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Chapter 25 : Human Molecular Genetics

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Human Molecular Genetics, Page 1 of 2

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Abstract:

Human genetics works the same way as dog genetics in terms of chromosomes, genes, enzymes, and other proteins. There are two basic approaches to learning about human genetics. In the classic approach, geneticists do what can only be described as detective work. First, a condition that seems to be inherited must be recognized. This chapter discusses many of the genes that work in dogs and experimental animals, like mice and fruit flies, because people have bred them for generations and created pure breeds that differ very little in genetic makeup from one individual to another. Proto-oncogenes are normal, essential parts of our genetic material that belong to the group of genes in charge of causing and regulating cell growth and division. It is actually changes in these genes that can lead to the development of cancer. Oncogenes are abnormal forms of proto-oncogenes. The most common oncogene in human cancers is . Genetic analysis of families with hereditary cancer and individual cancer patients is helping us identify additional genetic loci associated with cancer development. So far, the genetic picture of most common cancers looks very complicated, and no clear interpretation is available. It is clear that cancer is actually many diseases. It is also clear that different sets of mutations can cause similar cancers.

Citation: Kreuzer H, Massey A. 2008. Human Molecular Genetics, p 250-263. In Molecular Biology and Biotechnology: A Guide for Students, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817480_ch25

Key Concept Ranking

UV-Induced DNA Damage
0.4749008
DNA Synthesis
0.4489075
Chronic Myeloid Leukemia
0.4261917
DNA Damage and Repair
0.4196818
0.4749008
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Figures

Image of Figure 25.1
Figure 25.1

Pigment production from tyrosine.

Citation: Kreuzer H, Massey A. 2008. Human Molecular Genetics, p 250-263. In Molecular Biology and Biotechnology: A Guide for Students, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817480_ch25
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Image of Figure 25.2
Figure 25.2

The PH enzyme converts the amino acid phenylalanine into the amino acid tyrosine.

Citation: Kreuzer H, Massey A. 2008. Human Molecular Genetics, p 250-263. In Molecular Biology and Biotechnology: A Guide for Students, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817480_ch25
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Image of Figure 25.3
Figure 25.3

(A) Red blood cells (magnification, ×4,600). (Photograph copyright M. Bessir-D. Fawcett/Visuals Unlimited.) (B) Sickle-cell anemia. (Photograph copyright Science VU/Visuals Unlimited.). (C) Normal and sickled red blood cells (magnification, ×943). (Photograph copyright George J. Wilder/Visuals Unlimited.)

Citation: Kreuzer H, Massey A. 2008. Human Molecular Genetics, p 250-263. In Molecular Biology and Biotechnology: A Guide for Students, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817480_ch25
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Download as Powerpoint
Image of Figure 25.4
Figure 25.4

Electrophoresis of hemoglobin from a normal individual (lane A), from an individual with sicklecell anemia (lane B), and from an individual with sicklecell trait (lane C).

Citation: Kreuzer H, Massey A. 2008. Human Molecular Genetics, p 250-263. In Molecular Biology and Biotechnology: A Guide for Students, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817480_ch25
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Image of Figure 25.5
Figure 25.5

Extracellular growth signals are relayed to the cell nucleus via a series of protein-protein interactions, beginning at the cell membrane. The change in shape triggered by a growth factor binding to its receptor initiates a cascade of changes in associated proteins, resulting in a signal being transmitted to the nucleus.

Citation: Kreuzer H, Massey A. 2008. Human Molecular Genetics, p 250-263. In Molecular Biology and Biotechnology: A Guide for Students, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817480_ch25
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Image of Figure 25.6
Figure 25.6

The cell division cycle. The stages were named for what could be seen under the light microscope. G stands for gap, because no visible activity was occurring; S signifies DNA synthesis; and M stands for mitosis. Most nondividing cells are in G1. Together, G1, S, and G2 constitute interphase.

Citation: Kreuzer H, Massey A. 2008. Human Molecular Genetics, p 250-263. In Molecular Biology and Biotechnology: A Guide for Students, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817480_ch25
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References

/content/book/10.1128/9781555817480.chap25
1. Cancer special issue. 1996. Scientific American 275(3). This issue contains articles on how cancer arises and spreads, new therapies, genetic testing for cancer genes, and more.
2. Cavenee, W. K.,, and R. L. White. 1995. Genes and cancer. Scientific American 272(3):7279.
3. Greider, C.,, and E. Blackburn. 1996. Telomeres, telomerase, and cancer. Scientific American 274(2):92.
4. Pasternak, J. 1999. An Introduction to Human Molecular Genetics . Fitzgerald Scientific Press, Bethesda, MD.
5. Perera, F. 1996. Uncovering new clues to cancer risk. Scientific American274(5):54.

Tables

Generic image for table
Table 25.1

Some cancer genes and the physiological roles of their products

Citation: Kreuzer H, Massey A. 2008. Human Molecular Genetics, p 250-263. In Molecular Biology and Biotechnology: A Guide for Students, Third Edition. ASM Press, Washington, DC. doi: 10.1128/9781555817480_ch25

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