TCF12 (Transcription Factor 12)

This study emphasizes the role of alternative splicing in glioma cellular heterogeneity, highlighting the importance of an isoform-centric approach to better understand the complex biological processes driving tumorigenesis.

This study reveals how cancer cells abnormally upregulate SLC7A11 by hijacking multi-level mechanisms, gaining strong antioxidant/anti ferroptotic abilities, which are the core basis for their survival, proliferation, and resistance to treatment. This study also identified SLC7A11 as a convergence point for multiple key pathways, making it an ideal hub target for intervening in cancer and overcoming drug resistance.

Our results highlight the potential utility of Cisd2 and its activator hesperetin in chemotherapy involving doxorubicin.

Prognostic models based on tumor microenvironment and immune score stratification and the construction of related genes have potential applications for prognostic analysis of GBM patients.

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.

In contrast, among cases with a high Immunoscore, the AS score effectively distinguished outcomes (p < 0.0001), identifying a subgroup with poor prognosis but potential sensitivity to immunotherapy. This combined classification using the AS score and Immunoscore has prognostic relevance in sarcoma, suggesting that angiosarcomas with an immunologically active microenvironment (high Immunoscore) and poor prognosis (high AS score) may be prime candidates for immunotherapy and this approach warrants prospective validation.

This multi-omics study provides unprecedented insights into the transcriptional and epigenetic heterogeneity of t(8;21) AML, providing a potential actionable tool for clinical risk stratification.

Additionally, Sorafenib treatment upregulates TRIM21, enhancing ID1 ubiquitination, increasing SLC31A1 expression, and inducing cuproptosis. These findings uncover the TRIM21-ID1-TCF12-SLC31A1 axis as a critical pathway in ESCC progression, suggesting that targeting this axis with Sorafenib can offer a promising therapeutic strategy for inhibiting tumor growth and improving patient outcomes.

Moreover, TCF12 silencing inhibited tumorigenesis in vivo. TCF12 targeted SLC38A1 to promote HCC cell proliferation, migration and invasion and restrained ferroptosis, providing a novel sight for HCC pathogenesis.

In conclusion, the project investigated the prognosis and classification value of nitrogen metabolism-related genes in GBM from multiple perspectives, predicting the sensitivity of different subtypes of patients to immunotherapy response and drug sensitivity. These findings are expected to show new research directions for further exploration in these fields.

Finally, by interacting with the aforementioned targets, cells, Res is thought to impede the evolution of OS. In conclusion, ferroptosis and alterations in the immunological milieu are significant factors in the development of OS, and Res may one day be employed as a therapeutic drug to treat OS.

Further analysis of glioma-infiltrating immune cells reveals potential isoform-level regulation of protein glycosylation in regulatory T cells and a link between MS4A7 AS in macrophages and clinical response to anti-PD-1 therapy. This study emphasizes the role of AS in glioma cellular heterogeneity, highlighting the importance of an isoform-centric approach to better understand the complex biological processes driving tumorigenesis.