Richard L. Schilsky, MD

In this interview we discuss the American Society of Clinical Oncology’s (ASCO) health information and patient record initiative called CancerLinQ.

Our knowledge of how to best develop and use targeted therapies for cancer remains nascent, and optimizing the use of such treatments will likely require answering one other question that I have paraphrased from the Passover Haggadah: How is this tumor different from all other tumors?

Capecitabine (Xeloda) is a new, orally administered, enzyme-activated fluoropyrimidine carbamate designed to generate high levels of fluorouracil (5-FU) in tumor cells. Selective tumor activation of 5´-deoxy-5-fluorouridine,

Capecitabine (Xeloda) is a new, orally administered, enzyme-activated fluoropyrimidine carbamate designed to generate high levels of fluorouracil (5-FU) in tumor cells. Selective tumor activation of 5´-deoxy-5-fluorouridine,

An important, though as yet elusive, goal of cancer chemotherapy is the development of agents that are selectively toxic to tumor cells and, thus, permit effective cancer treatment to be administered without severe, often life-threatening toxicity to normal tissues. Until such agents are available, an alternative strategy to improve the therapeutic index of cancer chemotherapy is the administration of cytoprotective agents to selectively protect normal tissues from injury by cytotoxic drugs.

Recent strategies to improve the outcome of fluoropyrimidine chemotherapy for patients with cancer have focused on better selection of patients likely to respond to such therapy and on protracted exposure to 5-fluorouracil (5-FU). Cellular

The cellular and clinical pharmacology of fluoropyrimidines is characterized by marked interpatient variability in tumor response and patient tolerance. Understanding the metabolic pathways followed by 5-fluorouracil (5-FU) has