You are studying cancer progression in mice. Your results show the following pathway in which two proteins play important roles in how mouse cell division is regulated. nutrients cell division Prot 1 Prot 2 You isolate a mutant strain of mice that have a Prot 1 mutation (Prot 1-). These mutant mice frequently develop cancer as young adults. Which of the following can you conclude from these observations? Select all that apply Prot 1- mutation can be classified as dominant Prot 1 can be classified as a proto-oncogene Prot 1- mutation can be classified as recessive Prot 1 can be classified as a tumor suppressor gene

You are studying cancer progression in mice. Your results show the following pathway in which two proteins play important roles in how mouse cell division is regulated. nutrients cell division Prot 1 Prot 2 You isolate a mutant strain of mice that have a Prot 1 mutation (Prot 1-). These mutant mice frequently develop cancer as young adults. Which of the following can you conclude from these observations? Select all that apply Prot 1- mutation can be classified as dominant Prot 1 can be classified as a proto-oncogene Prot 1- mutation can be classified as recessive Prot 1 can be classified as a tumor suppressor gene

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter8: The Structure, Replication, And Chromosomal Organization Of Dna

Section8.4: The Watson-crick Model Of Dna Structure

Problem 2GR

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You are studying cancer progression in mice. Your results show the following pathway in which two proteins play important roles in how mouse cell division is regulated. nutrients cell division Prot 1 Prot 2 You isolate a mutant strain of mice that have a Prot 1 mutation (Prot 1-). These mutant mice frequently develop cancer as young adults. You isolate a mutant strain of mice that have a Prot 2 mutation (Prot 2-). These mutant mice frequently develop cancer as young adults. Which of the following can you conclude from these observations? Select all that apply O Function of wild-type Prot 2 is to promote cell division when nutrients are present Function of wild-type Prot 2 is to promote cell division when nutrients are absent Function of wild-type Prot 1 is to inhibit cell'division when nutrients are absent Function of wild-type Prot 1 is to inhibit cell division when nutrients are present
Tumor-suppressor genes are normal human genes that prevent uncontrollable cell growth. Starting with a normal laboratory humancell line, describe how you could use transposon tagging to identifytumor-suppressor genes. (Note: When a TE hops into a tumorsuppressorgene, it may cause uncontrolled cell growth. This is detected as a large clump of cells among a normal monolayer of cells.)
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)…
Tumor suppressor genes and oncogenes are implicated in carcinogenesis. However, one can predict whether a gene potentially encodes for a protein that influences carcinogenesis by examining their mutational profile. You sequence the genome of 4 cancers and identify 3 genes of interest. Which of the following genes has the best potential to an oncogene? Tumor 1 Tumor 2 Tumor 3 Tumor 4 Gene A S24F, N465T R33T T345S, G366R P367E, P368Y Gene B S34R, F360I S34R V254I S34E, T67Y Gene C S24F, I322E C255I, E344D S34E, P367E
Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings. Please sort as a list.
Below are data from Jimenez et al (2022) depicting cellular expression patterns of the tumor suppressor transcription factor p53 (a gene commonly mutated in cancers). They explored oscillating expression patterns found in a mutated human cell line. Panel D shows measurements of changes in p53 mRNA levels measured using two different approaches; figure E shows measurements of protein levels from the same samples. The numbers on either side indicate the observed fold change (FC) in relative abundance of these molecules (note that any difference in values obtained between the two methods are not relevant for this question). Answer part b as pictured in the question
One hallmark of cancer cells is their ability to divideindefinitely, in contrast with most normal somaticcells that undergo senescence after 30 to 50 generations of divisions. We saw in this chapter that one reason for this difference is that many cancer cellsexpress the telomerase enzyme that can mediate telomere lengthening.Interestingly, about 15% of tumors do not expresstelomerase. Instead, they lengthen their telomeres byan alternative pathway. Tumor cells of this class appear to have telomeres that are highly heterogenous inlength; some telomeres have many more TTAGGGrepeats than others.a. Diagram an event involving homologous recombination that would allow some telomeres in thesecells to become longer. What feature(s) of telomeresmake(s) such homologous recombination possible?b. Does this recombination need to occur between homologous telomeres (that is, telomeres of the samearm of the same chromosome)? If such recombination could occur between nonhomologous telomeres, how might…
Why is it important to model cancer through the generation of induced pluripotent stem cells ? Explain in detail the main findings.
A current focus of molecular medicine is to trigger or promote apoptosis of specific cells. several components of the apoptotic pathways are being targeted using this approach. for each of the following, state specifically how the treatment would be expected to stimulate or inhbit apoptosis. b. exposing cells to recombinant TRAIL protein, a ligand for thr tumor necrosis factor family of receptors
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.
Two genes associated with breast cancer, BRCA1 and BRCA2, were discovered in 1994 and 1995, respectively, and shortly thereafter, were patented by Myriad Genetics, a company based in Utah. Under the patents, testing for mutations in these genes could only be performed by Myriad, at costs from 300 to 3,000. Myriad also patented the process of analyzing the results of such tests, preventing anyone who obtains the sequence of their BRCA genes by other means (which itself would probably be patent infringement) from interpreting the information. The idea that genes can be patented has been a contentious issue from the beginning. Patents are not granted for products of nature, meaning that genes inside the body are not patentable, but biotech companies successfully argued that by removing a gene from the human body, purifying it, and then obtaining its DNA sequence, they created something not found in nature, and which is therefore a patentable invention. The U.S. Patent Office found the argument persuasive, but opponents argue that genes are parts of our bodies and can be identified but not invented. Biotech companies argue that without the protection offered by patents, they would have no incentive for research and development of diagnostic tests. In Europe, patents for BRCA1 and BRCA2 were revoked in 2004 because they did not meet the standards for a patent. After more than a decade of legal disputes, the patents were partially restored in 2008 on a very restricted basis. In the United States, a lawsuit, focused on the patents for the BRCA genes, was filed in May 2009. The suit challenges the basic idea that genes are patentable. In November 2009, the judge ruled that the lawsuit can proceed, and the case is moving forward. In March 2010, a federal court invalidated Myriad Genetics patent on these genes. In August 2011, the U.S. Court of Appeals reversed the lower courts decision and ruled that gene sequences isolated from cells are not a product of nature and are therefore patentable. The case went to the U.S. Supreme Court, which ordered the appeals court to reconsider the case. The Federal Appeals Court did not change its decision, and the case once again, went to the U.S. Supreme Court. A unanimous decision in June 2013 invalidated Myriads patents on the basis that isolating a gene from nature does not make it patentable. This is a landmark decision on gene patenting with widespread ramifications for the biotechnoloogy industry. Will this decision reduce the incentives for companies to invest in new diagnostic tests that would be used by cancer victims or those with serious genetic disorders?
Like Hurler syndrome, Fabry disease involves an abnormal accumulationof substances within lysosomes. However, the lysosomesof individuals with Fabry disease show an abnormal accumulationof lipids. The defective enzyme is α-galactosidase A, which is alysosomal enzyme that functions in lipid metabolism. The enzymaticdefect causes cell damage, especially to the kidneys, heart,and eyes. The gene that encodes α-galactosidase A is found on theX chromosome. Let’s suppose a phenotypically unaffected coupleproduces two sons with Fabry disease and one phenotypicallyunaffected daughter. What is the probability that the daughter willhave an affected son?