ANKRD1 (Ankyrin Repeat Domain 1)

A panel comprising seven key IPF genes was identified, which may have diagnostic and prognostic value for IPF. A comprehensive analysis of the Dgidb database revealed potential drugs that may be antitumor agents against IPF, such as Lygodii Spora, Smilacis Glabrae Rhizoma, and Aloe.

Our data highlights mutational variation across demographic cohorts. These patterns are vital to future studies into identifying diagnostic markers or therapeutic targets.

Importantly, survival analysis revealed that non-TCR TLX1+ patients had significantly poorer outcomes compared to their TCR TLX1⁺ counterparts (3y-OS: 55% vs. 90%, P < 0.001 and 3y-DFS: 45% vs. 75%, P = 0.02). These findings, consistent with our previous observations in TAL1-driven T-ALL, confirm that the clinico-biological impact of an oncogene is influenced by the specific mechanism underlying its deregulation.

EBF3 transcriptionally activates ACADL and blocks the Hippo/YAP pathway to inhibit BC progression.

Notably, we discovered two small molecules, Treprostinil and 10-HCPT, as potent DHHC9 inhibitors that effectively suppressed adenocarcinoma cell migration. Our findings define the DHHC9-STRN4-YAP axis as a novel mechanism linking palmitoylation to phosphatase regulation and Hippo pathway dysregulation, unveiling DHHC9 as a highly promising therapeutic target in cancer treatment.

These results indicated that IL-6, which is upregulated by UBE2T, may be crucial for maintaining mesenchymal traits and motility in OSCC cells. Collectively, these findings suggested that the UBE2T/IL-6/JAK axis may serve as a potential therapeutic target for OSCC.

One tumor from each cohort had high tumor mutational burden and microsatellite-instability with PMS2 and ARID1A mutation. These findings suggest shared genomic characteristics among HIV + DLBCL in Africa, offering opportunities for tailored biomarkers and therapeutic targets for this underserved population.

Mechanistically, PP7080 executed its functions via promoting ubiquitination of EZH2 and sponging miR-3614-5p to regulate the downstream target gene ANKRD1. Taken together, these findings suggest that PP7080 is a novel and effective biomarker for GC therapy and may facilitate the development of lncRNA-directed diagnostics and therapeutics against GC.

Clinically, higher ANKRD17 expression correlated with aggressive HCC progression. These findings suggest that ANKRD17 enhances metastatic progression in HCC by activating pro-metastatic and pro-survival pathways.

Immunohistochemical examination of surgical specimens revealed high expression of Ankrd1 in metastatic RCC tissues compared with that in primary RCC tissues from the same patients. Collectively, these findings suggest that Ankrd1 plays a critical role in the motility of ccRCC cells through lamellipodia formation.

Data analyses and functional assays indicated ANKRD11 as a predictive biomarker for BM-LUAD. This result addresses, to some extent, the existing gap in biomarkers for BM-LUAD.

Our study deciphered the molecular mechanisms forcing EC to differentiate into the YST lineage, which is accompanied by the acquisition of cisplatin resistance, confirming that YST formation is an escape mechanism for GCT under therapy. Thus, GCT patients should be screened for YST elements under therapy to identify patients at risk of developing therapy resistance.