RARG (Retinoic Acid Receptor Gamma)

Importantly, CFI did not affect TC cell-autonomous proliferation, suggesting that its pro-tumoural effects are mediated by the TME rather than directly on tumour cells. Collectively, Our findings establish RARγ/CFI signalling as a microenvironmental rheostat controlling TAM polarisation and provide new insights into the immunobiology of thyroid cancers.

Analysis of ClinPGx/PharmGKB data emphasizes ABCB1 as a potential resistance marker and supports pre-treatment genotyping of genes like TPMT and NUDT15 to prevent severe toxicities. Future advances should include the expansion of pharmacogenetic studies in underrepresented populations and the clinical validation of new markers in prospective trials, aiming to consolidate precision medicine as a routine part of the therapeutic management of acute leukemias.

Taken together, RARγ-mediated transcriptional regulation is multi-faceted and context-dependent. The delineation of these key RARγ targets and signaling pathways should allow the development of new therapeutics for OCSCC.

In recent years, a novel type of tripartite retinoic acid receptor (RAR) fusion genes has been identified in atypical APL (aAPL), exhibiting distinct structural characteristics and pathogenic mechanisms compared to the classical bipartite fusion. This article systematically introduces relevant content in this field: it begins by outlining the long-standing scientific puzzle of inconsistent clinical resistance versus in vitro sensitivity in aAPL patients; subsequently, it describes the discovery process and structural features of tripartite fusion genes in all RARG and specific RARA-related cases, and elucidates the key molecular mechanism by which tripartite fusion leads to all-trans retinoic acid (ATRA) resistance at the protein conformational level; finally, the discovery of transposon involvement in the formation of tripartite fusions and its implications for the mechanism of fusion gene are discussed.

The former partner gene is RARG, with clinical manifestations, bone marrow morphology, and immunophenotype similar to APL. The latter partner gene is HOXC13, with the characteristics of NUP98-AML patients.

Although gemcitabine plus cisplatin (Gem/Cis) represents a standard chemotherapy option, treatment resistance significantly limits the outcomes. This resulted in increased cancer cell apoptosis and a remodeled immune microenvironment, characterized by reduced PD-L1 expression and enhanced CD8+ T cell activation. Taken together, this study identified LA as a novel metabolic modulator that potentiates chemotherapy response in BTC through RARγ activation, orchestrating a dual antitumor response by promoting cancer cell apoptosis and enhancing antitumor immunity.

Our findings provide new insights into the TNBC microenvironment, emphasizing the complex spatial interactions between different cell types and highlighting key regulatory pathways that could be targeted for future therapeutic interventions. This spatial cell atlas lays the foundation for further exploration of tumor microenvironment dynamics and precision oncology approaches.

The attention maps also enhance the model's interpretability. Such a novel and rapid diagnostic approach for APL subtypes, which achieves high - precision identification and pixel - level visualization, holds significant clinical value.

In a three-dimensional tumor spheroid model, immunosuppressive macrophages enhanced the proliferation of HCT116 colorectal cancer cells, which was significantly hindered by RARγ inhibition. These findings suggest that targeting RARγ reprograms immunosuppressive macrophages and mitigates the tumor-promoting effects of TAMs, highlighting RARγ as a promising therapeutic target for developing novel anti-cancer strategies.

Notably, we found that supplementing the mTeSR1 basal medium with XAV939, a Wnt/β-catenin pathway inhibitor, supported robust self-renewal and pluripotency maintenance of SD-iPSCs. Furthermore, using a bovine trophoblast stem cells (TSC) induction protocol, we successfully derived CDX2-positive trophoblast-like cells from SD-iPSCs. The establishment of SD-iPSCs not only offers a valuable model for studying mammalian pluripotent stem cells but also provides a versatile platform for biotechnological and translational research.

Upon identifying the tripartite fusion gene, the treatment was switched to idarubicin combined with cytarabine chemotherapy. At the most recent follow-up of 16 months post-transplantation(May 2025), the patient remained in continuous remission. Sequence and fusion protein structural analyses revealed that the tripartite fusion leads to truncation of the ligand-binding domain of RARG gene, which is the key molecular mechanism underlying ATRA resistance.