Modern concepts of neoplasia rely on the evidence that a tumorarises from the clonal progeny of a single transformed cell.This ancestral cell of the neoplasm has multiple sites of acquired,and sometimes inherited, DNA damage that all its progeny share.During the early steps of carcinogenesis, there may be geneticalterations that lead to an intrinsic genetic instability, allowingadditional mutations to accumulate. These genetic changes conferselective advantages on the clone of tumor cells by disruptingthe regulation of cell proliferation. This mechanism permitsthe evolution of tumor-cell subclones and favors neoplasticprogression. The analysis of tumors . . . [Full Text of this Article]
Source Information
From the Department of Pathology, Baystate Medical Center, Springfield, MA 01199, where reprint requests should be addressed to Dr. Naber.
Segev, D. L., Saji, M., Phillips, G. S., Westra, W. H., Takiyama, Y., Piantadosi, S., Smallridge, R. C., Nishiyama, R. H., Udelsman, R., Zeiger, M. A.
(1998). Polymerase Chain Reaction-Based Microsatellite Polymorphism Analysis of Follicular and Hurthle Cell Neoplasms of the Thyroid. J. Clin. Endocrinol. Metab.
83: 2036-2042
[Abstract][Full Text]
Buer, J., Probst, M., Atzpodien, J., Puglisi, F., Naber, S. P.
(1995). Molecular Diagnosis of Neoplasms. NEJM
333: 193-194
[Full Text]
Previous
