BTG1 (BTG Anti-Proliferation Factor 1)

Importantly, peripheral blood BTG1 mRNA expression levels reliably predicted therapeutic response to decitabine, establishing BTG1 as a robust biomarker of decitabine efficacy in AML management. Clinical trial registration: ChiCTR2000037928.

Clinicopathological characteristics, including hemophagocytic lymphohistiocytosis (HLH), hepatosplenomegaly, International Prognostic Index (IPI) score, treatment with chemotherapy plus rituximab, CD5 expression, histopathological patterns, germinal center B-cell-like subtype and follow-up duration, did not differ significantly between the two groups...BTG1 mutation is associated with adverse outcomes, highlighting their potential as prognostic biomarkers or therapeutic targets. These findings advance our understanding of the molecular landscape and prognostic stratification of PBM-LBCL.

BTG1 mutation was promising prognostic predictor for DLBCL. The mechanism driving different survival outcomes may be attributed to the tumor metabolic reprogramming.

Chemotherapy efficacy in relapsed pediatric B-ALL is influenced by hematologic, cytokine, and genetic factors.

While BTG1 provides insights into gastric carcinogenesis, its clinical utility is limited due to the need for tissue samples. The serum-based PGI/PGII ratio shows greater promise as a non-invasive screening tool for GC.

Low expression of BTG1 was associated with CR and MRD negativity in newly diagnosed AML patients treated with a decitabine-containing regimen, suggesting that BTG1 is a potential marker for predicting the response to decitabine in newly diagnosed AML.

Together, we demonstrate variable clonal B-cell dynamics in LPL/WM patients developing DLBCL, and the occurrence of clonally unrelated DLBCL in about one-quarter of LPL/WM patients. Moreover, we identified commonly mutated genes upon DLBCL transformation, which together with preserved mutations already present in LPL characterize the mutational landscape of DLBCL occurrences in LPL/WM patients.

The identification of specific mutations in each subgroup, which were largely consistent with previous studies, indicates that the LymphGen classifier may be valuable in individualized treatment approaches for DLBCL patients. Additionally, this study demonstrates that unclassified group ("Other") may potentially be established as a distinct subgroup.

The rescuing experiments verified that upregulation of miR-421 promoted cell viability and colony formation, and reduced apoptosis, which were abrogated by overexpression of circITCH or BTG1. In conclusion, this study identified a novel circITCH/miR-421/BTG1 axis that restrained the development of HCC, and our findings provided novel biomarkers for the treatment of this disease.

Additionally, compared to control groups, CAR.15.amiR-BTG1 NKTs mediated durable antitumor activity in an aggressive model of metastatic neuroblastoma, inducing complete tumor regression in all treated animals (Fig 2G-I). These results establish BTG1 as a novel mediator of hyporesponsiveness in human NKT and non-naïve T cells and suggest that BTG1 silencing may broadly benefit the development of cancer immunotherapy.

This effect was conferred by a small shift in MYC protein induction kinetics but resulted in aggressive invasive lymphomas, which in humans are linked to dire clinical outcomes. Our findings reveal a delicate evolutionary trade-off between natural selection of B cells to provide immunity and potentially dangerous features that recall the more competitive nature of unicellular organisms.