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It is now clearly recognized that a large variety of human cancers (including many solid tumors) display recurring chromosome abnormalities. However, what is the biologic significance of these findings? How do these chromosomal changes relate to changes in expression of important growth regulatory genes, e.g., cellular oncogenes? What clinical significance, if any, do specific cytogenetic abnormalities have, particularly for solid tumors, in which they are often found against a background of other genetic alterations? These and other related questions have received a significant amount of attention over the past 5 years. In general, it appears that recurring sites of chromosome change may indeed represent the byproduct of molecular events, which themselves may participate in the generation or progression of human cancers. Our recognition and ultimately our molecular understanding of chromosome abnormalities will unquestionably provide further insights into neoplasms generally and solid tumors particularly. The diversity of structural chromosome alterations across the spectrum of human cancers is enormous and increasing rapidly. Information on cancer-associated chromosome alterations is currently accumulating at a rate in excess of 2,000 new cases per year, with well over 15,000 cases of chromosome abnormalities in cancers now reported in the literature (7,2). Recent attempts of a special committee (2) to summarize this immense amount of technical information has resulted in the identification of 149 nonrandom chromosome changes involving 43 types of neoplastic disorders, including now many benign proliferations (2). These changes include a plethora of genomic alterations including deletions, translocations, isochromosomes, insertions, inversions, etc. Taken together, every human chromosome except the Y can now be included in some form of neoplasia-associated alteration. With the explosion in our knowledge base of human chro

Clinical Correlations of Chromosome Change in Human Solid Tumors: The Tip of the Iceberg?