CD4-Targeted T Cells Rapidly Induce Remissions in Mice with T Cell Lymphoma.

Objective: To explore the immune cell therapy for T cell lymphoma, we developed CD4-specific chimeric antigen receptor- (CAR-) engineered T cells (CD4CART), and the cytotoxic effects of CD4CART cells were determined in vitro and in vivo.

Methods: CD4CART cells were obtained by transduction of lentiviral vector encoding a single-chain antibody fragment (scFv) specific for CD4 antigen, costimulatory factor CD28 fragment, and intracellular signal transduction domain of CD3 fragments. Control T cells were obtained by transduction of reporter lentiviral vector.

Characterizing the Tumor Suppressor Role of CEACAM1 in Multiple Myeloma.

Background/aims: Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), also known as CD66a, is a member of the immunoglobulin (Ig) superfamily that belongs to the carcinoembryonic antigen (CEA) family which plays a dual role in cancer. Previous studies showed high expression of CEACAM1 in multiple myeloma (MM). The aim of this study was to investigate the biological consequences of CEACAM1 overexpression in MM.

Monitoring tyrosine kinase inhibitor therapeutic responses with a panel of metabolic biomarkers in chronic myeloid leukemia patients.

The aim of this study is to investigate the potential biomarkers associated with chronic myeloid leukemia (CML), reveal the metabolite changes related to the continuous phases of tyrosine kinase inhibitors (TKIs), and find the potential biomarkers associated with treatment effects. Fifty-two patients with CML and 26 matched healthy people were enrolled as the discovery set. Another 194 randomly selected CML patients treated with TKI were chosen as the external validation set.

High Tim-3 expression on AML blasts could enhance chemotherapy sensitivity.

T-cell immunoglobulin and mucin domain-containing molecule3 (Tim-3) represents a novel mechanism of T-cell dysfunction and exhaustion. Tim-3 has also been identified in various solid tumors. However, the role of Tim-3 expression on blast cells in acute myeloid leukemia (AML) is not well understood.

Knockdown of connexin 43 attenuates balloon injury-induced vascular restenosis through the inhibition of the proliferation and migration of vascular smooth muscle cells.

Coronary artery disease (CAD) or atherosclerotic heart disease is one of the most common types of cardiovascular disease. Although percutaneous coronary intervention [PCI or percutaneous transluminal coronary angioplasty (PTCA)] is a mature, well-established technique used to treat atherosclerotic heart disease, its long‑term therapeutic effects are compromised by a high incidence of vascular restenosis (RS) following angioplasty. In our previous study, we found that the principal gap junction protein, connexin 43 (Cx43), in vascular smooth muscle cells (VSMCs) was involved in the development of vascular RS following angioplasty-induced balloon injury.