The efficacy and safety of chidamide, a new subtype-selective histone deacetylase (HDAC) inhibitor, have been demonstrated in a pivotal phase II clinical trial, and chidamide has been approved by the China Food and Drug Administration (CFDA) as a treatment for relapsed or refractory peripheral T cell lymphoma (PTCL). This study sought to further evaluate the real-world utilization of chidamide in 383 relapsed or refractory PTCL patients from April 2015 to February 2016 in mainland China. For patients receiving chidamide monotherapy (n = 256), the overall response rate (ORR) and disease control rate (DCR) were 39.06 and 64.45%, respectively. The ORR and DCR were 51.18 and 74.02%, respectively, for patients receiving chidamide combined with chemotherapy (n = 127). For patients receiving chidamide monotherapy and chidamide combined with chemotherapy, the median progression-free survival (PFS) was 129 (95% CI 82 to 194) days for the monotherapy group and 152 (95% CI 93 to 201) days for the combined therapy group (P = 0.3266). Most adverse events (AEs) were of grade 1 to 2. AEs of grade 3 or higher that occurred in ≥5% of patients receiving chidamide monotherapy included thrombocytopenia (10.2%) and neutropenia (6.2%). For patients receiving chidamide combined with chemotherapy, grade 3 to 4 AEs that occurred in ≥5% of patients included thrombocytopenia (18.1%), neutropenia (12.6%), anemia (7.1%), and fatigue (5.5%). This large real-world study demonstrates that chidamide has a favorable efficacy and an acceptable safety profile for refractory and relapsed PTCL patients. Chidamide combined with chemotherapy may be a new treatment choice for refractory and relapsed PTCL patients but requires further investigation.Electronic supplementary materialThe online version of this article (doi:10.1186/s13045-017-0439-6) contains supplementary material, which is available to authorized users.

Purpose: For classical Hodgkin lymphoma (cHL), programmed death-l (PD-1) is a well-recognized attractive target. This multicenter, single-arm, phase II study evaluated the efficacy and safety of camrelizumab, a humanized highaffinity IgG4 mAb against PD-1, in Chinese patients with relapsed or refractory cHL.Patients and Methods: Patients who had failed to achieve a remission or experienced progression after autologous stem cell transplantation or had received at least two lines of systemic chemotherapies were given camrelizumab 200 mg every 2 weeks. The primary endpoint was objective response rate per independent review committee (IRC) assessment. This study is registered with ClinicalTrials.gov (NCT03155425).Results: Between June 9, 2017 and September 18, 2017, 75 patients were enrolled and treated. At a median follow-up of 12.9 months, 57 of 75 (76.0%; 95% CI, 64.7-85.1) patients achieved an IRC-assessed objective response, including 21 (28.0%) and 36 (48.0%) patients who had complete and partial remission, respectively. Median duration of response was not reached (range, 0.0 þ -12.8 þ months). Treatmentrelated adverse events (AE) occurred in all patients. The most common ones included cutaneous reactive capillary endothelial proliferation (97.3%, 73/75) and pyrexia (42.7%, 32/75). Grade 3 or 4 treatment-related AEs occurred in 20 patients (26.7%); the most common AE was decreased white blood cell count (4.0%, 3/75). There were no grade 5 treatment-related AEs.Conclusions: Camrelizumab demonstrated a high response rate, durable response and controllable safety in Chinese patients with relapsed or refractory cHL, becoming a new safe and effective treatment option in this setting.

Key Points• The present study shows, for the first time, that Gas6 produced by endothelial cells contributes to venous thrombus formation.• Gas6 is required for the expression of tissue factor in endothelial cells.Gas6 (growth-arrest specific gene 6) plays a role in thrombus stabilization. Gas6 null (؊/؊) mice are protected from lethal venous and arterial thromboembolism through platelet signaling defects induced only by 5M ADP and 10M of the thromboxane analog, U46619. This subtle platelet defect, despite a dramatic clinical phenotype, raises the possibility that Gas6 from a source other than platelets contributes to thrombus formation. Thus, we hypothesize that Gas6 derived from the vascular wall plays a role in venous thrombus formation. Bone marrow transplantation and platelet depletion/ reconstitution experiments generating mice with selective ablations of Gas6 from either the hematopoietic or nonhematopoietic compartments demonstrate an approximately equal contribution by Gas6 from both compartments to thrombus formation. Tissue factor expression was significantly reduced in the vascular wall of Gas6 ؊/؊ mice compared with WT. In vitro, thrombin-induced tissue factor expression was reduced in Gas6 ؊/؊ endothelial cells compared with wild-type endothelium. Taken together, these results demonstrate that vascular Gas6 contributes to thrombus formation in vivo and can be explained by the ability of Gas6 to promote tissue factor expression and activity. These findings support the notion that vascular wall-derived Gas6 may play a pathophysiologic role in venous thromboembolism. (Blood. 2013;121(4):692-699) IntroductionVenous thromboembolism (VTE) is a common cause of morbidity and mortality in clinical medicine. The pathophysiology of VTE was first described by Virchow in 1853 and describes a triad of entities accounting for VTE. VTE could be triggered by alterations in the blood composition (thrombophilia), changes in blood flow (eg, stasis), and/or activation of the endothelium. 1 Under normal conditions, the endothelial surface inhibits coagulation because of the presence of various proteins, such as tissue factor (TF) pathway inhibitor, thrombomodulin, and the endothelial cell protein C receptor. 2 However, physical (eg, vascular damage) or functional (eg, hypoxia) perturbation of the endothelium promotes thrombosis because of reduced expression of anticoagulants and the induction of the expression of the transmembrane procoagulant protein TF. 3 Gas6, the product of growth arrest specific gene 6 (Gas6), is a member of the vitamin K-dependent family of proteins, which includes the procoagulant factors II, VII, IX, and X and the anticoagulant factors, protein C and S, as well as protein Z. 4 Even though Gas6 was discovered as a homolog of protein S more than a decade ago, it plays no role in the generation of fibrin and its role in vivo remains incompletely characterized. 5,6 Originally identified in fibroblasts, Gas6 is expressed in various cell types, including endothelial cells, 7 smooth muscle, 8 and bon...