TAF15 (TATA-Box Binding Protein Associated Factor 15)

This SOX10-TAF15 complex subsequently enhanced ACAT2 protein levels, stimulated cholesterol synthesis, suppressed apoptosis, and ultimately drove melanoma proliferation. Our findings reveal that the SOX10-TAF15-ACAT2 axis is a key regulator of cholesterol synthesis and melanoma proliferation, presenting a promising therapeutic target.

The structure is unable to incorporate wild-type TAF15, despite the individual being heterozygous, suggesting that this variant drives TAF15 filament assembly. This study provides structural and genetic evidence that TAF15 amyloid filaments underlie the diverse group of neurodegenerative diseases currently termed FTLD-FET, which we therefore rename FTLD-TAF15.

LINC01940 is a cancer-testis lncRNA that promotes GC progression and cisplatin resistance by enhancing ribosome biogenesis via the METTL16/IGF2BP3-TAF15-NOL11 axis. These findings suggest its potential as a prognostic biomarker and therapeutic target in GC.

The developed M2pep-LNP-siTAF15 nanodelivery system not only overcomes the challenge of targeted delivery, but its remarkable antitumor efficacy highlights strong potential for clinical translation. This work fundamentally advances our understanding of stromal-immune crosstalk in cholangiocarcinoma while offering a clinically actionable therapeutic strategy.

CD10, CD19 and MPO in one flow cytometry tube facilitated distinguishing B-cell acute lymphoblastic leukemia with dim expression of MPO versus B/myeloid mixed phenotype acute leukemia. B-ALL chemotherapy followed by blinatumomab bridging to allogeneic stem cell transplantation was successful in our patient.

Our work shows, for the first time, a broad overview on the extra-telomeric role of TRF2 in human cancer, further revealing a new axis through which TRF2 contributes to cancer progression.

Furthermore, ALS-linked mutations in TAF15 impair its ability to undergo phase separation, reduce binding to hnRNPA0, and eliminate transcriptional enhancement. These findings suggest that TAF15's C-terminal LC domain connects hnRNPA0 to transcriptional regulation, and that this mechanism is disrupted in ALS-associated mutations.

No spontaneous activation in the absence of antigen was observed. Together, our work demonstrates IDRs as a new toolset for improving CAR-T function through inducing biomolecular condensation.

These data suggest that FET oncoproteins act together with fully assembled and functional SWI/SNF complexes and recruited interaction partners. Finally, our data reveal that the SWI/SNF compositions, interactomes, and epigenetic background contribute to the tumor type in FET sarcoma. Trial registration Clinical trial number: not applicable.

B-ALL patients harboring the TAF15::ZNF384 fusion gene often present with complex chromosomal abnormalities at the initial diagnosis and the immunophenotype is often characterized by B lymphatic system with positive myeloid markers. CAR-T immunotherapy followed by allo-HSCT may offer a promising approach to improving their prognosis.

Treatment with the small molecule SP-2509 results in reversal of the transcriptional activity of the FET fusion that causes Ewing sarcoma, EWSR1::FLI1. This included reversal of FET-fusion transcriptional signatures for EWSR1::WT1, EWSR1::ATF1, and EWSR1::ERG. Though novel inhibitors are unlikely to display single-agent efficacy in the clinic, these data suggest seclidemstat remains a promising new treatment strategy for patients with FET-rearranged and other fusion positive sarcomas.

Similar to other translocation-associated sarcomas, the number of co-occurring SGAs in EMC is low; however, when present, they are associated with worse survival. Although a higher number of SGAs showed a trend to be associated with non-EWSR1 fusion variants, larger multi-institutional studies are needed to further evaluate the correlation between fusion variants with SGAs and survival.