The study of tumour resistance to anticancer drugs has been the subject of many publications since the initial discovery of the phenomenon by J. H. Burchenal and colleagues in 1950. Many papers have been published since then reporting development of resistance to most of the well-known anticancer agents in many different animal tumour systems, both in vivo and in vitro. Many different mechanisms of resistance have been described, and it is clear that the tumour cell has a wide diversity of options in overcoming the cell-killing activity of these agents. Definition of the magnitude of the phenomenon in the clinic is, however, much more problematical, and it is with this in mind that the initial chapter, seeks to out line the problem as the clinicians see it. It appears that the phenomenon of true resistance to a drug, as the biochemist would recognise it, is an important cause of the failure which clinicians experience in treating the disease. The extent of the contribution of this phenomenon to the failure of treatment cannot easily be evaluated at the present time, but it is hoped that the development and application of new and more sophisticated techniques for the analysis of cellular sub populations may help to give a more exact estimate and to shed some light on the causes of failure of many of the present therapeutic techniques."

Chromosome abnormalities of cancer cells have been recognized for a long time, and have generally proven to be a highly specific marker ofmalignancy. The contri- butions collected in this book, "Tumor Aneuploidy", cover several major aspects of present knowledge conceming the occurrence and clinical significance of chromo- some abnormalities as delineated by karyotype analyses or measurements of the cellular DNA content. Certain non-random clonal chromosome losses, deletions and translocations ap- pear to represent primary genetic lesions of malignancies and reflect their clonal origin. Secondary intraneoplastic genetic evolution is suggested by major clonal ab- normalities of chromosome number and cellular DNA content. Both types of ge- netic changes have been reaching great relevance in cancer medicine, today. Although the Philadelphia chromosome was first discovered in chronic myelo- cytic leukemia (CML), by Nowell and Hungerford in 1960, new banding techniques developed in the 1970's were needed to identity this abnormality as a translocation between chromosomes 9 and 22 (t(9; 22)). Soon thereafter, further non-random translocations were detected and attributed to special diseases like t(8; 21) and t(15; 17) to acute myeloid leukemias (AML) and t(9; 22), t(4; 11), t(8; 14) to acute lymphoblastic leukemia (ALL).