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.

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.

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter16: Gene Expression

Section: Chapter Questions

Problem 22RQ: Targeted therapies are used in patients with a set gene expression pattern. A targeted therapy that...

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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.
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 explanation: 19
Some autoimmune diseases show a positive correlation with dramatically decreased expression of histone deacetylase 9 (HDAC9, an enzyme that removes acetyl groups from histones). Why would the decreased expression of HDAC9 cause immune cells to produce inflammatory genes at inappropriate times?
Targeted therapies are used in patients with a set gene expression pattern. A targeted therapy that prevents the activation of the estrogen receptor in breast cancer would be beneficial to which type of patient? patients who express the EGFR receptor in normal cells patients with a mutation that inactivates the estrogen receptor patients with lots of the estrogen receptor expressed in their tumor patients that have no estrogen receptor expressed in their tumor
Which statements are true? Explain why or why not.1 In terms of the way it interacts with DNA, thehelix–loop–helix motif is more closely related to the leu-cine zipper motif than it is to the helix–turn–helix motif.2 Once cells have differentiated to their final spe-cialized forms, they never again alter expression of theirgenes.3 CG islands are thought to have arisen during evo-lution because they were associated with portions of thegenome that remained unmethylated in the germ line.4 In most differentiated tissues, daughter cells retaina memory of gene expression patterns that were presentin the parent cell through mechanisms that do not involvechanges in the sequence of their genomic DNA.
''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.'' Is this statement true? Explain why or why not.
Wilms tumor 1, or nephroblastoma, is caused by mutations in the WT1 gene, which encodes a transcription factor. You have identified a novel variant in WT1: Arg422Pro. You have control cells and cells that have been engineered to carry the homozygous WT1 p.Arg422Pro mutation. You want to assess effects of this mutation on a variety of endpoints. For each endpoint listed below, choose the one technique is best suited to answer the question. Choose from: array CGH, qRT-PCR, qPCR, RNA-seq, FISH, in situ hybridization, western blot, immunostaining, WT1 ChIP-seq, WT1 ChIP-PCR, ATAC-seq, 3C Endpoint Technique? WT1 protein amount (quantitative) Western blot WT1 protein binding to all enhancers, genome-wide Chip-seq WT1 mRNA amount (quantitative) WT1 protein subcellular localization Quantitative assessment of all mRNAs in these cells (genome-wide) RNAseq Chromatin interactions between a specific WT1 chromatin binding site (identified above)…
The PYK gene codes for the expression of pyruvate kinase, which is one of the enzymestargeted for anti-cancer drug design. You have identified an RNAi that targets the mRNAof PYK gene. To study the effect of the RNAi towards pyruvate kinase, the respected RNAiis expressed in Saccharomyces cerevisiae. The level of pyruvate kinase can be detectedwith a fluorescent antibody.(a). Predict the result that you will obtain in recombinant S. cerevisiae that expresses therespected RNAi.(b). Compare the result in Q3a(i) with the wild-type S. cerevisiae.
expand 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…
5) 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…
THE CHROMOSOMAL INSTABILITY PATHWAYS IN COLON CANCER Provide exmaples of genes give evidence
Describe the various post-translational modifications of HIF- 1alpha and how it affects the regulation of HIF-1al pha signaling. How might HIF- alpha alter the tumor microenvironment to promote tumor growth? Propose a strategy to prevent HIF-alpha signaling in the TME. What do you think would happen in a transgenic mouse with a total knockout of HIF-alpha?