Mammalian cells have a limitless replicative potential. During carcinogenesis, the cancer cell is not eradicated by the body's immune system. A breast cancer patient treated with Trastuzumab shows no benefits suggesting that the cancer is caused by HER- 2 receptors.
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- Q20. Dr. Rose Lees is a world expert on breast cancer. Choose True or False. Of all the receptors involved, the HER2+ has a worse [ Choose ] prognosis. [ Choose ] BRCA1 helps repair damaged DNA, or destroy cells if DNA cannot be repaired. True False The nuclear hormone receptors contain a DNA binding domain towards the C-terminus. [Choose] The nuclear hormone receptors contain a ligand binding domain toward the C-terminus. [ Choose] The main function of the estrogen receptor is as a DNA binding transcription factor. [ Choose ] The last a-helix, helix 12, folds into a groove on the side of the structure upon ligand binding. [Choose ] Upon binding of tamoxifen to the estrogen receptor, helix 12 exposes the coactivator-binding site. [ Choose ] >Q25. Choose True or False Mammalian cells have a limitless replicative potential. [Choose ] [Choose ] During carcinogenesis, the cancer cell is not eradicated by the body's immune system. False True A breast cancer patient treated with Trastuzumab shows no benefits suggesting that the cancer is caused by HER- [Choose ] 2 receptors. An inactive precursor of an enzyme is referred to as a [Choose ] zymogen. CAR T-Cell Therapy employs the use of T-cells because [Choose] they have memory. Maintenance of blood pressure is not a basic function of the lymphatic system. [Choose ] Fluids squeezed out of blood vessels describes the origin [Choose ] and composition of lymph. A covalent bond is formed between the receptor and the [Choose ] growth factor. >If a cell developed a mutation in its MAP2K1 gene (encodes the MEK protein) that prevented MIEK from being recognized by phosphatases, how would the EGFR signaling cascade and the cell’s behavior change?
- How does PKC’s signaling role change in response to growth factor signaling versus an immune response? PKC interacts directly with signaling molecules in both cascades, but only exhibits kinase activity during growth factor signaling. PKC interacts directly with signaling molecules in growth factor cascades, but interacts with signaling inhibitors during immune signaling. PKC amplifies growth factor cascades, but turns off immune cascades. PKC is activated during growth factor cascades, but is inactivated during immune response cascades.Which statements are true? Explain why or why not.1 The chemical carcinogen dimethylbenz[a]anthra-cene (DMBA) must be an extraordinarily specific mutagensince 90% of the skin tumors it causes have an A-to-T alter-ation at exactly the same site in the mutant Ras gene.2 In the cellular regulatory pathways that controlcell growth and proliferation, the products of oncogenesare stimulatory components and the products of tumorsuppressor genes are inhibitory components.3 Cancer therapies directed solely at killing the rap-idly dividing cells that make up the bulk of a tumor areunlikely to eliminate the cancer from many patients.4 The main environmental causes of cancer are theproducts of our highly industrialized way of life such aspollution and food additives.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)
- 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.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…True or False? p21 inhibits the S-cyclin/S-Cdk complex.
- em 92 of 145 Z 92. During an experiment, a researcher inactivates the fibroblast growth factor receptor gene expressed on grandiosa celih Which of the folog A) Absence of androgen production B) Formation of tumors from thecal cells C) Inhibition of formation of the follicular antrum D) Premature ovulation E) Transformation of thecal cells into granulosa cellsexpand this into 1000 words. the context is Identification of Differentially Expressed Genes in Breast Cancer Using RNA-Seq "In investigating the impact of TONSL overexpression on cellular physiology and gene regulation, differential expression analysis emerges as a pivotal analytical approach. By comparing gene expression profiles between primary cells and TONSL-overexpressing cells, researchers can identify genes whose expression levels are significantly altered. This analysis not only sheds light on the direct targets of TONSL but also unveils broader regulatory networks and pathways influenced by TONSL overexpression. Moreover, by pinpointing key genes involved, researchers can discern potential molecular mechanisms underlying the observed phenotypic changes associated with TONSL overexpression, offering valuable insights into TONSL's role in cellular homeostasis and function. Furthermore, functional enrichment analysis stands as a complementary approach to understanding the…Need help Intaractions of FAK kinase which directly depend on the tyrosine residue 397 (Y397) are inhibbited by a chemical compound in cancercells. Intaraction of FAK kinase with what proteins are blocked by this inhibition? (please give a listt of them all, and that's it)