BTG2 (BTG Anti-Proliferation Factor 2)

A prognostic nomogram integrating miR-15b-5p, BTG2 and clinical parameters demonstrated robust predictive accuracy (C-index: 0.78). The miR-15b-5p/BTG2 axis represents a novel regulatory mechanism in ESCA progression with significant potential as both a prognostic biomarker and therapeutic target.

The pharmacokinetics study strengthened our results that the identified drugs can be used as a therapeutic for PDAC as they obey Lipinski's rule. In conclusion, identified genes can act as prognostic markers, and drugs could be used as potential therapeutics for PDAC.

Although not associated with immune subtypes, IBC showed differences in HER2 and P53 pathways. The association of IBC with rurality and poverty underscores the importance of health care access for timely diagnosis and treatment of IBC.

In conclusion, these findings suggest that MLN4924 exerts an anti-tumor effect on AML by inducing apoptosis through the ROS-EGR1-BTG2 signaling axis. Our research provides a novel theoretical basis for the clinical potential of MLN4924 in improving the treatment of AML patients, offers novel strategies for AML treatment, and thereby advances the implementation of precision medicine.

The carcinogenic role of NOX2 in ESCC may be associated with the regulation of BTG2 expression. The aberrant expressions of NOX2 and BTG2 are associated with the prognosis of patients with ESCC, suggesting that NOX2 and BTG2 could serve as potential biomarkers and therapeutic targets.

These findings indicate that Nkx2-2as acts as a negative regulator of Wnt/β-catenin signaling through BTG2 activation, suggesting its potential role as a tumor suppressor and a candidate for RNA-based therapeutic strategies in BC. Targeting the Nkx2-2as/BTG2 axis may provide a conceptual framework for future studies aimed at developing RNA-based interventions to enhance chemosensitivity and overcome therapy resistance in BC.

This review comprehensively examines the dysregulated expression patterns and functions of KIAA1429 in NSCLC, elucidating its m6A-dependent modulation of key downstream effectors (Such as the HOXA1, DAPK3, and BTG2) that orchestrate malignant transformation. We highlight the emerging potential of KIAA1429 as a novel molecular target for precision therapy in NSCLC.

5-Azacitidine (5-Aza) is a hypomethylating agent with demonstrated therapeutic efficacy for myeloid leukemia...The results revealed that two genes (HDC and MICALL2) with increased expression in leukemia cells after 5-Aza treatment were associated with better overall survival, while six genes (BTG2, CD52, PECAM1, PIK3IP1, PTGS2, and TREML2) correlated with worse overall survival. This study revealed that the epigenetic regulation by DNA demethylation in intron 1 has an important role of 5-Aza treatment in myeloid leukemia cells, and suggests novel targets for the development of combination therapy with 5-Aza.

In three MAG neuropathy patients we find evidence that the self-reactive B cells responsible for their disease acquired a classical lymphoma driver somatic mutation early in their clonal expansion.

LncRNA SNHG5 inhibited GC cell growth and migration by modulating the PI3K/AKT pathway via the miR-92a-3p/BTG2 axis.

hsa-miR-125a-5p and -99b-5p are causal protective factors against PCa, modulating oncogenic pathways and survival. These miRNAs offer potential as noninvasive biomarkers and therapeutic targets, advancing precision oncology.