title: Personalizing treatment for chronic lymphocytic leukemia.
abstract: Over the past few years, more effective therapies have emerged in the treatment of chronic lymphocytic leukemia (CLL); these are mainly combinations of immunotherapy with fludarabine-based regimens. Despite the higher response rates obtained with these more intensive treatments, they may not always be applicable. Patients with several comorbidities have an increased toxicity with these newer therapies. Effective tools to distinguish between fit and nonfit patients and new therapeutic approaches suitable for fragile patients with CLL are therefore necessary. Moreover, there is still a subset of patients who are refractory to standard fludarabine-based treatments who continue to have very poor survival. Efforts to understand the mechanisms of resistance to treatment in order to develop new therapeutic agents for those patients are mandatory. Finally, advances in the knowledge of the pathogenesis of CLL are promoting the emergence of drugs directed to new biological targets of this disease. Consequently, trials exploring the toxicity profile and efficacy of these new therapeutic agents, alone or in combination with standard treatments, are warranted.
authors.affiliation: Department of Hematology, University Hospital of Vall d'Hebron 119-129, 08035 Barcelona, Spain.
authors.forename: Pau
authors.initials: P
authors.lastname: Abrisqueta
authors.forename: Marta
authors.initials: M
authors.lastname: Crespo
authors.forename: Francesc
authors.initials: F
authors.lastname: Bosch
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D019008:Drug Resistance, Neoplasm; D006801:Humans; D007167:Immunotherapy; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000188:drug therapy*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D057285:Precision Medicine; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D016315:Proto-Oncogene Proteins c-abl / Q000037:antagonists & inhibitors / Q000378:metabolism; D019718:Receptors, CXCR4 / Q000037:antagonists & inhibitors / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000037:antagonists & inhibitors / Q000378:metabolism; D025521:Tumor Suppressor Proteins / Q000378:metabolism; D014740:Vidarabine / Q000031:analogs & derivatives / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D000970:Antineoplastic Agents; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins; D004268:DNA-Binding Proteins; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D017346:Protein Serine-Threonine Kinases; D016315:Proto-Oncogene Proteins c-abl; D019718:Receptors, CXCR4; D016159:Tumor Suppressor Protein p53; D025521:Tumor Suppressor Proteins; D014740:Vidarabine; C576324:ATM protein, human; C024352:fludarabine