The B-raf kinase (BRAF oncogene) controls cell proliferation and survival through the mitogen-activated protein kinase (MAPK) pathway. By contrast, constitutively activated mutated BRAF causes uncontrolled tumorigenesis while small-molecule inhibition arrests growth to cause tumor regression.
T-cell exhaustion is a differentiation state of T cells associated with tumor progression in the context of cancer. One of the co-stimulatory molecules in the tumor microenvironment, 4-1BB, triggers a signaling cascade resulting in cytokine secretion and upregulation of antiapoptotic molecules.
Although FMS-like tyrosine kinase 3 (FLT3) inhibitors have shown success treating FLT3-mutated acute myeloid leukemia (AML), around 30% to 50% of patients show primary resistance to both type I and type II inhibitors. Therefore, identifying therapeutic strategies to overcome this resistance and enhance the efficacy of FLT3 inhibitors remains an urgent need.
The SLC6A6 gene encodes the transporter of the amino acid taurine. In recently presented work, researchers from the Institute of Molecular and Clinical Ophthalmology Basel, University of Basel and affiliated organizations aimed to investigate the molecular pathology of a novel mutation in SLC6A6 and its association with a syndromic form of Leber congenital amaurosis (LCA).
Tonix Pharmaceuticals Holding Corp. has received FDA clearance of its IND application to support a phase I trial with TNX-1500, an anti-CD40L monoclonal antibody. The first indication Tonix is seeking for TNX-1500 is the prevention of organ rejection in patients receiving a kidney transplant. Enrollment in the phase I study is expected to open in the third quarter of this year.
XNK Therapeutics AB has entered into a preclinical research agreement with a global pharma company to study XNK’s autologous natural killer (NK) cell therapy candidate XNK-04 in combination with a well-documented PD-L1 antibody in liver cancer.
Researchers from Hangzhou Polymed Biopharmaceuticals Inc. have reported the discovery and preclinical evaluation of HPB-092, an FMS-like tyrosine kinase 3 (FLT3) and interleukin-1 receptor-associated kinase 4 (IRAK-4) dual inhibitor, being developed for the treatment of acute myeloid leukemia (AML).
The use of therapies based on immune checkpoint blockade (ICB) in melanoma patients has greatly improved survival rates; however, many individuals either develop resistances or are nonresponsive to treatment.
The activation of GPR65 on tumor-associated macrophages (TAMs) is a key tumor-promoting process and GPR65 has been previously described as a genetically validated target in cancer. It was demonstrated that GPR65 functions as an immune checkpoint in acidic tumor microenvironment (TME), as it is activated by low pH in the TME.
Patients suffering from neuropathic pain, a chronic condition, have few treatment options and often develop tolerance to existing pain therapy that decreases its effectiveness. Now, a group of scientists from the University of Alabama at Birmingham (UAB) and the Baylor College of Medicine have described the pathophysiological mechanism of initiation, transmission and maintenance of neuropathic pain and identified a potential therapeutic target to treat it efficiently.
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.webp?height=488&t=1670008838&width=650 "Acute myeloid leukemia")
