The Eukaryotic Cell Cycle and Cancer

Name:____________________________________ Date:________________________ The Eukaryotic Cell Cycle and Cancer 1. What is the role of growth factors? Growth factors stimulate cell growth and differentiation by binding to specific receptors on the cell surface, triggering signaling pathways that lead to cellular responses like division 2. Cells divide, differentiate, or die. What is differentiation? Differentiation is when a less specialized cell transforms into a more specialized one, acquiring distinct features and functions to perform specific tasks within the body 3. What is apoptosis? Explain TWO purposes for apoptosis. Apoptosis is programmed cell death, serving two main purposes: sculpting tissues during development and removing damaged or unnecessary cells to maintain tissue health 4. Name one harmless result of too little cell division. _______________ Too little cell division can result in slower tissue regeneration, potentially delaying wound healing or cell turnover 5. Name one harmless result of too much cell division. _______________ Too much cell division can lead to callus formation, which serves as a protective barrier on the skin without causing harm 6. In general, what is the purpose of a checkpoint in the cell cycle? The purpose of a checkpoint in the cell cycle is to ensure accurate completion of each stage before cell progression 7. What is one potential outcome when errors occur in this highly regulated cell cycle process? One potential outcome of errors in the cell cycle process is the accumulation of mutations, leading to uncontrolled cell division or genetic diseases 8. What are the most important cell cycle regulators? The most important cell cycle regulators include cyclins, cyclin-dependent kinases (CDKs), and tumor suppressor genes like p53 and retinoblastoma protein (Rb) 9. What is kinase, and what does it do? A kinase is an enzyme that catalyzes the transfer of phosphate groups from ATP to specific target molecules, often proteins. Kinases play crucial roles in cell signaling pathways, regulating various cellular processes such as cell growth, differentiation, and division 10. When are cyclin-dependent kinases (CDKs) present inside the cell during the cell cycle? Cyclin-dependent kinases (CDKs) are present inside the cell throughout the cell cycle, but their activity is regulated by the availability of specific cyclin proteins 11. When are cyclins present inside the cell during the cell cycle? Cyclins are proteins that undergo cyclic fluctuations in concentration during the cell cycle. They are synthesized and degraded at specific times in the cell cycle, with their levels peaking and declining at different stages 12. CDKs form molecular complexes with cyclins. What do activated CDK-cyclin complexes do? Activated CDK-cyclin complexes phosphorylate target proteins involved in regulating the cell cycle. These phosphorylation events trigger the progression of the cell cycle, such as initiation of DNA replication, transition between cell cycle phases, and entry into mitosis 13. Go to “Cell Cycle Phases” and click on “G0” The G0 phase is the resting or non-dividing stage. What three factors determine whether a cell enters the G0 phase? The three factors that determine whether a cell enters the G0 phase are signals from the environment, the cell's own internal state, and regulatory proteins 14. Provide an example of a fully differentiated cell that is (A) permanently in G0 and (B) one that can leave G0 to progress through the cell cycle and divide again. A. ____________________ B. _____________________ A. Example of a fully differentiated cell permanently in G0: Neurons in the brain are typically in G0 and do not divide once fully differentiated B. Example of a cell that can leave G0 to progress through the cell cycle: Liver cells (hepatocytes) can exit G0 in response to specific signals or stimuli and re-enter the cell cycle to divide and regenerate liver tissue 15. Cancer is the result of an improperly regulated cell cycle. Name two basic reasons why cells can form tumors. Two basic reasons why cells can form tumors are: - Loss of cell cycle control mechanisms, such as checkpoints, leading to uncontrolled cell division. - Mutations in genes involved in cell growth regulation, such as oncogenes or tumor suppressor genes 16. What causes uncontrolled cell division at the genetic level? Uncontrolled cell division at the genetic level is caused by mutations in genes that regulate cell growth, division, and apoptosis. These mutations can lead to the activation of oncogenes or the inactivation of tumor suppressor genes, disrupting normal cell cycle control mechanisms 17. To cause cancer, proto-oncogenes require ___ allele(s) to be mutated and are therefore considered (dominant / recessive) (circle one.) This results in _____ of function. To cause cancer, proto-oncogenes require one allele to be mutated and are therefore considered dominant. This results in a gain of function, as the mutated allele promotes uncontrolled cell growth and division 18. To cause cancer, tumor suppressor genes require ___ allele(s) to be mutated and are therefore considered (dominant / recessive) (circle one.) This results in _____ of function. To cause cancer, tumor suppressor genes require both alleles to be mutated and are therefore considered recessive. This results in a loss of function, as the mutated alleles fail to inhibit abnormal cell growth and division 19. Watch the video clip. a. Using the gas pedal analogy, explain the impact on the cell cycle of a proto-oncogene versus an oncogene. Using the gas pedal analogy, a proto-oncogene acts like a gas pedal stuck in the "on" position, leading to continuous stimulation of cell division. An oncogene, on the other hand, is like a gas pedal that is constantly pressed down, causing uncontrolled and excessive cell division without the need for external signals b. Using the gas pedal analogy, explain the impact on the cell cycle of one mutated tumor suppressor gene allele versus two mutated tumor suppressor gene alleles. Using the gas pedal analogy, one mutated tumor suppressor gene allele is like having a faulty brake pedal, reducing the cell's ability to stop or slow down division when necessary. Two mutated tumor suppressor gene alleles are like having both brake pedals malfunctioning, completely losing the ability to control cell division, which can lead to uncontrolled proliferation and tumor formation 20. p53 is a tumor suppressor gene, and some scientists refer to it as “the guardian of the genome.” a. Explain its normal role and why scientists would regard it as “the guardian of the genome.” p53's normal role is to monitor DNA damage and cellular stress, triggering cell cycle arrest, repair, or apoptosis. Scientists call it "the guardian of the genome" because it prevents damaged cells from proliferating b. Explain what happens to the cell cycle if both p53 alleles are mutated. If both p53 alleles are mutated, the cell loses its ability to respond effectively to DNA damage, increasing the risk of accumulating mutations and developing cancer 21. Explain why people who inherit one mutated allele of the BRCA1 gene have a higher likelihood of developing cancer. Individuals inheriting one mutated BRCA1 allele have higher cancer risks because BRCA1 helps repair DNA damage. With one mutated allele, DNA repair capability decreases, increasing cancer susceptibility 22. Predict a potential outcome of a mutated MAD protein. Be specific. mutated MAD protein could disrupt the spindle assembly checkpoint during mitosis, potentially causing chromosome misalignment and contributing to cancer development 23. Use the model illustrated in the figure below to answer the following questions. a. The human gene EGFR located on chromosome 7 is a proto-oncogene that codes for a growth factor cell surface receptor. The binding of growth factor ligands to this receptor can lead to cell proliferation. Hypothesize what potential impact a mutated EGFR allele will have on a cell. Give TWO possible impacts. A mutated EGFR allele may lead to increased receptor activity, promoting exaggerated cell proliferation and potentially fueling tumor growth. It could also alter downstream signaling pathways, aiding in cell survival or growth b. RAS is a G-protein that is activated when a growth factor attaches to EGFR. Its activation results in the replacement of a GDP molecule with a GTP molecule, thus allowing a signal transduction pathway to be activated. Considering the signal pathway illustrated on this page, what is one potential outcome of a mutation in the RAS gene that leads to RAS protein hyperactivity. Be specific. Hyperactive RAS resulting from a mutation can continuously activate signaling pathways like the MAP kinase pathway, promoting uncontrolled cell proliferation and differentiation, which may lead to tumor formation c. Mutations in genes that code for proteins in this pathway have been linked to various types of cancer (i.e., RAS-pancreatic, RAF-colon, MEK-melanoma, EGFR-lung). If you were developing a new cancer drug, what approach might you take? Targeting key proteins like RAS, RAF, MEK, or EGFR in the MAP kinase pathway could be effective in halting cancer growth by disrupting aberrant signaling cascades that promote tumor progression