ATF7IP (Activating Transcription Factor 7 Interacting Protein)

Our findings emphasize the intricate transcriptomic profiles in oral leukoplakia and proliferative verrucous leukoplakia development, laying the groundwork for future studies to enhance clinical management and patient outcomes in oral oncology. Syndecan 3 gene polymorphisms may represent a key point in proliferative verrucous leukoplakia differential diagnosis and prognostic prediction.

To be brief, circ-ATF7IP is a newly identified biomarker for PTC related LNM. Targeting circ-ATF7IP/miR-488-3p/IL13RA1 axis is a promising therapeutic strategy for PTC.

Meanwhile, ATF7IP stabilizes the antioxidant sensor Parkinsonism-associated deglycase (PARK7) protein which preserves the transsulfuration pathway to produce GSH, also leading to the inhibition of Sorafenib-induced ferroptosis. In conclusion, our findings identify ATF7IP as a critical ferroptosis inhibitor and represent ATF7IP as a novel therapeutic target for Sorafenib-based combination therapies of hepatocellular carcinoma.

Notably, depletion of ATF7IP by two complementary cre-recombinase alleles in mice (CAG-CreERT2 and Mx1-iCre) impedes the migration of hematopoietic progenitors to the thymus, resulting in declined T lymphopoiesis. These findings establish the role of ATF7IP/SETDB1-mediated epigenetic programming in governing T lymphoid progenitor trafficking and differentiation, with implications for understanding the pathogenesis of human T lymphoid diseases.

Our large study extends the number of genome-wide significant risk loci identified for endometrial carcinoma by about one-third and proposes a role of NAV3 as a tumour suppressor in this common cancer.

In this review, we first discuss the role of SETDB1 in gene regulation through its histone methyltransferase activity, including an overview of its structural features and key cofactors. We then highlight the lineage-specific roles of SETDB1 in both normal hematopoietic processes and hematological malignancies, emphasizing its function as an immune checkpoint molecule that suppresses natural killer (NK) cell-mediated antileukemia responses.

Multi-compartment correlation analysis revealed three ecosystem-level patterns: (1) Inverse association between Epi_Diff and Epi_pEMT (Spearman R = -0.43); (2) Negative correlation between mCAF1 abundance and cCAF frequency (R = -0.48); (3) TAM(SPP1) dominance inversely correlating with both TAM(C1Q) (R = -0.43) and NK/T infiltration (R = -0.36). These axes suggest a potential hierarchical ecology framework where lineage-specific polarisation and inter-compartment synergies may collectively govern disease progression.

Additionally, we identified two fibroblast subgroups in a transforming state, indicating a potential epithelial-mesenchymal transition. Our research offers profound insights into the heterogeneity of fibroblasts between the PT and MLN in OSCC, serving as an essential resource for future drug discovery endeavors.

Monocytic acute myeloid leukemia (AML) responds poorly to current treatments, including venetoclax-based therapy...We also identified the expression of myeloid cell nuclear differentiation antigen (MNDA) and its murine counterpart Ifi203 as biomarkers to predict the sensitivity of AML to SETDB1 depletion. Our study highlights the critical and selective role of SETDB1 in AML with granulo-monocytic differentiation and underscores its potential as a therapeutic target for current unmet needs.

CNAs were detected in 5/11 (45%) cases, with copy gains involving chromosome 12 occurring in 3/11(27%). In conclusion, no recurrent fusions or pathogenic variants have been detected in the present COF cohort, with copy gains involving chromosome 12 occurring in 27% of cases.