Drug A323 inhibits the activity of the cyclin-dependent kinase (CDK) - G1 cyclin complex. Consider possible effects of the drug on the cell cycle of normal and malignant cells. Predict what is likely to happen if the drug is added to the cell types described in A). Motivate your answers and describe the role of cycle-regulatory pathways that are relevant with respect to the action. of drug A323. A) Carcinoma cells in which both allels of the Rb gene carries loss of function mutation.

Drug A323 inhibits the activity of the cyclin-dependent kinase (CDK) - G1 cyclin complex. Consider possible effects of the drug on the cell cycle of normal and malignant cells. Predict what is likely to happen if the drug is added to the cell types described in A). Motivate your answers and describe the role of cycle-regulatory pathways that are relevant with respect to the action. of drug A323. A) Carcinoma cells in which both allels of the Rb gene carries loss of function mutation.

Name: Drug A323 inhibits the activity of the cyclin-dependent kinase (CDK) -
Uploaded: 2024-03-20T06:42:55.000Z
Channel: Bartleby
Description: Drug A323 inhibits the activity of the cyclin-dependent kinase (CDK) - G1 cyclin complex. Consider possible effects of the drug on the cell cycle of normal and malignant cells. Predict what is likely to happen if the drug is added to the cell types d

Biochemistry

6th Edition

ISBN:9781305577206

Author:Reginald H. Garrett, Charles M. Grisham

Publisher:Reginald H. Garrett, Charles M. Grisham

Chapter32: The Reception And Transmission Of Extracellular Information

Section: Chapter Questions

Problem 21P

See similar textbooks

Similar questions

Plasma PDGF levels can be a diagnostic marker for severity and progression of breast cancer. The assay data below shows the plasma levels of PDGF in normal individuals, Stage II and Stage IV (More severe). You are treating a patient with breast cancer and assay indicates that their plasma PDGF level 6 fmoles/ 100 uL.Based on this info, in which stages has this patient's cancer progressed? Explain what process this patient's tumor has likely undergone and which cell types you would expect to now be associated with this tumor.
Although numerous treatments are available for advanced hormone receptor- positive (HR+) and human epidermal growth factor receptor 2 negative (HER2-) breast cancers, they are rarely curable. Drugs such as palbociclib that inhibit cyclin-dependent kinase 4 and 6 (CDK4/6) are rapidly altering this therapeutic environment. Discuss the function of CDK4 and CDK6 in promoting cell growth as well as the overall effects of their inhibition by palbociclib on the progression of the cell cycle.
Cancer-promoting mutations are likely to have different effects on the activity of proteins encoded byproto-oncogenes than they do on proteins encodedby tumor-suppressor genes. Explain.
Which ONE of these statements is the most accurate definition of the mode of action of imatinib? Select one: A.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by competing with adenosine triphosphate (ATP) binding B.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by competing with adenosine triphosphate (ATP) binding C.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by interaction with the enzyme site D.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by interaction with the enzyme site
I just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.
Distinguish between What is known of CD105 (endoglin) as an hepatcellular carcinoma marker and it’s potential as a drug target. Discuss: - Is anything known about its biology? E.g does it have known ligands and normal functions? - if you were to target it would you just use it to get growth inhibiting compound into the new blood vessels or is CD105 required for neovascularization?
A current focus of molecular medicine is to trigger or promote apoptosis of specific cells. several components of the apoptotic pathways are being targeted using this approach. for following, state specifically how the treatment would be expected to stimulate or inhibit apoptosis. c. Treatment of cells with organic compounds that enter the cell and bind with high affinity to the active site of Caspase-3
describe the outcome of EGFR inhibition as well as the differences between erlotinib and panitumumab’s mechanisms of action. EGFR- driven cancer cells can become resistant to tyrosine kinase inhibitors. Explain the two types of EGFR blockade acquired resistance and propose a subsequent treatment option.
The mechanisms that “trigger” micrometastases to develop into macrometastases (which can be clinically detected) are still poorly understood. However, elucidating these pathways could offer valuable insights into the long term treatment of cancer patients. Interestingly, the efficiency of this process is believed to be very low (indeed, many patients exhibit micrometastases that never develop into full blown clinical metastases). Which mechanism has a stronger influence on the outcome of colonization? What is the main driver leading to the development of macrometastases from micrometastases?
Changes in the activity of a variety of Cdks are essential for accurate progression through the cell cycle, and yet the levels of Cdk expression are fairly constant during the cell cycle. Briefly describe three mechanisms by which the activity of Cdks is regulated.
If somatic tumors cause local regions in their vicinity to have an increased pOH, how is this strategic for the survival of the tumor? Select one: a. It allows the increased hydroxide concentrations to cause a conformational change in nearby hemoglobin to the R state so that ample oxygen is deposited for tumor growth. b. It allows the increased proton concentrations to cause a conformational change in nearby hemoglobin to the R state so that ample oxygen is deposited for tumor growth. c. It allows the increased proton concentrations to cause a conformational change in nearby hemoglobin to the T state so that ample oxygen is deposited for tumor growth. d. It allows the increased hydroxide concentrations to cause a conformational change in nearby hemoglobin to the T state so that ample oxygen is deposited for tumor growth. e. None of these.
TNF-alpha treatment of prostate carcinoma, LNCAP cells decreases cell survival as shown in the graph below. Which of the following would you observe in these cells treated with TNF- alpha? Select all that apply TNF-a 120 100 80 - 60 40 20 0. 24 72 (hrs) Control + TNF-a 100 ng TNFA 10 ng O Activation of extrinsic pathway of apoptosis O Activation of intrinsic pathway of apoptosis Activation of executioner caspases Recruitment of adapter protein FADD to the TNF-alpha receptor LNCAP cell viability (% of control)