In a patient with a constitutively active receptor tyrosine kinase that increases the activity of PI3K, the administration of a drug that increases PTEN expression will likely inhibit tumorigenesis because; Group of answer choices PTEN prevents growth factor binding to RTK PTEN competitively inhibits the catalytic subunit of PI3K

In a patient with a constitutively active receptor tyrosine kinase that increases the activity of PI3K, the administration of a drug that increases PTEN expression will likely inhibit tumorigenesis because; Group of answer choices PTEN prevents growth factor binding to RTK PTEN competitively inhibits the catalytic subunit of PI3K

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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Which of the following statements are correct about cytoplasmic signaling in cancer cells? Multiple answers. A. Only minor modifications of cell control machinery are required for normal cells to become highly proliferating cancer cells B. Immediate early genes are induced in the presence of protein synthesis inhibitors C. Many immediate -early genes are oncogenes D. Delayed early genes are highly expressed in the presence of protein synthesis inhibitors E. Delayed early genes are highly expressed in normal cells in the absence of growth factors
You are looking at the results of a western blot from the lysates of cells harvested from a suspected breast cancer tumor and you see that there is an increased expression of INK4-p16, you suspect that this will______________? Group of answer choices Increase S to G2 phase transition Initiate a cell cycle arrest in G1 Block M to G1 phase transition Promote tumorigenesis
Cell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.
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 of the following defects in RAS would be tumorigenic? multiple answers A. Deletion of nucleotide binding domain B. Inactivation of Guanine Exchange Factor (GEF) C. Mutation at amino acid 61 that prevents hydrolysis of bound GTP D. Inactivation of GTPase Protein (GAPS) E. Mutation that prevents binding of GTP
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
Studies suggest that the presence of oncogenic Ras is not sufficient to drive tumorigenesis. Instead, the activity of Ras needs to be amplified and sustained to induce pathological consequences. Recent studies have suggested a role for inflammatory stimuli on tumor development in the context of oncogenic Ras. Is the presence of oncogenic Ras necessary for transient inflammatory stimulation to induce chronic pathologies (such as cancer) OR is chronic inflammation essential for oncogenic Ras to induce tumorigenesis?
TGF-β1 is a protein that affects cell growth and differentiation. Scientists conducted an experiment where epithelial cells were treated with transforming growth factor beta 1 (TGF-β1) in the laboratory. At the end of the experiment, the epithelial cells had transformed through several stages from epithelial cells to embryonic stem cells (ESCs) to neural progenitor cells (NPCs), and finally to cortical neurons (CNs). The scientists observed the transformation of the cells by analyzing gene expression at certain stages (M1-M7) and determined the relative gene expression level, as shown in the graph. The graph shows the relative gene expression level for cells at different stages of differentiation. Which of the following claims could account for the differences in gene expression at each stage of cell differentiation, and how does this correlate with the distance of the genes on the chromosome? A - Cell differentiation is controlled by RNA translation, but there is no…
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
Which of the following associated with cancer development would you expect to be tumor promoters and not genotoxic carcinogens (select all that apply)? A. Excessive alcohol consumption that kills liver cells B. Bisphenol A which mimics the activity of estrogen C. Chemical in pesticides that binds and activates a transcription factor that cause activation of NFkB D. Chemical in cigarette smoke that forms adduct with DNA E. A viral infection that causes ulcerative coilitis of GI tract
Tumor cells from a person with leukemia have been analyzed to determine which oncogene is involved in the transformation. After partial sequencing of the gene, the predicted gene product is identified as a tyrosine kinase. Which of the following proteins would most likely be encoded by an oncogene and exhibit tyrosine kinase activity? A. Nuclear transcriptional activator B. Epidermal growth factor C. Membrane-associated G protein D. Platelet-derived growth factor E. Growth factor receptor
1. VHL is a tumor suppressor because a. it causes cancer cells to become hypoxic b. it inhibits the enzyme proline hydroxylase c. it promotes the degradation of a powerful transcription factor. d. in the absence of VHL, HIF-1 is ubiquitylated by proline hydroxylase 2. NF-1 is a tumor suppressor because A. it inactivates Ras by promoting the hydrolysis of GTP to GDP B. it promotes the methylation of the Ras gene promoter C. it is a phosphatase that dephosphorylates the kinases in the Ras effector pathways D. it inhibits the GEF (guanine exchange factor) that activates Ras please answer both question cause this is my last posting question thank you