with Nonpolyposis colorectal cancer and his biopsy pathology report reveals a defect in some TSGs involved in DNA mismatch repair, which of these genes is least likely to be implicated in this patients cancer? Group of answer choices SMAD4 MSH2 MLH1 PMS1
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- how do i expand this into 1000 words The objective is to interpret the results of an RNA-Seq analysis to identify differentially expressed genes in breast cancer using figure 1. The data provided includes gene symbols, chromosome location, start and end points, strand, fold change, log2 fold change, p-value, and false discovery rate (FDR). The RNA-Seq analysis has identified several genes that are differentially expressed in breast cancer. These genes are located on various chromosomes and have varying levels of fold change, indicating the degree to which their expression levels differ between normal and cancerous cells. The gene with the highest fold change is EYA4, located on chromosome 6, with a fold change of 3604.4176. This indicates that the expression of this gene is over 3600 times higher in cancer cells compared to normal cells. The log2 fold change is 11.81555, which is a measure of the magnitude of the difference in gene expression. The p-value for this gene is extremely low…You are in charge of a new gene therapy clinic. Two cases have been referred to you for review and possible therapy. Case 1. A mutation in the promoter of a proto-oncogene causes the gene to make too much of its normal product, a receptor protein that promotes cell division. The uncontrolled cell division has caused cancer. Case 2. A mutation in an exon of a tumor-suppressor gene makes this gene nonfunctional. The product of this gene normally suppresses cell division. The mutant gene cannot suppress cell division, and this has led to cancer. What treatment options can you suggest for each case?Describe the progression of cancer from an early benign lesion to a genetically heterogeneous malignant tumour and how this knowledge is used to design current and future antineoplastic treatments can you please give this in maximum detail as i am trying to understand this in extensive detail
- This is homework not a test! From NTSA case study https://static.nsta.org/case_study_docs/case_studies/cystic_fibrosis.pdf Please help with questions 2, 3 and 4 of part four 2. "The successful use of gene therapy to cure SCID syndrome (2000) is hoped to be a permanent cure for those patients because a good copy of the problem gene was inserted into the patients' blood stem cells in the bone marrow (hematopoietic stem cells). Once white blood cells enter the blood stream they have a limited life span, on the order of a few week to months. The blood stem cells are the cells that create more white blood cells to replace those that are lost. If the gene was only inserted into the circulating mature white blood cells, the patient would only be temporarily cured until those cells were used up or died." The current gene therapy approaches to cure CF involve inserting a functional CFTR gene into the mature epithelial cells of the lungs. In light of the preceding paragraph, do you think that…hi, can I please get help on a case study on nueroanatomy I have been struggling for a couple of hours now and can't seem to understand the study to answer the following questions. is there any way or format that i can get help. I would really appreciate it. thanks! 1. Based on the information in the case, what is the most likely neuroanatomic location for a single lesion that can explain all of the patient’s symptoms and signs? In your own words, explain how you arrived at that localization. 2.What are some possibilities for the nature of the lesion (e.g., stroke, tumor, trauma, etc.)? In your own words, explain your rationale for these options. 3. How does the laboratory data and neuroimaging demonstrate the actual lesion for the patient? Describe how you interpret the data in your own words. 4.How was the patient was treated, and how did they subsequently fare? Describe the treatment plan in your own words.how do i expand this into 1000 words The methodology employed to identify differentially expressed genes (DEGs) in breast cancer using RNA-Seq data involves several systematic steps integrating data retrieval, analysis, normalization, DEG identification, and functional annotation. Initially, raw RNA-Seq data is retrieved from the NCBI GEO database, specifically from dataset GSE216238 (Nakshatri, 2023), which encompasses samples from both breast cancer and normal tissue. Subsequently, the raw data was imported into Excel for initial analysis, leveraging its widespread availability and user-friendly interface. Gene expression data for breast cancer analysis was obtained from the Gene Expression Omnibus (GEO) database. The GEO homepage (https://www.ncbi.nlm.nih.gov/geo/) was accessed, and the "Query & Browse" tab was selected. Advanced Search: Under "Search GEO DataSets," an advanced search was conducted (https://www.ncbi.nlm.nih.gov/gds/advanced). Keywords "breast" and "cancer" were…
- Answer and explain your choice to the following multiple-choice questions about cancer-promoting mutations. The ABC gene undergoes multiple gene duplication events, producing multiple copies of this gene in the genome. This gene duplication event is associated with cancer. What would best describe the normal function of ABC gene? Inhibit cell growth and division Oncogene Inhibit apoptosis Metabolic enzyme EXPLAIN in 1-2 sentences: A mutation in the epidermal growth factor receptor (EGFR) causes it to send a positive signal along its intracellular signaling pathway, even without the EGF ligand bound to it. Knowing the function of a growth factor, how would you classify this mutation? an activating mutation in a tumor suppressor gene an activating mutation in a proto-oncogene a loss of function mutation in a tumor suppressor gene a loss of function mutation in a proto-oncogene EXPLAIN in 1-2 sentences: In an otherwise normal cell, what would be the immediate result of a…Which of the following effectively describes the situation of someone with an inherited predisposition to cancer such a familial adenomatous polyposis or BRCA-associated familial breast cancer? Choose all that apply Group of answer choices None of the other answers effectively describes the situation If they get malignant cancer, somatic mutations will not have been a factor Their cancer will most likely arise in their germ cells, not their somatic cells Most cells in their body contain multiple cancer-causing mutations Every cell of their body contains a gain-of-function allele of an oncogene Every cell of their body contains a defective, loss-of-function allele of a tumor suppressor gene134 LABORATORY MANUAL IN HUMAN HISTOLOGY ells U23T RAIUDBAL Size of the Cells Shape of the Nucleus Degree of Chromatin Condensation Presence or Absence of Nucleoli CE 1215) 1-XXI Blood Cells Cytoplasmic Staining Presence of Cytoplasmic Granules Bone Marrow Cell 29 3000 va 010 Na Y
- Discussion: (1 or 2 paragraphs with your own opinion like how Circulating Tumor DNA as Biomarkers for Cancer Detection technology can be early detector of cancer)Hello! My question is: Discuss the evidence used to establish the causal association between virus infection and cancer. How can this knowledge be used in the diagnosis, treatment and prevention of virus-associated tumours? Thank you!!!! Mr. Yeboah, diagnosed with a malignant tumour of the liver had it removed and was given a course of chemotherapy. Initially, tumour marker (AFP) activity activity was 7500KU/L (which is very high) but after treatment, this gradually declined to only 5KU/L. A routine follow up test was perfomedafter 3 months and the results was 15KU/L for AFP. The doctor suspected a relapse of the tumour and so referred Mr. Yeboahto an oncologist at a cancer centre who also did a re-check. AFP was recorded to be 5KU/L. Enquiries revealed that the hospital and the cancer centre use different instruments for the measurement of AFP. Both results are normal even though the values are significantly different because different methods were used.a) How can both labs confirm that the results are not clinically significant? b) How can both labs avoid this happening again?