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- . The website CBioPortal (http://www.cbioportal.org)is an exceptionally useful program for visualizing thecancer genes and genomes of tumors from thousandsof patients with different kinds of cancer that havebeen analyzed by whole genome sequencing and insome cases, by RNA-Seq.Go the the CBioPortal site and click All underSelect Cancer Study and in Enter Gene Set typePTEN, then hit Submit. On the page that is returnedyou will see how the coding region of the PTEN geneis altered in tumors investigated in the various studies.Hitting the tab Mutations will let you see the detailsof these mutations relative to the PTEN protein, whilethe tab Expression lets you see how the gene’s expression (in terms of cDNA reads) is altered in individual tumor samples.a. Is PTEN an oncogene or a tumor suppressor gene?What kinds of evidence lead you to this conclusion?b. What kinds of cancer are most likely to involvealterations of PTEN?c. How would you identify patients whose tumorcells are particularly…Isothiocyanates arè compounds found in vegetables such as broccoli. Such compounds have been shown to induce the expression of proteins called caspases in cervical cancer cells. Outside of Cell Toxins DNA Damage p53 Apoptosis Inside of Cell Based on the above diagram, would you expect ingestion of broccoli to promote, suppress or have no effect on the progression or survival of cervical cancer cells? Promote progression of cervical cancer cells Suppress progression of cervical cancer cells O Have no effect on progression of cervical cancer cellsThis is a blank question. Thank you in advance, Bloom Syndrome Bloom syndrome is a rare genetic disorder. It is characterized by short stature and a long narrow face with prominent nose and ears. There is also increased sensitivity to light. People who have the disorder often develop rashes on their face, forearms, and hands when they have been exposed to the sun. In addition, these people often suffer from chronic obstructive pulmonary disorder (COPD) and have a higher chance of developing cancer. The cause of this genetic disorder is a mutation in the BLM gene located on chromosome 15. The immediate effect of this mutation is that there is a defect in the functioning of the DNA helicase enzyme. What would be the effect of this mutation on DNA replication? What stage of the cell cycle would be most affected?
- Genetic tests that detect mutations in the BRCA1 and BRCA2 tumor-suppressor genes are widely available. These tests reveal a number of mutations in these genes—mutations that have been linked to familial breast cancer. Assume that a young woman in a suspected breast cancer family takes the BRCA1 and BRCA2 genetic tests and receives negative results. That is, she does not test positive for the mutant alleles of BRCA1 or BRCA2. Can she consider herself free of risk for breast cancer?Relatively few inherited forms of cancer involve the inheritance of mutant oncogenes. Instead, most inherited forms of cancer are defects in tumor-suppressor genes. Give two or more reasons why inherited forms of cancer seldom involve activated oncogenes.6 of 16 Which gene would most likely be under inducible expression control? O A gene that encodes for a protein required for the electron transport pathway O A gene that encodes for a protein critical for assembly of the bacterial cell wall A gene that encodes for a subunit of the RNA polymerase holoenzyme A gene that encodes for a protein that is produced in response to oxidative stress A gene that encodes for a component of a bacterial flagellar assembly
- 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.1. Describe which enzymes are required for lactose and tryptophan metabolism in bacteria when lactose and tryptophan, respectively, are (a) present and (b) absent. 2. Contrast positive versus negative regulation of gene expression. Describe the role of the repressor in an inducible system and in a repressible system.THE CHROMOSOMAL INSTABILITY PATHWAYS IN COLON CANCER Provide exmaples of genes give evidence
- The chemical carcinogen dimethybenzialanthracene (DMBA) must be an extraordinarily specific mutagen since 90% of the skin tumors it causes have an A-to-Talteration at exactly the same site in the mutant Ras gene is true or false1. Cancer genetics Breast cancers can be divided into several classes. One type of breast cancer, classified as HER2 positive ("HER2+"), represents 15-20% of breast cancers. Most HER2+ cancers arise due to amplification of the HER2 gene (without any mutation of the HER2 protein coding region). HER2 amplification is also associated with several other types of cancer (e.g. stomach cancer). Would the HER2 gene be considered a proto-oncogene or a tumor suppressor gene? Justify your answer based on the function of the HER2 protein (look it up). b. How does amplification of HER2 promote cancer? c. Some HER2+ cancers have become resistant to the antibody drug. These cells were found to have mutations of the PTEN gene (look for information about the PTEN gene). Are these likely to be recessive loss of function mutations or dominant gain of function mutations of PTEN? Justify your answer, relating PTEN mutations to drug resistance.5. Please discuss the effect of epigenetic posttranslational modifications on cancer development according to the reading article week 10. Would you think that epigenetic posttranslational modifications could be used as potential therapeutic cancer agents?