SEC31A (SEC31 Homolog A COPII Coat Complex Component)

Mechanistically, we show that AMPK and ULK1 signaling orchestrate this process independent of autophagy, with ULK1-mediated phosphorylation of SEC31A driving SEC24C-dependent COPII reorganization. These findings establish ER-to-Golgi trafficking as a nutrient-sensitive regulatory node that links metabolic stress to cell surface remodeling and metastatic potential.

Their prognostic value remained significant after adjusting for copy number alterations and transcriptomic subtypes. A 4-feature model integrating these two promoter activities with two clinical variables (Tumor size, Ki67 index) achieved an AUROC of 0.73 and improved patient risk stratification, with a Net Reclassification Improvement (NRI) of 0.40-0.48 over the clinical-only model, underscoring the potential of promoter activity as a biomarker in TNBC.

The circKLHL24/Sec31A/miR-615-5p/CXCL12 axis is critical for CAF-induced PNI in PDAC. Therefore, circKLHL24 could serve as a potential therapeutic target for PDAC.

Pre-analytic evaluation of the manufacturer's recommended 20% tumor content cut-off is essential to ensure valid results. The Idylla MSI assay offers several advantages over other PCR-based assays including minimal hands-on time, rapid turn-around-time, no requirement for a paired normal sample and the use of FFPE directly without an extraction step.

We present seven cases of ALK+ LBCL, discussing the correlation between fusion genes and ALK protein expression, and enhancing our understanding of the genetic attributes of this tumour. This study also shows the loss of 5hmC in nearly all seven ALK+ LBCL cases, independently of TET2 mutations.

Moreover, Nlp deficient mice were prone to spontaneous B cell lymphoma, since the developments and functions of lymphocytes significantly depended on secretory proteins through ER-to-Golgi vesicle trafficking, including IL-13, IL-17 and IL-21. Thus, perturbations of Nlp altered ER-to-Golgi communication and cellular homeostasis, and might contribute to the pathogenesis of B cell lymphoma.

Notably, this is the first reported instance of a solid tumor featuring a SEC31A-BRAF gene fusion. The discovery of this novel fusion gene expands our understanding of BRAF fusion partner profiles, particularly in the context of paediatric PACC.

The patient whose tumor harbored SEC31A::PDGFRA was treated after multiple relapses with imatinib and sunitinib therapy, with progression-free periods of 5 and 2 years, respectively. Despite its bland appearance, myxoid inflammatory myofibroblastic sarcoma harbors a significant risk for disseminated disease, particularly when it occurs in the peritoneum. Targeted therapy could be considered for patients with disseminated disease.

Notably, exogenous PTN supplementation ameliorated the differentiation deficits of these OPCs. Collectively, our findings indicate that the association between TRAPPC12 and MEA6 is important for cargo trafficking and white matter development.

The functional inhibition of KLHL12 by LZTR1 provides important evidence that LZTR1 may be a repressor of BTB-Kelch family members. These results provide clues to the mechanism of LZTR1-deficiency carcinogenesis.

The Idylla MSI Test was successfully technically validated as an adequate tool for the evaluation of the MSI status in CRC.

We reported a novel rare ALK fusion SEC31A: EXON20~ALK: exon20 and showed the effectiveness of crizotinib against the fusion. This study provided strong evidence for the efficacy of ALK-TKI for rare ALK fusion.