You established two cell lines (Cell line X and Cell line Y) from colon cancer patients and both of them can proliferate without the Wnt ligand. When you analyze the tumor suppressor APC (Adenomatous Polyposis Coli) protein in these lines, X does not express functional APC but Y expresses functional APC. How can Y keep proliferating without Wnt? Which function (protein) within the Wnt signaling pathway might be defective in Y?
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- 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.Aberrant signaling through the EGF receptor signal transduction pathway drives many forms of breast cancer, while misregulation of PI3K drives many prostate cancers. PI3K is one of MANY downstream effectors of EGF receptor signaling, and there are several known activating mutations of PI3K. Would a small molecule that targets PI3K be an effective treatment for a breast cancer that is driven by aberrant signaling through the EGF receptor? Briefly explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY IN ABOUT EIGHT WORDS.)What is the most likely outcome is we lose the tumor suppressor proteins, cyclin- dependent kinase inhibitors. Select one: o a. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will not proceed. o b. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will not proceed. o c. Cyclin-cylin dependent kinase complex will not phosphorylate retinoblastoma protein and cell-cycle will proceed. o d. Cyclin-cylin dependent kinases will phosphorylate retinoblastoma protein and cell- cycle will proceed.
- A temperature-sensitive mutant yeast strain stops dividing when shifted from 25°C to 37°C. These cells are analyzed at different temperatures by a machine that measures the amount of DNA they contain, and the following graphs are obtained. number of cells number of cells [ Select] [Select] [Select] 25°C [Select] مل Cells in G1 phase should have [Select] Which of the following would explain the behavior of your mutant? Mark yes or no for each of the following choices. 2 amount of DNA/cell (arbitrary units) 37°C 1 2 amount of DNA/cell (arbitrary units) unit(s) amount of DNA. ✓ Inability to initiate DNA replication Defect in chromosome condensation ✓Defect in centrosome duplication ✓Defect in cytokinesisThe Human papillomavirus (HPV) has been linked to an increased risk of cervical cancer. The HPV E6 and E7 proteins govern the cell via altering cellular proteins. The E6 protein interacts with the tumor suppressor protein p53 and directs its ubiquitin-mediated destruction. Can you elaborate about the P63 gene: its function and if it can be altered/mutated by HPV? If it does, what is the relationship between P53 and P63? Thank you!One important role of Fas and Fas ligand is to medi-ate the elimination of tumor cells by killer lymphocytes.In a study of 35 primary lung and colon tumors, half thetumors were found to have amplified and overexpressed agene for a secreted protein that binds to Fas ligand. How doyou suppose that overexpression of this protein might con-tribute to the survival of these tumor cells? Explain yourreasoning.
- A tumor cannot grow to be very large without the development of new blood vessels (angiogenesis) to provide access to oxygen and nutrients. During the 1990s, it was discovered that Factor X stimulates the proliferation and migration of the cells that form blood vessels, thereby inducing the formation of new blood vessels. Factor X binds to specific receptor tyrosine kinases (RTKs) on the cell surface and causes the RTKs to dimerize and become active, initiating an intracellular signaling cascade that stimulates cell division and inhibits apoptosis. Many cancer cells secrete high levels of Factor X, and increased Factor X expression in a tumor is correlated with a poor medical outcome for the patient. Some evidence suggests that blocking Factor X-dependent signaling may prevent the formation of new blood vessels and lead to the death of immature blood vessels without disturbing mature blood vessels. You work for a biotechnology company that seeks to create anticancer drugs that…A growth factor Fsh3 stimulates the proliferation of culture fish cells. The receptor that binds Fsh3 is a receptor tyrosine kinase (RTK) and there are numerous fish tumor cell lines that have a mutation for the gen for this receptor. Which of the following mutations would be expected to promote uncontrolled cell proliferation. a mutation that inactivates the protein tyrosine phosphatase that acts on the receptor a mutation that prevents the binding of the normal extracellular signal to the receptor a mutation that inhibits the Ras GEF a mutation that destroys the kinase activity of the receptor a mutation that prevents dimerization of the receptorwhich 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
- 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.One important role of Fas and Fas ligand is to mediate the elimination of tumor cells by killer lymphocytes. In a study of 35 primary lung and colon tumors, half the tumors were found to have amplified and overexpressed a gene for a secreted protein that binds to Fas ligand. How do you suppose that overexpression of this protein might contribute to the survival of these tumor cells? Explain your reasoning.TLRs activate NFkB, AP-1, and IRF transcription factors to induce the expression of inflammatory cytokines and type I interferons. A key feature of TLR signaling is the ability to induce inflammatory cytokine gene expression extremely rapidly following TLR stimulation. This is accomplished by signaling pathways using several mechanisms to activate transcription factors that are already present in the cell prior to TLR stimulation, but are kept in an inactive state. These signaling pathways use all of the following mechanisms EXCEPT: Induced ubiquitination leading to protein degradation Induced ubiquitination inducing protein–protein interactions Induced phosphorylation leading to nuclear translocation Induced phosphorylation leading to kinase activation Induced phosphorylation preventing protein degradation