18 research outputs found
P1153: UTILITY OF THE FRAILTY SCORE FOR PREDICTING PROGNOSIS AND INDIVIDUALIZING TREATMENT INTENSITY IN ELDERLY PATIENTS WITH DIFFUSE LARGE B-CELL LYMPHOMA
Hemoglobinâplatelet index as a prognostic factor in patients with peripheral Tâcell lymphoma
Abstract Peripheral Tâcell lymphoma (PTCL) is a heterogeneous group of aggressive lymphomas with a poor prognosis. The International Prognostic Index (IPI) and the Prognostic Index for PTCLâunspecified (PIT) is used to predict the prognosis of PTCL. The hemoglobinâplatelet index (HPI), based on anemia and thrombocytopenia status, is associated with the prognosis of diffuse large Bâcell lymphoma. However, its significance in terms of predicting the prognosis of PTCL has not been fully investigated. We herein retrospectively analyzed 100 patients with newly diagnosed PTCL in our department. At a median followâup of 3.2Â years, the median progressionâfree survival (PFS) and overall survival (OS) was 0.72 (95% confidence interval [CI]: 0.56â1.2) years and 2.0 (95% CI: 1.5â4.7) years, respectively. Multivariate analysis revealed that elevated lactic dehydrogenase (LDH) and hypoalbuminemia were independent adverse variables for PFS. The HPI showed significant predictive value for both PFS and OS. As a new prognostic model comprising the HPI, LDH, and albumin, the LAâHPI allowed the stratification of patients into four distinct risk subgroups: low risk (zero risk factors), lowâintermediate risk (one risk factors), highâintermediate risk (two or three risk factors), or high risk (four risk factors). The PFS and OS differed significantly among the patients by the LAâHPI score. The LAâHPI demonstrated better predictive performance compared to the IPI, PIT, and HPI. Our data demonstrated the prognostic utility of the HPI in patients with PTCL. The LAâHPI, incorporating four readily obtainable parameters, exhibited superior performance compared to traditional indices
Clinical outcomes in transplantâeligible patients with relapsed or refractory diffuse large Bâcell lymphoma after secondâline salvage chemotherapy: A retrospective study
Abstract Objective The prognosis of patients with relapsed or refractory (R/R) diffuse large Bâcell lymphoma (DLBCL) is poor. Although patients who fail firstâline salvage chemotherapy are candidates for secondâline salvage chemotherapy, the optimal treatment strategy for these patients has not yet been established. Methods The present, singleâcenter, retrospective study included transplantâeligible patients with R/R DLBCL who received secondâline salvage chemotherapy with curative intent. Results Seventyâsix patients with R/R DLBCL received secondâline salvage chemotherapy. Eighteen (23.7%) patients were responders to the firstâline salvage chemotherapy. The overall response rate was 39.5%, and overall survival (OS) was significantly longer in patients who responded to secondâline salvage chemotherapy than those who did not. Fortyâone patients who proceeded to potentially curative treatment (autologous hematopoietic stem cell transplantation [ASCT], chimeric antigen receptor [CAR] Tâcell therapy, or allogeneic hematopoietic stem cell transplantation) had a better prognosis than those who did not. Among the 46 patients who failed to respond to the secondâline salvage regimen, only 18 (39.1%) could proceed to the curative treatments. However, among the 30 patients who responded to the secondâline salvage regimen, 23 (76.7%) received one of the potentially curative treatments. Among 34 patients who received CAR Tâcell therapy, OS was significantly longer in those who responded to salvage chemotherapy immediately prior to CAR Tâcell therapy than in those who did not respond. In contrast, the number of prior lines of chemotherapy was not identified as a statistically significant prognostic factor of survival. No significant difference was detected in OS between patients receiving ASCT and those receiving CAR Tâcell therapy after the response to secondâline salvage chemotherapy. Discussion In this study, we demonstrated that chemosensitivity remained a crucial factor in predicting survival outcomes following CAR Tâcell therapy irrespective of the administration timing, and that both ASCT and CAR Tâcell therapy were acceptable after the response to secondâline salvage chemotherapy
CD74 Is a Novel Prognostic Factor for Patients with Pancreatic Cancer Receiving Multimodal Therapy
Cellular Polymer Ferroelectret: A Review on Their Development and Their Piezoelectric Properties
Impact of stress factors on carotenoid composition, structures, and bioavailability in microbial sources
Induction of GADD45α expression contributes to the anti-proliferative effects of polymethoxyflavones on colorectal cancer cells
The chemotherapeutic drug oxaliplatin differentially affects blood DC function dependent on environmental cues.
Item does not contain fulltextIt has become evident that the tumor microenvironment plays a pivotal role in the maintenance of cancerous growth. One of the acquired functions of the tumor microenvironment is the suppression of immune responses. Indeed, blocking the inhibitory pathways operational in the microenvironment results in enhanced T-cell-dependent, anti-tumor immunity. Chemotherapeutic drugs not only directly kill tumor cells but also shape the tumor microenvironment and potentiate anti-tumor immunity. Here, we demonstrate that the chemotherapeutic compound oxaliplatin acts as a double-edged sword. Besides killing tumor cells, oxaliplatin bolsters immunosuppressive pathways, resulting in decreased activation of T cells by human plasmacytoid dendritic cells (pDCs). Exposure to oxaliplatin markedly increased expression of the T-cell inhibitory molecule programmed death receptor-ligand 1 (PD-L1) on human pDCs and also TLR9-induced IFNalpha secretion. Furthermore, oxaliplatin decreased TLR-induced STAT1 and STAT3 expression, and NF-kappaB-mediated responses. The oxaliplatin induced upregulation of PD-L1 and downregulation of costimulatory molecules CD80 and CD86 resulted in decreased T-cell proliferation. Our results demonstrate that platinum-based anticancer drugs adapt TLR-induced signaling in human pDCs and myeloid DCs (mDCs), thereby downgrading their immunostimulatory potential.1 juli 201