Fluoropyrimidines have been the standard care as ajuvant or palliative treatment for malignant gastrointestinal carcinoma over several decades. Their common adverse effects include gastrointestinal effects, myelosuppression, and hand-foot syndrome. Besides, fluoropyrimidines are the second cause of chemotherapy-induced cardiotoxicity and have the different manifestation and machanisms from anthracyclines. With the development of onco-cardiology, increasing concern is raised on fluoropyrimidine-induced cardiotoxicity. This review addresses the epidemiology, clinical manifestation, and proposed mechanisms; and also highlights the diagnosis, monitoring and management of fluoropyrimidine-induced cardiotoxicity.
Objective To observe the early efficacy and toxicity of gemcitabine plus tegafur, gimeracil and oteracil potassium (S-1) regimen (GS regimen) in patients with metastatic castration-resistant prostate cancer (mCRPC) after docetaxel failure. Methods From July 2013 to December 2015, sixteen mCRPC patients who failed in the treatment of docetaxel-based chemotherapy in West China Hospital of Sichuan University were collected. And the patients were treated with gemcitabine 1 000 mg/m2 intravenously on Day 1 and S-1 40–60 mg/m2 orally dividedly twice daily on Day 1–10, which repeated every two weeks. The main outcome measures were total prostate-specific antigen (T-PSA) decline rate and pain remission rate. Results Of the 13 evaluable patients, the T-PSA decline rate≥50% was observed in 4 patients (30.8%). Among the 11 patients with bone pain, remarkable pain relief was observed in 4 cases (36.4%). Myelosuppression, gastrointestinal reaction, rash and fatigue were the commonly observed adverse reactions and the toxicity of chemotherapy was tolerable. Conclusion The GS regimen is active and tolerable in patients with mCRPC after docetaxel failure.
The poor treatment effect and short survival period of patients with acute leukemia are mainly due to the lack of effective early diagnosis and treatment targets. Lipid metabolism reprogramming meets the material and energy requirements for rapid proliferation and division of tumor cells, and is associated with the invasiveness, recurrence, and chemotherapy resistance of acute leukemia. This article reviews the carcinogenic and chemotherapy resistance mechanisms of lipid metabolism reprogramming in leukemia cells, and summarizes the latest findings on targeted fatty acid metabolism pathways, aiming to provide a new perspective on the role of intracellular fatty acid metabolism in the occurrence and development of acute leukemia. It is expected to provide a theoretical basis for the elucidation of its resistance mechanism and the development of corresponding targeted therapies.