AHNAK2 (AHNAK Nucleoprotein 2)

Our findings indicated that the rondom froest model based on five autoantibodies might help identify preclinical and early-stage PC.

These hits exhibited lower free energies (ΔG) as compared to the benchmark inhibitors, Galunisertib and Vactosertib. The results offer valuable insights into the binding mechanism of protein TGFßR1 and its role in the disease, suggesting that targeting the TGF-ß signaling pathway may represent a promising therapeutic strategy.

Conversely, AHNAK2 overexpression in HCT116/5-FU cells produced the opposite effects. Collectively, these findings demonstrate that AHNAK2 reduces the chemosensitivity of CRC to 5-FU by activating the AKT/GSK-3β signaling pathway, underscoring its potential as a therapeutic target to improve CRC treatment strategies.

We assessed SUMOylation expression patterns and function in PDAC using Western blot and the SUMOylation inhibitor TAK-981...This study underscores the role of SUMOylation in PDAC and introduces the Sscore as a prognostic tool. SAFB2 is identified as a potential tumor suppressor, offering new therapeutic targets for PDAC.

qRT-PCR confirmed that, except for NLRP10, all prognostic genes exhibited expression patterns consistent with TCGA-NSCLC data. This study highlights the significant role of FRGs in NSCLC prognosis and regulation, offering novel insights for personalized treatment strategies.

Our study posits AHNAK2 as a valuable diagnostic biomarker in PDAC, now demanding prospective validation. Determination of mechanisms regulating AHNAK2 subcellular localisation may help explain its biological role.

Additional members of this genetic framework were identified when the low-frequency (0.01 < MAF < 0.05) pathological/deleterious genetic variants were analyzed with the low-frequency biallelic AHNAK2, GLI3, PTIRM1, and ZNF254 variants, warranting a closer look at their potentially important role in fALS as C9ORF72 genetic modifiers as well as their link to both neuromuscular disorders/ALS and cancer. Therefore, in addition to the current genetic screening using a standard panel of ALS-related genes, a supplementary screening by WES could be very beneficial for the development of personalized treatment of ALS patients as well as in search of the respective efficient disease-modifying drugs.

Our study provided comprehensive insights into genomic alterations in a cohort of Chinese MIBC, which could provide potential clues for clinical applications.

Our study provides novel insights into the genomic landscape of BTC and highlights the potential of whole-genome sequencing analysis to identify actionable gene mutations and understand the molecular mechanisms underlying this malignancy. The high mutational burden, structural variations, and copy number alterations observed in BTC samples in this study underscore the genetic complexity and heterogeneity of this disease.

The expression of chemoresistance genes has been detected, including KLF4 (doxorubicin and ifosfamide), ULK1, LUM, GPNMB, and CAVIN1 (doxorubicin), and AHNAK2 (gemcitabine) in tumor cells and ETS1 (gemcitabine) in TME. This study provides the first description of the single-cell transcriptome of UPS with resistance to two lines of chemotherapy, showcasing the gene expression in subpopulations of tumor cells and TME, which may be potential markers for personalized cancer therapy.

These genes play significant roles in the PI3K-Akt pathway and potentially interact with vitamin D. Molecular docking and single-cell RNA sequencing analyses suggest that vitamin D may improve the prognosis of glioma patients infected with COVID-19 by regulating these key genes and the PI3K-Akt pathway. The findings reveal molecular links between glioma and COVID-19, thereby providing new insights for developing targeted therapeutic strategies.