title: Advances in the treatment of hematologic malignancies. Part 1 of a 3-part series: Aggressive lymphomas.
abstract: The treatment of patients with aggressive lymphomas has improved significantly in recent years, primarily due to the introduction of targeted therapy with the anti-CD20 monoclonal antibody rituximab in combination with chemotherapy. Rituximab has significantly improved overall survival and progression-free survival in patients with aggressive lymphomas, even those with high-risk disease. Ongoing research aims to determine the optimal uses of rituximab for inducing and maintaining remission in a variety of settings. Another important area of focus has been the investigation into prognostic and predictive factors. Assessing each patient according to different prognostic factors allows clinicians to best determine a patient's risk and develop a suitable therapy. Microarray analysis is being used in this area to determine gene expression patterns associated with responses to therapy and, ultimately, to identify specific genes associated with various outcomes. The identification of relevant genes could indicate specific patients that might benefit from targeted therapy, and may reveal additional therapeutic targets. These investigations have already identified several candidate genes that may be appropriate targets for therapy, such as Bcl-2, protein kinase C-beta, and nuclear factor-kappa B. The future of therapy for aggressive lymphomas will likely involve identifying the molecular profile for each patient and designing an appropriate targeted therapy based on their specific situation. Recent and ongoing studies are moving us closer towards that goal.
authors.affiliation: James P. Wilmot Cancer Center, University of Rochester, NY, USA.
authors.forename: Richard I
authors.initials: RI
authors.lastname: Fisher
authors.forename: Bertrand
authors.initials: B
authors.lastname: Coiffier
authors.forename: Julie M
authors.initials: JM
authors.lastname: Vose
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D015703:Antigens, CD / Q000378:metabolism; D018951:Antigens, CD20 / Q000378:metabolism; D000951:Antigens, Neoplasm / Q000378:metabolism; D000971:Antineoplastic Combined Chemotherapy Protocols / Q000627:therapeutic use; D001402:B-Lymphocytes / Q000378:metabolism / Q000473:pathology; D000074301:CD52 Antigen; D003520:Cyclophosphamide / Q000627:therapeutic use; D018572:Disease-Free Survival; D004317:Doxorubicin / Q000627:therapeutic use; D020869:Gene Expression Profiling; D015973:Gene Expression Regulation, Leukemic / Q000187:drug effects / Q000235:genetics; D006023:Glycoproteins / Q000378:metabolism; D006801:Humans; D016393:Lymphoma, B-Cell / Q000175:diagnosis / Q000235:genetics / Q000378:metabolism / Q000628:therapy; D020411:Oligonucleotide Array Sequence Analysis; D011241:Prednisone / Q000627:therapeutic use; D011379:Prognosis; D016499:Radioimmunotherapy / Q000379:methods; D016032:Randomized Controlled Trials as Topic; D033581:Stem Cell Transplantation; D016896:Treatment Outcome; D014750:Vincristine / Q000627:therapeutic use
chemical_list: D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D018951:Antigens, CD20; D000951:Antigens, Neoplasm; D000074301:CD52 Antigen; C000613862:CD52 protein, human; D006023:Glycoproteins; D014750:Vincristine; D004317:Doxorubicin; D003520:Cyclophosphamide; D011241:Prednisone