Palmar-plantar erythrodysesthesia in patients receiving capecitabine and intratumor thymidine phosphorylase and dihydropyrimidine dehydrogenase: is there a pharmacologic explanation?

Background: Palmar-plantar erythordysesthesia (PPE) is the most common toxicity of capecitabine. Preclinical studies have shown that radiation therapy (RT) upregulates thymidine phosphorylase (TP), which could in turn increase the efficacy of capecitabine. Capecitabine is degraded by dihydropyrimidine dehydrogenase (DPD), and a deficiency in this enzyme can increase the toxicity of capecitabine.

Continuing reassessment of the risks of erythropoiesis-stimulating agents in patients with cancer.

Purpose: Erythropoiesis-stimulating agents (ESA) are approved for the treatment of anemia in patients with nonmyeloid malignancies whose anemia is due to the effect of concomitantly administered chemotherapy. Since the 1993 approval of epoetin alfa in patients with cancer, the risk of thrombovascular events, decreased survival, and poorer tumor control have been increasingly recognized. The risks of ESAs in patients with cancer and the design of trials to assess these risks have been the topic of discussion at two Oncologic Drugs Advisory Committees in 2004 and 2007.

Long-term assessment of cardiac function after dose-dense and -intense sequential doxorubicin (A), paclitaxel (T), and cyclophosphamide (C) as adjuvant therapy for high risk breast cancer.

Objectives: This study evaluated the incidence of late cardiotoxicity after dose-dense and -intense adjuvant sequential doxorubicin (A), paclitaxel (T), and cyclophosphamide (C) for breast cancer (BC) with > or = 4 involved ipsilateral axillary lymph nodes.

Methods: Patients were enrolled from 1994 to 2001 after definitive BC surgery if > or =4 axillary nodes were involved. Planned treatment was A 90 mg/m(2) q 14 days x 3, T 250 mg/m(2) q 14 days x 3, C 3 g/m(2 )q 14 days x 3 with filgrastim (G) support.