BCL9L (BCL9 Like)

The mechanical properties of CSCs and TCs are strongly correlated with tumor type, stage, and grade, while regulatory genes such as BCL9L contribute to these biomechanical variations. Importantly, the combined biomechanical profiles of CSCs and TCs outperform the individual properties of either cell type as biomarkers for tumor classification.

Genomic diversity and BCL9L mutational status in CTC pools emerged as strong predictors of survival in mCRC, underscoring the potential of CTC genomic profiling as a minimally invasive and clinically relevant prognostic tool in mCRC.

miR-136-5p is downregulated in glioma tissues and closely correlates with tumor CT signs. It may serve as a promising biomarker to assist in glioma diagnosis using CT scans.

This study, through intergroup comparative analysis, found that immunotherapy (using programmed death 1/programmed death-ligand 1 inhibitors) may improve the prognosis of patients with short survival and chemotherapy resistance. Additionally, the study revealed that mutations in BCL9L and WHSC1 could serve as biomarkers for breast cancer prognosis, while CRTC1 mutations and Signature.3 could predict chemotherapy response. The study also found that the JAK-STAT pathway might be a potential therapeutic target for chemotherapy resistance. Therefore, this study identifies molecular characteristics that influence the prognosis of breast cancer patients, providing important theoretical insights for the development of personalized treatment strategies.

Together, we demonstrate that targeting BCL9/BCL9L plays a crucial role in cDC1-modulated antigen presentation of tumor-derived antigens, as well as CD8+ T cell activation and tumor infiltration. Targeting BCL9/BCL9L to regulate cDC1 function and directly orchestrate a positive feedback loop necessary for optimal antitumor immunity could serve as a potential strategy to counter immune suppression and enhance cancer immunotherapy.

Previous work has revealed that the ability of β-HPV8 E6 protein to inhibit Notch and transforming growth factor β signaling importantly contributes to this activity. Here, we present evidence that HPV8 E6 also subverts Hippo and Wnt signaling and that these activities also aid in restraining keratinocyte differentiation.

However, inhibition of β-catenin signaling via genetic deletion of Bcl9/Bcl9l in either Apc-deficient or mutant β-catenin mouse models restored Hnf4a, Hnf4g, and Btnl gene expression and γδ T-cell infiltration into tumors. These observations highlight an immune-evasion mechanism specific to WNT-driven colon cancer cells that disrupts γδIEL immunosurveillance and furthers cancer progression.

Our results suggest that sarcomatoid transformation exhibits adaption to hypoxia via a TGF-β/TEAD/EMT axis which is reversible by PRX3 inhibition.

Whole exome sequence showed ESCA and its subtypes, tissue block shared similar single nucleotide variants, such as TP53, ARHGAP35, CDH3 mutations, while relatively large difference in copy number variations on the basis of some common variants, such as amplification of FGFR3 (chr.4) and BCL9L (chr.11) genes.Conclusion ESCA cell line is the very first cell line of UCS until now, which showed infinite multiplication and tumorigenicity in vivo. ESCA harbored TP53, ARHGAP35, CDH3 mutations and amplification of FGFR3 and BCL9L genes, which would probably be a good model for exploring the molecular mechanism of UCS.

We identified a mutant KRAS-m6A axis in CRC leading to increased expression of BCL9L, which in turn drives an immunosuppressive tumor microenvironment by regulating CD4+ T cells and CD4+ Treg cells. BCL9L is a potential therapeutic target and prognostic marker for KRAS-mutant CRC.

Molecular typing indicated that 3 cases of UCS were of high copy number type/p53 mutation type, and 1 case had POLD1 mutation. Microsatellite stability, low PD-L1 expression and TMB results suggested that UCS patients have no obvious advantage in immunotherapy.

Lastly, Mutational signature had difference in both groups, assuming that the early-onset group had been through different event attributing to mutational changes. Although these findings should be further validated by detailed functional experiments, our genomic and transcriptomic analysis provide additional insights into understanding of young CRC patients.