Chemical basis of heredity, the genetic code

New York University School of Medicine Department of Biochemistry New York U.S.A.
Bulletin of the New York Academy of Medicine 06/1964; 40(2):387-411. DOI: 10.1007/BF02151242
Source: PubMed
261 Reads
  • Source
    CA A Cancer Journal for Clinicians 01/1965; 15(1):2-13. DOI:10.3322/canjclin.15.1.2 · 115.84 Impact Factor
  • Progress in Biophysics and Molecular Biology 02/1966; 16:191-240. DOI:10.1016/0079-6107(66)90007-1 · 2.27 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Summary Human neoplasia is a heterogenous group of diseases, and hence it is not unexpected that the karyotypic findings in cancer and leukemia are protean in nature. The chromosomal constitu tions in these conditions ranges from diploidy, impressive hypo- diploidy, to high hyperploidy. Except for chronic myelocytic leukemia, no consistent karyotypic picture has emerged for any group of cancer or leukemia. As a matter of fact, no 2 similar karyotypes have been found in human cancer (primary and metastatic). These findings coupled with the high frequency of diploidy in acute leukemia indicate that gross genomic aberra tions cannot be imputed as being involved in the direct causation of neoplasia. The Ph1chromosome in chronic myelocytic leukemia appears to be the only plausible case for the direct participation of a chromosomal abnormality in the causation of a cancerous state. Even though the possibility exists that submicroscopic gene involvement may induce gross chromosomal changes, the latter leading to the initiation of cancer or leukemia, it is more likely (at least in the author's mind) that the chromosomal abnormalities in these diseases described to date are secondary phenomena to the neoplastic state. Thus, the escape of the can cerous cell from normal growth controls is due to genie malfunc tion and the karyotypic changes are mere epiphenomena of the metabolic parameters resulting from the abnormal growth. Future studies on isolated human normal and abnormal chromo somes, ultrastructural and metabolic, may shed considerable light on the role of genomic changes in cancer causation. Presently held concepts ascribe to malfunctioning DNA a direct and obligatory role in the causation of cancer. The changed function of DNA may not be necessarily accompanied by dis cernible structural changes in chromosomes. The contribution of gross chromosomal changes to the direct causation of cancer has been a subject of debate and controversy for over half a century, and a number of erudite and comprehensive papers dealing with various facets of the problem have appeared re cently (6, 14, 15, 24, 27, 28, 38). That not all gross chromosomal aberrations lead to neoplasia is evident from the infrequent oc currence of cancer in the rather frequently encountered aneuploidy in human subjects. Until the human genome is com pletely, or even partially, mapped (an almost forbidding, formi dable, and herculean genetic task), we are obliged to evaluate the role of genomic malfunction in oncogeny as it is reflected in grossly microscopic chromosome changes. Hence, the major aim of this paper will be to reflect on the nature of karyotypic changes 1Supported in part by Grants T-182from the American Cancer Society, Inc., and CA-08204from the National Cancer Institute. in human cancer and leukemia and to evaluate the chromosomal deviation as participants in the direct causation of human neo plasia.
    Cancer Research 10/1966; 26(9):2064-81. · 9.33 Impact Factor
Show more


261 Reads
Available from