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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 Moore’s 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 Moore’s 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 1990—n years after the case began—the 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?
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Chapter 15 Solutions
Human Heredity: Principles and Issues (MindTap Course List)
- The Adaptive Immune Response Is a Specific Defense Against Infection Researchers have been having a difficult time developing a vaccine against a certain pathogenic virus as a result of the lack of a weakened strain. They turn to you because of your wide knowledge of recombinant DNA technology and the immune system. How could you vaccinate someone against the virus, using a cloned gene from the virus that encodes a cell-surface protein?arrow_forwardWhy are the proteins called p53 and Ras studied so much these days?arrow_forwardYes or no? reverse genetics is RNA interference example. cellular differentiation potency in multipotent is greater than pluripotent stem cell. does digoxigenin UTO use to make dsrna and perform rna interference?arrow_forward
- DO NOT COPY IN GOOGLE OR IN BARTLEBY QUESTION: - Why is TP53 called the Guardian of the genome?arrow_forwardWhy does a muscle cell express a different set of genies compared to a white blood cell? Why do cells show changes Gene Expression in response to changing environmental Conditions? Which types Genes in our skin cells would be activated in response to Sunburn?arrow_forwardCan you please help me by drawing a serie of schematic figures that demonstrates the information in the paragraph below. The carboxy terminus of the p53 protein acts as an allosteric regulator of sequence-specific DNA binding. This was demonstrated initially by Hupp et al. (1992) using a bacterially expressed protein. Recombinant bacterial p53 bound poorly to DNA, and binding could be enhanced by the addition of antibodies specific to the C-terminal region of the protein. Phosphorylation of Ser315 and Ser392 within this domain also enhance sequence-specific DNA binding. Dephosphorylation of Ser376 of p53 after IR allows the association of 14-3-3 proteins with the C terminus of the protein (Waterman et al., 1998). Stavridi et al. (2001) demonstrate that this interaction is required for p53 to activate the downstream gene, p21waf1/cip1, and for the G1 cell cycle checkpoint arrest response. Interestingly, this dephosphorylation event seems to be ATM-dependent, possibly by a phosphatase…arrow_forward
- As the most junior member of a lab, you are tasked with generating cell lines that accumulate DNA damage to investigate how random mutations affect transformation of cells into cancer cells. You decide to mutate proteins in the p53 pathway. Which three proteins would you mutate? Explain your reasoning.arrow_forwardAre all pluripotent stem cells created equal, however?arrow_forwardcan you please help me out with this ? Mutations in the IL2RG gene cause approximately 30 percent of severe combined immunodeficiency disorder (SCID) cases in humans. These mutations result in alterations to a protein component of cytokine receptors that are essential for proper development of the immune system. The IL2RG gene is composed of eight exons and contains upstream and downstream sequences that are necessary for proper transcription and translation. Below are some of the mutations observed. For each, explain its likely influence on the IL2RG gene product (assume its length to be 375 amino acids). Nonsense mutation in a coding region Insertion in Exon 1, causing frameshift Insertion in Exon 7, causing frameshift Missense mutation Deletion in Exon 2, causing frameshift Deletion in Exon 2, in frame (g) Large deletion covering Exons 2 and 3arrow_forward
- Yes or no? is siRNA result of activity of argonaut? Does RNAi result permanently heritable in expression of genes? Does northern blotting use to detect the expression of a transcription in multiple tissues?arrow_forwardTrue or False? LINE elements encode functional transposition protein and thus can move autonomously in the human genome. True or False? Target-primed reverse transcription can mobilize information through an RNA intermediate.arrow_forwardGENETICS QUESTION!! Imagine that you are a geneticist at a hospital and you are given a file for a patient whose family has a history of cancer. The patient, John Doe, is 18 years old and has had a biopsy done on a tumorous growth in his adrenal gland. He has a sister, Jane, and a brother, Bob, who are younger than he is and who are both healthy. His mother, Betty, has a diagnosis of breast cancer. John’s father, Joe, and John’s paternal grandparents have no history of cancer. Betty is one of four children. Her brother, Tom, and sister, Lucy, have never had cancer or signs of cancer. Both Tom and Lucy are older than Betty. Betty had another brother, Jake, who died very young of leukaemia. Tom has monozygotic twin daughters who are healthy. Betty’s father, Don, died of soft tissue sarcoma in his thirties. Betty’s mother is alive and healthy. Betty’s paternal grandmother, Don’s mother, died of a brain tumor in her thirties. Don had no siblings. As part of your research, you also consult…arrow_forward
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