Rationale for consolidation to improve progression-free survival in patients with non-Hodgkin's lymphoma: a review of the evidence.

Non-Hodgkin's lymphoma (NHL) comprises both indolent forms, including follicular lymphoma (FL) and marginal zone lymphoma (MZL), and aggressive forms, including diffuse large B-cell lymphoma (DLBCL) and mantle cell lymphoma (MCL). FL and DLBCL are the most common subtypes of indolent and aggressive NHL, respectively. Although these lymphomas exhibit different clinical behaviors and outcomes, the prognosis is negatively affected in both DLBCL and FL by the lack of a complete response (CR) with standard treatment options. The aim of therapy should therefore be achievement of a CR, which is not only associated with longer progression-free survival (PFS) and overall survival times, but is also a prerequisite for a cure, particularly in DLBCL. Consolidation treatment with radioimmunotherapy (RIT) is an innovative treatment approach to increase CR rates. Phase II studies have indicated promising results with yttrium-90 ((90)Y)-ibritumomab tiuxetan and iodine-131 ((131)I)-tositumomab as consolidation following induction therapy for previously untreated patients with advanced FL. More recently, investigators reported a marked increase in CR rates and significant improvements in PFS using standard chemotherapy regimens followed by (90)Y-ibritumomab tiuxetan in a phase III randomized trial in patients with previously untreated FL. Data also suggest that RIT may play a role in the treatment of high-risk DLBCL, with encouraging PFS results from a phase II trial of (90)Y-ibritumomab tiuxetan consolidation following induction with rituximab plus chemotherapy in elderly patients with previously untreated DLBCL. With the higher CR rates and longer PFS times observed in patients with FL and DLBCL, as well as encouraging early data from MZL and MCL consolidation trials, RIT appears to have an important role in the treatment of patients with NHL

Lung cancer: Mechanisms of carcinogenesis by asbestos

Lung cancers have typically been reported in asbestos-exposed cohorts in smokers, and interactions between cigarette smoke and asbestos may be additive or multiplicative in the development of tumors. Research has indicated that some cellular and molecular events elicited by exposures to chemical carcinogens in cigarette smoke or asbestos fibers are different in lung epithelial cells, the target cells of lung carcinomas. We describe here contemporary concepts of lung cancer development and recent experimental studies providing an understanding of how asbestos and components of cigarette smoke act alone and together to cause lung cancers. We emphasize the importance of the tumor microenvironment including inflammation and fibrosis, interactions between different cell types in the lung that culminate in these events, and the role of epigenetics, a relatively new tool in understanding a number of common molecular events in carcinogenesis. Lastly, we provide a perspective on the multiple properties of different asbestos fiber types that may be critical in assessing their toxicity and carcinogenicity in lung tissue and the development of a quantitative model to predict the pathogenicity of mineral fibers in lung cancers