Early diagnosis of pancreatic cancer is difficult and lacks specific drugs. Recently, researchers from France and Spain have discovered that a substance that has been used to treat anxiety can interfere with the development of pancreatic cancer.
Pancreatic cancer is one of the deadliest tumors. At present, treatment is generally carried out through general chemotherapy regimens. Nupr1 protein is an “intrinsically disordered protein”. As early as the 1990s, scientists pointed out that it is involved in the development of pancreatic cancer. Now, scientists have discovered molecules that can inhibit the activity of this protein.
Experts say that this study screened molecules that effectively inhibit Nupr1 activity from more than 1,000 drugs that have been approved for the treatment of various diseases. Through the combination of computer simulation and pharmacological test, it can be known that the molecule can interact with Nupr1 protein. In vitro experiments show that it can reduce the viability and metastasis ability of tumor cells, and completely inhibit the possibility of colony formation. The effective compound has been tested in animals to prove that it can prevent the development of the disease. This compound is trifluoperazine.
Trifluoperazine was previously used only as an antipsychotic drug in clinic, and it is now shown that its antitumor efficacy is very good. This study has changed the direction of pancreatic cancer treatment. Inhibiting Nupr1 may become a new therapeutic direction for the treatment of this cancer.
Targeting FGFR4 and CD276 with CAR T-cells demonstrates a strong antitumor impact against children rhabdomyosarcoma
Chimeric antigen receptor (CAR) T-cells that specifically target Fibroblast Growth Factor Receptor 4 (FGFR4), a surface tyrosine receptor that is extensively expressed in rhabdomyosarcoma (RMS), are now undergoing clinical research. However, the effectiveness of these CAR T-cells may be hindered by tumor heterogeneity and inadequate activation. In this study, we present a method to enhance the co-stimulatory and targeting characteristics of a FGFR4 CAR through an optimization process. We substituted the hinge and transmembrane domain of CD8 as well as the 4-1BB co-stimulatory domain with the corresponding domains of CD28. The CARs produced exhibit heightened anti-tumor efficacy in multiple RMS xenograft models, with the exception of the RMS559 cell line, which is known for its aggressive nature.
