In many breast cancers, ER (alpha) activation by estrogens is generally considered responsible for enhanced proliferation, whereas that is counteracted by the presence of ER (beta),which exerts an antiproliferative effect. Please devise a strategy targeting both receptors for the treatment of this disease.
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In many breast cancers, ER (alpha) activation by estrogens is generally considered responsible for enhanced proliferation, whereas that is counteracted by the presence of ER (beta),which exerts an antiproliferative effect. Please devise a strategy targeting both receptors for the treatment of this disease.
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- Can I get help on creating a concept map for the Introduction provided below? The development of a multicellular organ (such as the brain) from stem cells involves complicated processing.1,2 Proliferating stem cells undergo the fate decision process before developing into tissues or organs. This process is controlled and regulated by a signaling pathway network (called gene regulatory network).3 The network comprises pathways created by the intrinsic and extrinsic factors of the cells, which form the signal transduction to control stem cell fate. There are various signal pathways that have been discovered and studied for tissue development and patterning, including Wnt signaling,4 Notch, and receptor tyrosine kinase.5–7 It has been suggested that cross-regulatory interactions between elements of the pathways (e.g., Wnt and Notch) affect the process of cell fate assignment.8,9 Most components of Wnt signaling have multiple interactions with other signaling pathways (e.g., Hippo/YAP and…Mutations in the BRCA genes have been shown to be related to a higher incidence of breast cancer in humans, and genetic tests are available that enable women to discover whether they carry versions of the gene associated with high risk. However, even early detection of breast cancer does not guarantee a cure. What considerations can you think of for and against advising women to take the tests? ·1. Match each of the terms in the left column to the bestfitting phrase from the right column.a. epistatic interaction 1. divide the body into identical units(segments)b. regulative 2. initiated by binding of ligand todetermination receptorc. modifier screen 3. individuals with cells of more thanone genotyped. RNAi 4. the fate of early embryonic cells canbe altered by the environmente. ectopic expression 5. assign identity to body segmentsf. homeodomain 6. substance whose concentrationdetermines cell fatesg. green fluorescent 7. suppression of gene expression byprotein double-stranded RNAh. genetic mosaics 8. method for identifying pleiotropicgenesi. segmentation genes 9. a DNA-binding motif found incertain transcription factorsj. homeotic genes 10. encode proteins that accumulate inunfertilized eggs and are needed forembryo developmentk. morphogen 11. double mutant has phenotype of oneof the two mutantsl. maternal effect 12. a gene is turned on in an inappropriategenes tissue or at…
- Hello! Discuss the onco-suppressive function of xenophagy + ( role of adaptors, compare and contrast evidence, opinion about the way forward for the field). Thank you!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?Briefly explain the role of genetic testing and the following inherited gene mutations linked to breast cancer: ATM BRCA1andBRCA2 BRIP 1 CDH1 CHEK2 PALB2 PTEN STK11 TP53
- • How does the hormone get from its secretory gland to its target tissue? • Are steroid hormones hydrophobic or hydrophilic? • How are steroid hormones transported to target tissues? • When the steroid hormone binds to the nuclear receptor it dimerizes and binds to HRES? What are the HRES? When the NR dimer binds to HRES how does it effect gene transcription? Serum binding protein with bound hormone Hormone Altered cell function New protein 4 DNA 2 HRE mRNA Plasma membrane Figure 12-30 Lehninger Principles of Biochemistry, Seventh Edition 2017 W. H. Freeman and Company Cytosol 1 translation on ribosomes Nucleus Nuclear receptor RNA polymerase transcription 3 Gene 2 Hormone, carried to the target tissue on serum binding proteins, diffuses across the plasma membrane and binds to its specific receptor protein in the nucleus. 4 Hormone binding changes the conformation of the receptor; it forms homo- or heterodimers with other hormone-receptor complexes and binds to specific regulatory…This is one given problem on my homework assignment for developmental biology. Thank you for the help!Describe the effects of FGF and RA on each other in limb bud development. Give a specific example of their effects on each other in this capacity. Knowing this, propose a question/hypothesis to investigate the mechanism of how a specific morphogen controls pattern if you know that the morphogen is both necessary and sufficient AND is expressed in the correct spatial/temporal frame.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.)
- 14 of 16 Which experimental technique would be useful in determining whether a particular chemical signal is a paracrine signal or not? Observation of the behaviour of single cells O Gene expression analysis Analysis of blood from nearby capillaries Chemical analysis of the signal molecule Analysis of extracellular fluid from the tissue in question5) Briefly explain why the formation of a tumour can pose a risk to a person's homeostasis. 6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug "vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief…You are given a project to characterize the effect of mutation on two newly discovered G protein coupled-receptors, GPCR-UCI and GPCR-UC2, both of which bind to the same ligand. For the cell signalling assay, you have the UMR-106 cell line that expresses both GPCR-UC1, CPCR- UC2, the corresponding G proteins, and adenyl-cyclase. A basal adenylyl cyclase activity, and thus, a baseline cAMP concentration, is detected in the cell line. (i) You found that, upon binding to the ligand, the mutation in GPCR-UC1 results in increased CAMP level but the mutation in GPCR-UC2 results in a low cAMP concentration. Based on these results, identify the subclass of G protein isoforms that the GPCRs activate. Explain your answer. (ii) If the mutation affects the G protein from GDP release, how would this affect the CAMP production after ligand binding? Explain your answer.