Mutational signatures of p53 are shown in this image (G.P. Pfeifer et al., Nature, 21(48), 2002) for the three types of cancer with the highest death rates in the United States: lung (~225,000 deaths in 2016), breast (246,000), and colorectal (381,000). These data can be obtained by sequencing the gene that encodes p53. Approximately 85 percent of lung cancers occur in smokers. Based on these data, calculate how many deaths due to lung cancer among nonsmokers were reported in 2016
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- Li- Fraumeni Syndrome (LFS) is a rare hereditary cancer disease due to a mutation in the TP53 gene. Propose a treatment strategy for LFS.The P63 and P53 have similar functionalities in the cell, however, p53 is rarely associated directly with p63, suggesting that p63 may indirectly act as an oncogene by blocking p53 function. This hypothesis may also explain why p63 is associated with other indications of misinterpretation. I do understand the above statement, however once piece not clear – why would p63 block p53 function? Have these genes been shown to have opposing functions? From the background information provided above, it seems like they would have seminar functions. Explain."Changes to the p53 protein structure can be caused by differences in DNA and can affect protein function." Can you give detailed explanation why this is causation and not correlation? The explanation should be related with mutation, structure changes during protein synthesis, chemical property changes in amino acids, and functions of p53 protein.
- MM, a 54-year old female presents to the Family Medicine Clinic due to a 2-week history of increasing shortness of breath and cough and mild/moderate pain in left side. She was diagnosed with infiltrating intraductal adenocarcinoma of the left breast 5 years ago; at that time, ER(-)/ PR(-); her-2/neu(+); p53(+); staged as having T3N1M0, stage IIIA, high-risk breast cancer. She underwent a modified radical mastectomy with axillary node dissection followed by 6 cycles of CMF chemotherapy. Her mother and sister also had a history of breast cancer. Past Medical History Gravida 4, para 4; menses onset age 13; HTN x 10 years; Type 2 DM x 8 years; breast CA described above; remained disease free until present follow up. Past Surgical History: Left modified radical mastectomy 5 years ago; cholecystectomy 14 years ago. Medications: Glyburide, 5mg PO BID Verapamil SR, 240mg PO daily Furosemide, 40mg PO daily Allergies: NKDA Physical Examination: GEN: Well-developed, obese woman in no…In Metastatic Breast Cancer [such as in Breast Invasive Ductal Carcinoma; Breast Invasive Carcinoma, NOS; Breast Invasive Cancer, NOS; Invasive Breast Carcinoma; Breast Invasive Lobular Carcinoma; Breast Mixed Ductal and Lobular Carcinoma] what role does the genes Tp53 and Tp63 have? Would one of them affect the other (i.e. mutation, etc) or there is not relationship among the two genes at all.Describe the nature of p53 reactivation as acancer-fighting strategy
- Equalizing the Expression of X Chromosome Genes in Males and Females Males have only one X chromosome and therefore only one copy of all genes on the X chromosome. Each gene is directly expressed, thus providing the basis of hemizygosity in males. Females have two X chromosomes, but one is always inactivated. Therefore, females, like males, have only one functional copy of all the genes on the X chromosome. Again, each gene must be directly expressed. Why, then, are females not considered hemizygous, and why are they not afflicted with sex-linked recessive diseases as often as males are?Who Owns Your Genome? John Moore, an engineer working on the Alaska oil pipeline, was diagnosed in the mid-1970s with a rare and fatal form of cancer known as hairy cell leukemia. This disease causes overproduction of one type of white blood cell known as a T lymphocyte. Moore went to the UCLA Medical Center for treatment and was examined by Dr. David Golde, who recommended that Moores spleen be removed in an attempt to slow down or stop the cancer. For the next 8 years, John Moore returned to UCLA for checkups. Unknown to Moore, Dr. Golde and his research assistant applied for and received a patent on a cell line and products of that cell line derived from Moores spleen. The cell line, named Mo, produced a protein that stimulates the growth of two types of blood cells that are important in identifying and killing cancer cells. Arrangements were made with Genetics Institute, a small start-up company, and then Sandoz Pharmaceuticals, to develop the cell line and produce the growth-stimulating protein. Moore found out about the cell line and its related patents and filed suit to claim ownership of his cells and asked for a share of the profits derived from the sale of the cells or products from the cells. Eventually, the case went through three courts, and in July 1990n years after the case beganthe California Supreme Court ruled that patients such as John Moore do not have property rights over any cells or tissues removed from their bodies that are used later to develop drugs or other commercial products. This case was the first in the nation to establish a legal precedent for the commercial development and use of human tissue. The National Organ Transplant Act of 1984 prevents the sale of human organs. Current laws allow the sale of human tissues and cells but do not define ownership interests of donors. Questions originally raised in the Moore case remain largely unresolved in laws and public policy. These questions are being raised in many other cases as well. Who owns fetal and adult stem-cell lines established from donors, and who has ownership of and a commercial interest in diagnostic tests developed through cell and tissue donations by affected individuals? Who benefits from new genetic technologies based on molecules, cells, or tissues contributed by patients? Are these financial, medical, and ethical benefits being distributed fairly? What can be done to ensure that risks and benefits are distributed in an equitable manner? Gaps between technology, laws, and public policy developed with the advent of recombinant DNA technology in the 1970s, and in the intervening decades, those gaps have not been closed. These controversies are likely to continue as new developments in technology continue to outpace social consensus about their use. Should the physicians at UCLA have told Mr. Moore that his cells and its products were being commercially developed?Who Owns Your Genome? John Moore, an engineer working on the Alaska oil pipeline, was diagnosed in the mid-1970s with a rare and fatal form of cancer known as hairy cell leukemia. This disease causes overproduction of one type of white blood cell known as a T lymphocyte. Moore went to the UCLA Medical Center for treatment and was examined by Dr. David Golde, who recommended that Moores spleen be removed in an attempt to slow down or stop the cancer. For the next 8 years, John Moore returned to UCLA for checkups. Unknown to Moore, Dr. Golde and his research assistant applied for and received a patent on a cell line and products of that cell line derived from Moores spleen. The cell line, named Mo, produced a protein that stimulates the growth of two types of blood cells that are important in identifying and killing cancer cells. Arrangements were made with Genetics Institute, a small start-up company, and then Sandoz Pharmaceuticals, to develop the cell line and produce the growth-stimulating protein. Moore found out about the cell line and its related patents and filed suit to claim ownership of his cells and asked for a share of the profits derived from the sale of the cells or products from the cells. Eventually, the case went through three courts, and in July 1990n years after the case beganthe California Supreme Court ruled that patients such as John Moore do not have property rights over any cells or tissues removed from their bodies that are used later to develop drugs or other commercial products. This case was the first in the nation to establish a legal precedent for the commercial development and use of human tissue. The National Organ Transplant Act of 1984 prevents the sale of human organs. Current laws allow the sale of human tissues and cells but do not define ownership interests of donors. Questions originally raised in the Moore case remain largely unresolved in laws and public policy. These questions are being raised in many other cases as well. Who owns fetal and adult stem-cell lines established from donors, and who has ownership of and a commercial interest in diagnostic tests developed through cell and tissue donations by affected individuals? Who benefits from new genetic technologies based on molecules, cells, or tissues contributed by patients? Are these financial, medical, and ethical benefits being distributed fairly? What can be done to ensure that risks and benefits are distributed in an equitable manner? Gaps between technology, laws, and public policy developed with the advent of recombinant DNA technology in the 1970s, and in the intervening decades, those gaps have not been closed. These controversies are likely to continue as new developments in technology continue to outpace social consensus about their use. Do you think that donors or patients who provide cells and/or tissues should retain ownership of their body parts or should share in any financial benefits that might derive from their use in research or commercial applications?
- List the regulatory mechanisms that might be lost in a cell producing faulty p53.Equalizing the Expression of X Chromosome Genes in Males and Females Individuals with an XXY genotype are sterile males. If one X is inactivated early in embryogenesis, the genotype of the individual effectively becomes XY. Why will this individual not develop as a normal male?Changes in epigenetic modifications alter the accessibility and transcription of DNA. Describe how environmental stimuli, such as ultraviolet light exposure, could modify gene expression.