TNF-alpha treatment of prostate carcinoma, LNCAP cells decreases cell survival asshown in the graph below.Which of the following would you observe in these cells treated with TNF-alpha? Select all that applyTNF-a12010080 -6040200.2472(hrs)Control+ TNF-a 100 ngTNFA 10 ngO Activation of extrinsic pathway of apoptosisO Activation of intrinsic pathway of apoptosisActivation of executioner caspasesRecruitment of adapter protein FADD to the TNF-alpha receptorLNCAP cell viability (% of control)

* TNF inhibitors are the drugs helps to prevent inflammation to grow which are used to to treat…

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 - 24 72 (hrs) • Control - TNF-a 10 ng + TNF-a 100ng 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)

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 - 24 72 (hrs) • Control - TNF-a 10 ng + TNF-a 100ng 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)

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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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 - 24 72 (hrs) + Control - TNF-a 10ng + TNF-a 100 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)
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.
All but which of the following best explains the advantage of cancer cells expressing PKM2 over PKM1? OPKM1 has lower activity PKM2 allows for accumulation of glycolytic intermediates Serine is a more potent allosteric effector of PKM2 Higher serine levels lead to increased activity of PKM2 O O
1 of 16 Data from an experiment is shown in the figure below. In the experiment, murine cells were treated with a specific a ligand that activates receptor R. In some cases, the cells were exposed to one of two drugs (X or Y) as well as the ligand or were left untreated (UT). After 30 minutes of treatment, the cells were lysed with a detergent-based buffer to release the soluble membrane, cyosolic and nuclear proteins. Samples from each cell extract were run (in duplicate) by SDS-PAGE (SDS-polyacrylamide gel electrophoresis) in order to separate the proteins by molecular mass (size). The separated proteins were then transferred to a nitrocellulose membrane which was then probed with different antibodies in a western blotting procedure to detect specific phosphorylated proteins or total proteins. If present in the cell extract, these proteins appear as a dark band in the relevant western blot image within the figure. Drug X Drug Y UT Ligand Ligand Ligand Western blotting antibodies…
PDGF 100 PI3K 740 751 PI3K 50 - GAP O771 O GAP PTP P 1009 O PTP protein P-site 1 12 4 5. 6. 7. PI3K 740, 751+ 1021 GAP 771 +] +] PTP 1009 PLC PLCy PLCT 1021 When activated by ligand binding, the PDGF (platelet-derived growth factor) receptor becomes phosphorylated on 5 tyrosine residues (left figure). These phosphorylated tyrosines serve as binding sites for proteins that contain SH2 domains (SH2 domains bind phosphorylated Y). These proteins include phospholipase C-gamma (PLC-gamma), a phosphotyrosine phosphatase (PTP), a Ras GTPase-Activating Protein (GAP), and a phosphotidylinositol 3-Kinase (PI3K). PDGF stimulates several changes in the target cell, one of which is DNA synthesis. To determine which effectors of the PDGF receptor is/are responsible for stimulating DNA synthesis, you construct several mutant forms of the receptor that retain individual or combinations of the phosphorylation sites. You express these in cells and monitor DNA synthesi The results are shown in the right…
Discuss the advantages and disadvantages of general chemotherapy like Etoposide compared to specific inhibition of EGFR.
Consider the following simplifieddiagram of a signal transductionpathway that regulatesprogrammed cell death inmammalian cells. Assume that thisdiagram represents the behavior ofa single cell within an organism.Key: TNF and SF are circulatingin the plasma; TNFR = TNFreceptor; SFR = SF receptor.Based on the regulatory networkdescribed above, state whethermutations that knockout each ofthe following proteins would either increase apoptosis or decrease apoptosis. TNF Bcl2 INH EFF SFR AKT TNFR SF
1. Basic of signal tranduction pathway in cancer disease 2. Specific of cellular response and organismal response in cancer disease.
Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.
A scientist observes a mutation in the transmembrane region of EGFR that eliminates its ability to be stabilized by binding interactions during dimerization after ligand binding. Which hypothesis regarding the effect of this mutation on EGF signaling is most likely to be correct? EGF signaling cascades would be active for longer in the cell. EGF signaling cascades would be active for a shorter period of time in the cell. EGF signaling cascades would not occur. EGF signaling would be unaffected.
Chemotherapeutic agents can promote apoptosis in cancer cells by these mechanisms except; Group of answer choices Downregulating MCL1 expression Increasing BCL-2 expression Increased p53 expression Increased BIM (BH-3) expression
which of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTP