Genes, fragile sites, chromosomal translocations, and cancer in aging

Jacqueline Whang-Peng, E. Lee, C. S. Kao-Shan, R. Boccia, T. Knutsen

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Use of cell synchronization techniques has allowed high resolution analysis of chromosomes and made it possible to show that the majority of tumors have cytogenetic abnormalities. Many non-random chromosomal abnormalities, both numerical and structural, have been correlated with specific neoplasms. Recently a remarkable concordance between the chromosomal location of human cellular oncogenes and breakpoints involved in various forms of cancer has been demonstrated. These chromosomal abnormalities may arise as a result of the action of specific agents on heritable or constitutional fragile sites. In a study of chromosome aberrations and fragile sites in different age groups, we have shown that there are significant increases in the degree of hypodiploidy and both minor and major aberrations with increasing age. In our study of fragile sites, we found increasing expression of breakpoints with increasing age, although the frequency of breaks at oncogene, c-fra, h-fra sites, and on the X chromosome did not change. The most common site of chromosome breakage occurred at 3p14.2, followed by breaks at lq21.3, 7q32.3, and llq13.3. These four sites are at or near known cancer break sites. The consequence of chromosome rearrangement is unknown, but may cause a change in a constitutional gene, cause a translocation of an oncogene, an alteration in gene dosage, or even activation of a normally quiescent oncogene which may lead to malignant transformation.
Original languageEnglish
Title of host publicationInterrelationship Among Aging, Cancer and Differentiation
Pages233-243
Publication statusPublished - 1985
Externally publishedYes

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Genetic Translocation
Oncogenes
Chromosome Aberrations
Genes
Chromosome Fragile Sites
Neoplasms
Chromosomes
Chromosome Breakage
Gene Dosage
X Chromosome
Age Groups

Cite this

Whang-Peng, J., Lee, E., Kao-Shan, C. S., Boccia, R., & Knutsen, T. (1985). Genes, fragile sites, chromosomal translocations, and cancer in aging. In Interrelationship Among Aging, Cancer and Differentiation (pp. 233-243)

Genes, fragile sites, chromosomal translocations, and cancer in aging. / Whang-Peng, Jacqueline; Lee, E.; Kao-Shan, C. S.; Boccia, R.; Knutsen, T.

Interrelationship Among Aging, Cancer and Differentiation. 1985. p. 233-243.

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Whang-Peng, J, Lee, E, Kao-Shan, CS, Boccia, R & Knutsen, T 1985, Genes, fragile sites, chromosomal translocations, and cancer in aging. in Interrelationship Among Aging, Cancer and Differentiation. pp. 233-243.
Whang-Peng J, Lee E, Kao-Shan CS, Boccia R, Knutsen T. Genes, fragile sites, chromosomal translocations, and cancer in aging. In Interrelationship Among Aging, Cancer and Differentiation. 1985. p. 233-243
Whang-Peng, Jacqueline ; Lee, E. ; Kao-Shan, C. S. ; Boccia, R. ; Knutsen, T. / Genes, fragile sites, chromosomal translocations, and cancer in aging. Interrelationship Among Aging, Cancer and Differentiation. 1985. pp. 233-243
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AU - Knutsen, T.

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N2 - Use of cell synchronization techniques has allowed high resolution analysis of chromosomes and made it possible to show that the majority of tumors have cytogenetic abnormalities. Many non-random chromosomal abnormalities, both numerical and structural, have been correlated with specific neoplasms. Recently a remarkable concordance between the chromosomal location of human cellular oncogenes and breakpoints involved in various forms of cancer has been demonstrated. These chromosomal abnormalities may arise as a result of the action of specific agents on heritable or constitutional fragile sites. In a study of chromosome aberrations and fragile sites in different age groups, we have shown that there are significant increases in the degree of hypodiploidy and both minor and major aberrations with increasing age. In our study of fragile sites, we found increasing expression of breakpoints with increasing age, although the frequency of breaks at oncogene, c-fra, h-fra sites, and on the X chromosome did not change. The most common site of chromosome breakage occurred at 3p14.2, followed by breaks at lq21.3, 7q32.3, and llq13.3. These four sites are at or near known cancer break sites. The consequence of chromosome rearrangement is unknown, but may cause a change in a constitutional gene, cause a translocation of an oncogene, an alteration in gene dosage, or even activation of a normally quiescent oncogene which may lead to malignant transformation.

AB - Use of cell synchronization techniques has allowed high resolution analysis of chromosomes and made it possible to show that the majority of tumors have cytogenetic abnormalities. Many non-random chromosomal abnormalities, both numerical and structural, have been correlated with specific neoplasms. Recently a remarkable concordance between the chromosomal location of human cellular oncogenes and breakpoints involved in various forms of cancer has been demonstrated. These chromosomal abnormalities may arise as a result of the action of specific agents on heritable or constitutional fragile sites. In a study of chromosome aberrations and fragile sites in different age groups, we have shown that there are significant increases in the degree of hypodiploidy and both minor and major aberrations with increasing age. In our study of fragile sites, we found increasing expression of breakpoints with increasing age, although the frequency of breaks at oncogene, c-fra, h-fra sites, and on the X chromosome did not change. The most common site of chromosome breakage occurred at 3p14.2, followed by breaks at lq21.3, 7q32.3, and llq13.3. These four sites are at or near known cancer break sites. The consequence of chromosome rearrangement is unknown, but may cause a change in a constitutional gene, cause a translocation of an oncogene, an alteration in gene dosage, or even activation of a normally quiescent oncogene which may lead to malignant transformation.

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