Although numerous treatments are available for advanced hormone receptor- positive (HR+) and human epidermal growth factor receptor 2 negative (HER2-) breast cancers, they are rarely curable. Drugs such as palbociclib that inhibit cyclin-dependent kinase 4 and 6 (CDK4/6) are rapidly altering this therapeutic environment. Discuss the function of CDK4 and CDK6 in promoting cell growth as well as the overall effects of their inhibition by palbociclib on the progression of the cell cycle.
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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 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)Hereditary retinoblastoma generally affects children in both eyes, while spontaneous retinoblastoma usually occurs during adulthood only in one eye. Explain the genetic basis for the epidemiological distinction between these two forms of retinoblastoma. Explain the apparent paradox: loss-of-function mutations in tumor-suppressor genes act recessively, yet hereditary retinoblastoma is inherited as an autosomal dominant.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.
- Explain with specific examples how oncogenic receptors would promote cellular proliferation in the absence of external growth factorsdescribe the outcome of EGFR inhibition as well as the differences between erlotinib and panitumumab’s mechanisms of action. EGFR- driven cancer cells can become resistant to tyrosine kinase inhibitors. Explain the two types of EGFR blockade acquired resistance and propose a subsequent treatment option.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)
- Below are two cell signalling pathways that work together to regulate cell growth, proliferation and ultimately the size of organs in O.Extremus. In other closely related organisms, dysfunction of these pathways has been associated with tumor growth. mTOR pathway: 1. Growth factors bind and stimulate the receptors. 2. Receptors can activate the phosphatidylinositol 3 kinase (PI3K) – Akt signaling pathway. 3. The activated Akt, a serine threonine kinase, inhibits theTSC1–TSC2 complex, allowing Rheb to activate mTORC1. 4. In parallel, amino acids activate the mTORC1 pathway through a mechanism requiring the Rag– Ragulator complex. Hippo pathway: 1. The binding of the ligand activates the receptors which activate Mst and Lats. 2. YAP activity is modulated by phosphorylation of Mst and Lats. YAP upregulates miR-29, which in turn downregulates PTEN, an inhibitor of PI(3)K and Akt. So, the two pathways crosstalk and coordinate cell number and growth. a) What purpose does this forward…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?Describe the effects of the over-expression of mdm2 on cell proliferation and apoptosis on cell signaling pathways and metabolism or cell cycle control. Briefly explain the normal role of each component in the context of the pathway and why its loss or modification would have the expected effect.
- Drug A323 inhibits the activity of the cyclin-dependent kinase (CDK) - G1 cyclin complex. Consider possible effects of the drug on the cell cycle of normal and malignant cells. Predict what is likely to happen if the drug is added to the cell types described in A). Motivate your answers and describe the role of cycle-regulatory pathways that are relevant with respect to the action. of drug A323. A) Carcinoma cells in which both allels of the Rb gene carries loss of function mutation.Because of oxygen and nutrient requirements, cells in a tissue must reside within 100 μm of a blood vessel. Based on this information, explain why many malignant tumors often possess gain-of-function mutations in one of the following genes: βFGF, TGF-α, and VEGF.Plasma PDGF levels can be a diagnostic marker for severity and progression of breast cancer. The assay data below shows the plasma levels of PDGF in normal individuals, Stage II and Stage IV (More severe). You are treating a patient with breast cancer and assay indicates that their plasma PDGF level 6 fmoles/ 100 uL.Based on this info, in which stages has this patient's cancer progressed? Explain what process this patient's tumor has likely undergone and which cell types you would expect to now be associated with this tumor.