Genetics: From Genes to Genomes
6th Edition
ISBN: 9781259700903
Author: Leland Hartwell Dr., Michael L. Goldberg Professor Dr., Janice Fischer, Leroy Hood Dr.
Publisher: McGraw-Hill Education
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Chapter 20, Problem 7P
B cells are specialized blood cells that secrete antibodies. Normally, human blood has millions of different types of B cells making millions of different kinds of antibody molecules. This variety occurs because, as described in the Fast Forward Box in Chapter 13 entitled Programmed DNA Rearrangements and the Immune System, antibody genes undergo rearrangements in the precursors of B cells. Individual B cell precursors rearrange their antibody genes in different ways.
In the blood of patients with cancers called B cell lymphomas, almost all of the antibody molecules are all of one type, but this single type of antibody is different in different lymphoma patients.
| a. | Based on this information, provide a brief description of the genesis of B cell lymphomas, focusing on the cells that are overproliferating. |
| b. | How does the nature of B cell lymphomas provide support for the clonal theory of cancer shown in Fig. 20.6? |
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Chapter 20 Solutions
Genetics: From Genes to Genomes
Ch. 20 - For each of the terms in the left column, choose...Ch. 20 - Characterize the differences between tumor cells...Ch. 20 - Prob. 3PCh. 20 - Prob. 4PCh. 20 - A carcinogenic compound is placed on the skin of...Ch. 20 - You have decided to study genetic factors...Ch. 20 - B cells are specialized blood cells that secrete...Ch. 20 - Molecules outside and inside the cell regulate the...Ch. 20 - Put the following steps in the correct ordered...Ch. 20 - a. Would you expect a cell to continue or to stop...
Ch. 20 - Two different protein complexes called SCF and APC...Ch. 20 - One of the hallmarks of mitotic anaphase is the...Ch. 20 - Concerning the Tools of Genetics Box Analysis of...Ch. 20 - Are genome and karyotype instabilities...Ch. 20 - Prob. 15PCh. 20 - Why dont all loss-of-function mutations that are...Ch. 20 - Chromothripsis is a rare phenomenon, first...Ch. 20 - The chromosome 9/22 translocation associated with...Ch. 20 - A female patient 19 years old, whose symptoms are...Ch. 20 - Prob. 20PCh. 20 - A generic signaling cascade is shown in the...Ch. 20 - Neurofibromatosis type 1 NF1; also known as von...Ch. 20 - Families with germ-line BRCA1 or BRCA2...Ch. 20 - The text explained that retroviruses can cause...Ch. 20 - Hepatocellular carcinoma is the most frequent form...Ch. 20 - Suppose that instead of microarrays, you analyzed...Ch. 20 - Prob. 27PCh. 20 - Glioblastoma multiforme GBM is the most common and...Ch. 20 - a. The legend to Fig. 20.29 identifies which of...Ch. 20 - The website CBioPortal http://www.cbioportal.org...
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- The Adaptive Immune Response Is a Specific Defense Against Infection In cystic fibrosis gene therapy, scientists propose the use of viral vectors to deliver normal genes to cells in the lungs. What immunological risks are involved in this procedure?arrow_forwardWho 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?arrow_forwardWho 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?arrow_forward
- Monoclonal antibodies are produced by immunizing a mouse with a particular antigen, then removing its spleen. Individual B cells producing mouse antibodies specific for the antigen are isolated from the spleen, then fused with cancer cells. Each of the resulting hybrid cells can be cloned, which means it can be cultured indefinitely in the laboratory. The resulting cell lines produce and secrete antibodies that recognize the antigen to which the mouse was immunized. These antibodies are called monoclonal antibodies. Some monoclonal antibodies are used for passive immunization. They are effective, but only in the immediate term. Antibodies that are produced by one’s own immune system can last up to about six months in the bloodstream, but those delivered in passive immunization often last for less than a week. Why the difference?arrow_forwardAtaxia-telangiectasis (ATM) is a rare genetic neurodegenerative disease. About 20% of people with ATM develop acute lymphocytic leukemia or lymphoma, cancers of the immune-system cells. Cells in many of these cancers exhibit chromosome rearrangements, with chromosome breaks occurring at antibody and T-cell-receptor genes (A. L. Bredemeyer et al. 2006. Nature 442:466–470). Many people with ATM also have a weakened immune system, which makes them susceptible to respiratory infections. Research has shown that the locus that causes ATM has a role in the repair of double-strand breaks. Explain why people who have a genetic defect in the repair of doublestrand breaks might have a high incidence of chromosome rearrangements in their immune-system cells and why their immune systems might be weakened.arrow_forwardWhen a mixture of different IgG antibody proteins are treated with the enzyme papain, each antibody is cleaved into three roughly equal size fragments. From each original antibody, two of the three fragments are identical to each other, and represent the ‘arms’ of the antibody ‘Y’. These fragments are known as Fab fragments. The third fragment is known as the Fc region, because this fragment will crystallize when purified. The reason a mixture of Fc fragments will crystallize is because: It is the only part of the antibody protein that can easily be purified at the high concentrations needed for crystallization. It has no disulfide bonds holding the domains together, as disulfide bonds will inhibit crystallization. It is the only fragment of the antibody that still has disulfide bonds, so it remains intact during the crystallization process. The Fc fragments of IgG are much more water soluble than the Fab fragments. All Fc fragments generated from a mixture of IgG molecules have the…arrow_forward
- Over time, cancer cells are known to produce weakly antigenic variants of cell surface proteins. This will result in ----. protection of cells from the immune system increase in cancer cell death by the immune system Neither A nor B. It will make no difference. Therapeutic antibodies used in the treatment of cancer are targeted at proteins located On the cell surface of cancer cells. On the cell surface of normal cells. In the nucleus of cancer cells. In the cytoplasm of cancer cells. C and D.arrow_forwardA wild-type mouse that is heterozygous for two immunoglobulin heavy chain alleles (IgHa/b) generates the population of B cells shown on the left of the figure below. A mouse strain, also IgHa/b, carries an inactivating mutation in the VpreB gene. In addition to producing fewer mature B cells than the wild-type mice, the VpreB-deficient mice generate B cells as shown on the right. What is the explanation of the difference seen between the wild-type and the VpreB-mutant B cells?arrow_forwardMice and humans with inactivating mutations in the gene encoding activation-induced cytidine deaminase (AID) have an immunodeficiency disease known as 'hyper IgM type 2'. Since AID is the enzyme that catalyzes the conversion of cytosines in the DNA to uracils, thereby initiating the process of somatic hypermutation, why do individuals with this deficiency only produce IgM antibodies?arrow_forward
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