In your own words, explain how cancer cells differ from normal cells in regard to the following: Molecular controls of the cell cycle (include Cdk and Cdk/cyclin complexes, p53 gene/protein, Rb gene/protein in response)
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In your own words, explain how cancer cells differ from normal cells in regard to the following:
Molecular controls of the cell cycle (include Cdk and Cdk/cyclin complexes, p53 gene/protein, Rb gene/protein in response)
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- Choose all of the TRUE statements. Hint: 4 statements are true. Cytokinesis occurs the same way in both plant and animal cells. Sister chromatids are genetically identical. The term chromosome can be used to describe both chromosomes composed of one and two chromatids. Mitosis results in daughter cells that are genetically identical to the parent cell. All eukaryotic somatic cells are diploid. Cyclin dependent kinases are present but not active in cell cycle regulation without the presence of cyclin proteins. Chromosomes are always visible in the cell.In your own words, explain how cancer cells differ from normal cells in regard to the following: Cell to cell communicationIn your own words, explain how cancer cells differ from normal cells in regard to the following: Apoptosis
- (Q) During M-phase of cell cycle, active M-Cdk phosphorylates several target proteins in order to regulate their activities. Identify TWO specific examples of such target proteins that are phosphorylated by active M-Cdk, and explain how each of them affects the cell (i.e. their respective biological significance). i) target protein phosphorylated: _______________________________ Biological Significance: ii) target protein phosphorylated: _______________________________ Biological Significance:Discuss the complete cell cycle in a human cell, mitosis and meiosis, and the regulatory components (i.e. the proteins associated with cellular checkpoints) of the cell cycle. Tumor growth results when the cell cycle checkpoints are ignored. Give an example of how tumor growth could result from either a loss-of-function or a gain-of-function mutation.p53 gene, as is the Rb gene, is a tumor suppressor gene. p53 protein binds to DNA leading to the simulation of p21 that work together with cdk2. When p21 is defective and cannot joined to cdk2 the cell cannot pass through to the next stage of cell division. Mutated p53 cannot bind to DNA in an effective way, and therefore the p21 protein is not available to act as the 'stop signal' for cell division. Thus cells divide uncontrollably, and form tumors. Hi, can you please elaborate on this: based on the info above, what is the relationship between genetics and environment in the development of these type of cancer. Which factor (genetics or environment) is playing a larger role in the generation of these types of cancers?
- The cell cycle is typically thought of as having four stages. Describe the stages of the cell cycle and identify the mechanism(s) involved in progressing or not progressing through the stages with reference to proteins and signalling processes involved. Please keep brief - 10 sentences/dot points max.#9) Cancer cells generally have missense mutations in p53 gene, resulting in truncated p53 normally active p53 dominant negative p53 inactive p53 #2) When cancer cells have not spread beyond its original site, the term used to describe it is benign growth intraepithelial neoplasia carcinoma stage 3 carcinoma in sit #10) Single or double stranded breaks in DNA activate Chk 1 and 2 kinases, which phosphorylates p53. This results in --- in the level of p53 in the cell. increase decrease please answer them all. they are very short and won't take your time. Thank you in advance.A cell begins to undergo apoptosis due to stress. Which of the following are true about this cell? (select all that apply) The cell can exit apoptosis if the stressful factor is removed The cell has high levels of p53. The cell's DNA will inevitably degrade The cell may undergo mitosis before completing apoptosis
- "Agent V" is the name of an anticancer (chemotherapy) drug. This drug works against cancer cells by inhibiting the formation of microtubules in sensitive cells. Consider a cell that is sensitive to agent V (in other words, agent V is effective at stopping growth of this cell). Based on this information, agent V would cause the cell to be frozen at which of the major cell cycle checkpoints (G1, G2 or M checkpoint)? ExplainCompare the characteristics of highly proliferating normal cells (including cells of the hair follicles, gastrointestinal tract, and bone marrow) with the characteristics of highly proliferating cancerous cellsDuring cell division cycle, cells need to monitor the process of DNA replication and segregation of replicated DNA so that these processes are error-free. Some potential errors that could occur include incomplete DNA replication, DNA damage in genome, and uneven separation of replicated genome. These mechanisms that cells used to monitor these processes are referred as the "cell cycle checkpoint, which can control specific Cdk activity to regulate the progression of cell cycle. For the following checkpoint mechanisms, indicate which Cdk activity is attenuated? Also indicate one of the key proteins or protein complexes involved in the following checkpoints. a) DNA damage checkpoint during S-phase b) Mitotic checkpoint during M-phase