: Faux Biology180: Genomic Instability Read Introduction Cancer develops through the multitude of that can occur from genome, a hallmark of. It is an increased risk of genome transformations during the cell cycle, which can negatively affect the body. Overtime, with age, as people s cells divide more, their susceptibility to mutations. How can mutations be prevented? Complete the diagram below Read What is Genome Instability? What are harmful mutations? How are cancer cells different than non-cancer cells? What are some selective advantages cancer cells have? What is the chance of a single nucleotide mutation occurring? Why are cancer mutations more likely than we think? What genes are known to lead to breast cancer?
14 Why is it important to get tested for cancer often? Has the death rate of cancer in the U.S. gone down in recent years? Look through the slideshow Do the Genome Instability Flashcards Take the multiple choice/interactive quiz!
15 Name: Period: Date: Inflammation as a Hallmark of Cancer 1. Work in pairs (share a computer). 2. So that you can get credit, turn in this paper! 3. Go to Kenneth Sieu s AP Biology Inflammation Qwizcards page. 4. Start exploring the page! Introduction Read the introduction and fill in the blanks below. Inflammation is natural process within the body to kill and promote. However, inflammation can inadvertently cause more damage to the body by aiding the growth and spread of cancer. It is one of the Hallmarks of cancer and is intertwined with, evading the, and. Inflammation, although a helpful process from the immune system, can assist in the growth, replication, and creation of. 2. Read Inflammation and DNA damage. Answer the questions below. How does inflammation lead to genomic instability? 3. Read What Happens Next? and Tumor Growth and Inflammation. Answer the questions below. What role does inflammation play in the promotion of angiogenesis? Inflammation and Cancer: Overview 1. Read What is Inflammation? Answer the questions below. What are the 2 types of inflammation and how are they different? How do cancer cells use cells from the immune response for their own purposes during inflammation? How is chronic inflammation related to cancer? (general)
16 Name: Period: Date: Inflammation as a Hallmark of Cancer 6. Now practice what you ve learned with the flashcard deck. See if you can get all 10 right before moving on! Write down three things you learned from the flashcard review. Label the diagram above. 1. a b 2. c d e 3. f g 4. Read How was the link between cancer and inflammation discovered? Summarize the study in two sentences. Finally, do the quiz. Now that you ve learned about how inflammation can cause cancer, write down a four sentence summary of this hallmark. 5. Read Treatments Write down one question you have about possible cancer treatments related to inflammation.
17 Name: Period: Date: Inflammation as a Hallmark of Cancer
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