CLTC (Clathrin Heavy Chain)

Furthermore, the inhibition of clathrin-coated vesicles (CCVs) by CHC downregulation or inhibition suppresses cell survival by reducing phosphorylated PTEN at the STT, suggesting that SCYL2 enhances PTEN phosphorylation through CCVs as a signaling platform. Our results indicate that SCYL2/CHC complex plays a pivotal role in regulating the PI3K/AKT signaling pathway through PTEN phosphorylation, thus leading to tumor development and may be a promising novel target for treating tumors.

UBR4 promotes clathrin-dependent EGFR degradation, enhancing anti-EGFR therapeutic efficacy, and may serve as a predictive biomarker in metastatic CRC.

Pediatric ALK+ ALCL with non-NPM1-ALK fusions exhibits diverse clinical features and outcomes. TPM3-ALK fusions might correlate with a more favorable course, while other variants may face a potentially higher relapse risk. ALK inhibitors showed promising efficacy in the salvage setting. These preliminary findings highlight the need for larger prospective studies to validate mutation-specific risk stratification and therapeutic strategies.

We suggest this impairment was linked to a significant decrease in clathrin heavy chain abundance and pointed to a disrupted clathrin-mediated endocytosis. This study highlights a novel role for myoferlin in focal adhesion recycling in PDAC and provides a consistent mechanism explaining how myoferlin contributes to PDAC cell migration, a significant event in metastatic dissemination, and reinforce its potential as a therapeutic target.

This study identifies ATT-1 as a promising multi-targeted therapeutic for colorectal cancer by leveraging PDOs for direct, de novo target discovery. We uniquely identified two novel, high-affinity targets, CLTC and XRCC5, and elucidated a convergent dual-targeting mechanism wherein ATT-1 binding disrupts DNA damage repair and triggers apoptosis. This novel mechanism and its potent synergy with standard chemotherapy in physiologically relevant models provide a compelling strategy for integrating traditional Chinese medicine into modern precision oncology.

Our data reveal novel insights into the role of amisulpride in modulating the differential expression of genes and proteins. These findings, which involve genes/proteins related to AP-1 transcription factor family gene regulation, cytoskeleton, histone binding activity, the intracellular trafficking of receptors and endocytosis of a variety of macromolecules, and nuclear localization signal, are particularly significant as they shed light on the molecular underpinnings of the clinical efficacy of amisulpride and the pathogenesis of schizophrenia.

These findings offer unprecedented insight into the functional diversity of a natural neoantigen-specific CD4+ T-cell response and show how immunotherapeutic intervention influences the phenotype, magnitude, and efficacy of the antitumor immune response. This information could lead to new approaches to immune monitoring in the clinical setting of checkpoint blockade immunotherapy and cancer vaccines. Furthermore, we show that Treg can be a potent source of TCRs that can mediate therapeutic benefit in the setting of ACT.

SP TACC3 efficiently penetrates cells and displaces TACC3 from the mitotic spindle, causing a delay in mitotic progression in two out of three cancer cell lines. This work showcases the novel application of hydrocarbon-stapled peptides to disrupt the TACC3/CHC protein-protein interaction in a cellular context, highlighting the potential of targeting this interface for future cancer therapies.

Various ALK fusion partners have been identified in EIMS, including RANBP2, RRBP1, EML4, and VCL. In this report, we present four cases of EIMS involving the abdominal cavity, including the first case with a CLTC::ALK fusion, which has previously been associated only with nonaggressive IMT.

Our study indicates that CMTM3 promotes CAC by aggravating colitis through causing vascular permeability, providing insights into targets for development of future therapies.

This information could lead to new approaches to immune monitoring in the clinical setting of checkpoint blockade immunotherapy and cancer vaccines. Furthermore, we show that T reg can be a potent source of TCRs that can mediate therapeutic benefit in the setting of adoptive cell therapy (ACT).

Herein, we present a poorly differentiated carcinoma involving lung and mediastinum. Next generation sequencing-based RNAseq identified a novel fusion, CLTC::RPS6KB1, while no other known drivers were present.