PBX3 (PBX Homeobox 3)

FET-rearranged MET are epigenetically unrelated to cutaneous and salivary gland MET, and their malignant counterparts are best classified as sarcomas rather than carcinomas.

This uncovered consistent synergy between menin and lysine-specific demethylase 1 (LSD1) inhibition, including with the clinical agent iadademstat...In vivo, the combination produced potent antileukemic effects in both MOLM-13 and MLL-r patient-derived xenografts, markedly reducing leukemic burden and extending survival without overt toxicity. These findings identify LSD1 as a critical cofactor of the menin-MLL-LEDGF axis and establish concurrent menin and LSD1 inhibition as a mechanistically informed combinatorial therapeutic approach in MLL-r AML.

Notably, ALDH2-high tumors exhibited resistance to immune checkpoint blockade (ICB), whereas combinatorial ARG2 inhibition and ICB therapy synergistically restored antitumor immunity. These findings nominate ARG2 as a novel therapeutic target and propose dual metabolic-immunologic intervention as a promising strategy for ICB-resistant CRC.

HCP5 acts as an oncogenic lncRNA in GC by promoting cell viability, migration, and proliferation via the miR-526b/PBX3 axis. Targeting the HCP5/miR-526b/PBX3 axis may represent a promising therapeutic strategy for GC.

AFH occurring in distal extremity/acral locations have a predilection for females, upper extremity locations, frequent unusual (solid, non-angiomatoid and myxoid) morphology and higher frequency of CREM over ATF1 fusions. Awareness of the morphologic spectrum of these rare neoplasms is essential for correct classification.

Positive correlations were observed between NUP210 and MEIS1/PBX3, with MEIS1 and PBX3 proteins interacting with the HOXA9 protein. Our results demonstrated that NUP210 was remarkably upregulated in AML and may promote the malignant behavior of AML cells by upregulate HOXA9 gene expression, offering new insights for AML treatment.

Methylation profiling showed case 1 to cluster with cutaneous squamous cell carcinoma, while case 2 was independent but positioned close to salivary gland epithelial-myoepithelial carcinoma. These findings expand on the histopathologic and molecular genetic features of basaloid tumors with apparent adnexal differentiation and raise awareness to carefully interpret and correlate molecular findings with morphology and immunophenotype to avoid misinterpretation as a mesenchymal neoplasm.

These findings provide novel insights into tumor metabolic reprogramming and uncover a previously unknown physiological function for PBX3. Moreover, these results suggest the potential of targeting PBX3 as an anti-tumor therapeutic strategy.

The present study identifies a cis-regulatory element, named SFE1, that interacts with PBX1/3 either directly or within a complex with cofactors to modulate SHH expression in the FEZ. This research establishes that PBX1 and PBX3 play complementary roles in SHH regulation during embryonic development.

HOX-PBX-WNT interactions contribute to the distinct biology of NPM1-mutated CN-AML. Targeting this axis may offer novel therapeutic strategies for AML, warranting further research into molecular-driven treatments for AML.

Notably, obeticholic acid, identified as an ETV5 inhibitor in this study, exhibited promising efficacy in suppressing NEPC development. This study highlights ETV5 as a key transcription factor that facilitates NEPC development and underscores its potential as a therapeutic target for this aggressive cancer subtype.

Accordingly, enhancing interferon response by interferon-α (IFNα) administration induces leukemic cell differentiation, and inhibiting MA9 transcriptional activity on top of the enhanced IFN signaling further delays leukemia progression. Our study underscores the importance of Pbx3-mediated suppression of interferon response genes in the progression of MA9-induced AML and highlights the potential application of type I interferon for its treatment.