I am extremely honored and pleased to have the opportunity to write a few introductory words for this timely volume on Na + /It exchange. This is a field of investigation that I entered into by challenge and necessity, embraced with passion and fmally left in my quest for new discoveries in growth control. Ten years, one third of my scientific life, has been devoted to uncovering the mysteries of intracellular pH (PH;) regulation with respect to growth factor action. I got started on this new topic in 1980, when I heard a rather provocative hypothesis presented by Enrique Rozengurt at an ICN-UCLA Keystone meeting on "Cell Surface and Malignancy." He showed that all mitogens induced amiloride-sensitive Na + entry into resting cells and proposed that, if a compound stimulates Na + influx, it could be a mitogen. In support of his proposal Enrique reported that the amphipathic polypeptide, mellitin, which induced Na+ influx, was indeed mitogenic for 3T3 cells. This was only correlation at this stage. However, I was fascinated by this talk. I immediately approached Enrique to inform him of my skepticism about this beautiful story, and to indicate that I would only be convinced when I succeeded in isolating mutant fibroblasts lacking the amiloride-sensitive Na+ transporter. ''Good luck " was his response.

Prostate Cancer Metabolism: From Biochemistry to Therapeutics shows the peculiarities of prostate cancer metabolism, emphasizing the targetable aspects - that have not been considered in conventional treatment protocols. The book specifically addresses treatment of the castration-resistant stage of prostate cancer proposing many repurposed drugs and nutraceuticals to complement, not replace, standard therapies. The large body of evidence supporting these concepts makes them deserving of further research and well-designed clinical trials. It discusses lipid, cholesterol, glutamine, and glucose metabolisms and their impact on prostate cancer. Additionally, it explains how current established drugs can be repurposed to improve treatment outcomes. The concepts set out in the book, that deal with cancer at the cellular/molecular level, help identify new avenues of research and treatments to pursue that do not affect well-being whilst offer consistent benefits. Since most practicing physicians have not studied basic biochemistry since medical school, each chapter begins with a brief review of the topic to facilitate an understanding of the metabolically-oriented approach to targeting prostate cancer. Conventional treatments are not discussed here since they are covered in textbooks and specialized updates that abound in the medical literature. It is a valuable resource for cancer researchers, oncologists, clinicians and members of biomedical field who want to learn more about prostate cancer metabolism and how to apply recent findings in the field to bedside.

I am extremely honored and pleased to have the opportunity to write a few introductory words for this timely volume on Na + /It exchange. This is a field of investigation that I entered into by challenge and necessity, embraced with passion and fmally left in my quest for new discoveries in growth control. Ten years, one third of my scientific life, has been devoted to uncovering the mysteries of intracellular pH (PH;) regulation with respect to growth factor action. I got started on this new topic in 1980, when I heard a rather provocative hypothesis presented by Enrique Rozengurt at an ICN-UCLA Keystone meeting on "Cell Surface and Malignancy." He showed that all mitogens induced amiloride-sensitive Na + entry into resting cells and proposed that, if a compound stimulates Na + influx, it could be a mitogen. In support of his proposal Enrique reported that the amphipathic polypeptide, mellitin, which induced Na+ influx, was indeed mitogenic for 3T3 cells. This was only correlation at this stage. However, I was fascinated by this talk. I immediately approached Enrique to inform him of my skepticism about this beautiful story, and to indicate that I would only be convinced when I succeeded in isolating mutant fibroblasts lacking the amiloride-sensitive Na+ transporter. ''Good luck " was his response.