PTEN (Phosphatase and tensin homolog)

Conversely, in prostate adenocarcinoma models, DNMT1 deletion leads to de-repression of neuroendocrine lineage genes with a loss of H3K27me3 marks. Our findings reveal a functional interplay between two repressive epigenetic machineries that mediates lineage plasticity in prostate cancer.

These alterations, together with oxidative stress, promote a pro-tumorigenic microenvironment. A deeper understanding of these mechanisms may enable early biomarker identification and the design of targeted preventive and therapeutic strategies for lung cancer in PLWH.

Brain MRI revealed multiple enlarged perivascular spaces involving the bilateral subcortical white matter and the corpus callosum, as well as callosal thickening. Genetic testing identified a heterozygous likely pathogenic variant in the PTEN gene, with maternal transmission confirmed on familial testing. Timely genetic diagnosis allows appropriate genetic counselling and clinical follow-up.

TP53, PTEN, and RB1 mutations were linked to inferior overall survival in LuPSMA-treated patients and may serve as prognostic biomarkers. Prospective validation is required to establish their predictive value.

The humane endpoint was reached after 6-8 weeks, allowing for timely treatment intervention and monitoring of tumor progression. Therefore, the AMG5 line provides a new tool in glioma research by generating reproducible GBM with features of mesenchymal subtype to address emerging questions and to better understand GBM development.

Our study has shown that FBXO32 facilitates HCC growth and metastasis via the PTEN/PI3K/AKT signaling through ubiquitination of TAL1. Consequently, FBXO32 emerges as a promising target for therapeutic intervention in the treatment of HCC.

By identifying 31 driver genes, mutational signatures, viral sequences, and tumor-predisposing germline variants, our study provides insight into the domestic cat oncogenome. We demonstrate key similarities with the human oncogenome, confirming the cat as a valuable model for comparative studies, and identify potentially actionable mutations, aligning with a "One Medicine" approach.

Importantly, PTEN expression partially rebounded by DPI-28, aligning with the intended transient activity window of the nanoscript system and supporting its translational safety. Through this combination of precise, nonintegrative gene modulation and broad downstream remodeling, NS-PTEN addresses both intrinsic neuronal limitations and extrinsic inhibitory features of the SCI microenvironment.

Notably, PTEN loss also results in a dependency on an activated DNA damage response pathway, leading to an exquisite vulnerability to CDK12 inhibition. Our study suggests an interferon adaptation model in which tumors driven by PTEN deficiency inherently activate the interferon response, enabling them to adapt to interferon cytotoxicity and gain resistance to immunotherapies.

Emerging data also link neutrophil-rich stromal inflammation with the tumor resident microbiome, suggesting composite TAN-microbiome biomarkers for refined risk stratification. In this review, we summarize current knowledge on phenotypic diversity, regulatory circuits and functional programs of TANs and NETs in RCC, and discuss their prognostic and predictive significance, as well as therapeutic strategies aimed at chemokine blockade, complement modulation, NET inhibition and neutrophil re-education.

Although many syndromes mimic HHT, few combine mucosal telangiectasias, high-flow AVMs, and recurrent hemorrhage. Integrating clinical, imaging, and genetic data enables precise diagnosis, risk stratification, and personalized management.

Furthermore, the inhibition of clathrin-coated vesicles (CCVs) by CHC downregulation or inhibition suppresses cell survival by reducing phosphorylated PTEN at the STT, suggesting that SCYL2 enhances PTEN phosphorylation through CCVs as a signaling platform. Our results indicate that SCYL2/CHC complex plays a pivotal role in regulating the PI3K/AKT signaling pathway through PTEN phosphorylation, thus leading to tumor development and may be a promising novel target for treating tumors.