The cell cycle is a set of coordinated events that culminate in the formation of two cells from one mother cell. This cycle is composed of four major phases; G1 (growth phase 1), S (DNA synthesis phase), G2 (growth phase 2) and M (mitosis), which function to integrate environment sensing signaling pathways with cell growth and proliferation. Cancer cell proliferation relies on the ability of cancer cells to grow, transition through the cell cycle, and divide. Cancer cells often deregulate the cell cycle and undergo unscheduled cell divisions. So, it makes sense that many anti- cancer drugs perturb the proliferation cycle of turhor cells by inhibiting/damaging cell cycle events, which activate checkpoints, arrest cells and induce apoptosis. Source *Your assignment is to conduct your own research and find examples of two such cancer research drugs and write a mini-report (one-half page length) about each. You should include the name of the drug and describe the specific mechanism of action on the cell cycle. Please identify where in the cell cycle the drug targets and cite ALL REFERENCES! Must be typed. REFERENCES: Peer Review scientific journals, .gov and .edu research institutions are appropriate web-sites

The cell cycle is a set of coordinated events that culminate in the formation of two cells from one mother cell. This cycle is composed of four major phases; G1 (growth phase 1), S (DNA synthesis phase), G2 (growth phase 2) and M (mitosis), which function to integrate environment sensing signaling pathways with cell growth and proliferation. Cancer cell proliferation relies on the ability of cancer cells to grow, transition through the cell cycle, and divide. Cancer cells often deregulate the cell cycle and undergo unscheduled cell divisions. So, it makes sense that many anti- cancer drugs perturb the proliferation cycle of turhor cells by inhibiting/damaging cell cycle events, which activate checkpoints, arrest cells and induce apoptosis. Source *Your assignment is to conduct your own research and find examples of two such cancer research drugs and write a mini-report (one-half page length) about each. You should include the name of the drug and describe the specific mechanism of action on the cell cycle. Please identify where in the cell cycle the drug targets and cite ALL REFERENCES! Must be typed. REFERENCES: Peer Review scientific journals, .gov and .edu research institutions are appropriate web-sites

Human Physiology: From Cells to Systems (MindTap Course List)

9th Edition

ISBN:9781285866932

Author:Lauralee Sherwood

Publisher:Lauralee Sherwood

Chapter1: Introduction To Physiology And Homeostasis

Section: Chapter Questions

Problem 6RE: Cell specializations are usually a modification or elaboration of one of the basic cell functions....

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Describe how Ras and p53 can alter the simplified genetic pathway controlling cell division shown below. For each of the two genes, would uncontrolled cell division result from a loss-of-function or a gain-of-function mutation? growth factors - receptors - cyclins - cyclin-dependent kinases - cell division
How can defects in the regulation of cell-cyle checkpoints would affect cells and explain how these defects relate to uncontrolled division in cancer and cancer progression? Describe the movements of chromosomes and the status of the microtubules spindle during interphase, prophase, metaphase, anaphase, and telophase? Explain the movement of chromosomes during stages of meoisis to produce sperm and eggs?
(a) the cell cycle is divided into different phases (referred to as M, G0, G1, S and G2); Can you account for what happens during the different parts of the cycle and out of it is checked? ( b) What is the difference between apoptosis and necrosis? ( c) What are caspases and what is their function in the cell?
"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)? Explain
Which of the following is true with respect to cyclins and CDKs? A) CDKs promote progression of the cell cycle, cyclins function to inhibit progression of the cell cycle B) CDKs are the checkpoints in the cell cycle, and when bound to cyclins, they stop progression of the cell cycle C) CDKs will only work to promote progression of the cell cycle when complexed with their designated cyclins D) CDKs are rarely expressed during a cell's cycle, unless cyclins are present to act as transcription factors .
A cell inherits a mutation in a gene that results in a transcription factor, called NF-kB, constantly being in its active conformation. When active, NF-kB stimulates the expression of cyclins that promote progression of the cell cycle, regardless of other conditions. As a result of this mutation, how would this cell's phenotype be affected by this mutation? A) This cell would have a cancer phenotype B) This cell would grow larger in size, but would never divide C) This cell would likely undergo apoptosis D) This cell would not duplicate its chromosomes .
Maturation promoting factor, MPF, is a cyclin-CDK complex that catalyzes the phosphorylation of other proteins to start mitosis. The activity level of MPF is dependent on the relative concentrations of the cyclin and CDK components of MPF (Figure 1). Based on Figure 1, which of the following describes the role of cyclin in the regulation of the cell cycle? a.During S phase, the cyclin level remains the same because DNA replication is occurring. b.During G2 phase, the cyclin level remains low, causing MPF activity to decrease, which leads cells to initiate mitosis. c.During G1 phase, the cyclin level decreases to signal the start of the resting phase of the cell cycle. d.During M phase, the cyclin level peaks, resulting in an increased binding frequency with CDK.
Describe the steps by which the TP53 gene responds to DNA damage and/or cellular stress to promote cell-cycle arrest and apoptosis. Given that TP53 is a recessive gene and is not located on the X chromosome, why would people who inherit just one mutant copy of a recessive tumor-suppressor gene be at higher risk of developing cancer than those without the recessive gene?
One important biological effect of a large dose of ionizing radiation (like X-rays) is to halt cell division. How does this occur? To answer this question, state the name and role of 2 specific and important proteins involved in the process. What happens if a cell has a mutation that prevents it from halting cell division after be irradiated? Be specific and detailed. An adult human who has reached maturity will die within a few days of receiving a radiation dose large enough to stop cell division. What does that tell you about cell division? In addition, name 2 different/unique cell types that would be primarily affected.
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.
The p53 gene encodes a tumor-suppressor protein, p53, which acts as a transcription factor for several genes. Discuss an example of a specific gene that is activated by p53 and how this gene activation will lead to a pause in the cell cycle for DNA repair to take place.
How does the dysregulation of cell cycle checkpoints contribute to the development of cancer?