The risk model constructed in this study effectively predicts the prognosis of LUAD patients. PLEK2 is highly expressed in LUAD and associated with EGFR-TKIs resistance, suggesting its potential as a prognostic biomarker and therapeutic target.
2 months ago
Journal
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KRAS (KRAS proto-oncogene GTPase) • TP53 (Tumor protein P53) • HMGA1 (High Mobility Group AT-Hook 1) • ID3 (Inhibitor Of DNA Binding 3, HLH Protein) • PLEK2 (Pleckstrin 2)
This prognostic model constructed based on CCCR genes represents a valid tool for the prognosis of LUAD patients. Our findings provide valuable insights into the prognostic and immunological relevance of CCCR genes in LUAD, offering a robust foundation for personalized treatment strategies and future research.
4 months ago
Journal • Tumor mutational burden
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TMB (Tumor Mutational Burden) • EREG (Epiregulin) • IGFBP1 (Insulin Like Growth Factor Binding Protein 1) • PLEK2 (Pleckstrin 2)
In conclusion, our study highlights the pivotal role of PLEK2 in BC cell dynamics and introduces HOXD9 as a novel regulator of PLEK2. Targeting the HOXD9/PLEK2/AKT signaling axis may offer a promising therapeutic strategy for treating breast cancer.
This study proposes a glycolysis assessment strategy based on the interquartile range, which effectively addresses the limitations of previous scoring methods, including insufficient resolution and limited robustness. The proposed method enables more accurate quantification of intracellular glycolysis levels and facilitates fine-grained characterization of metabolic states. Furthermore, it identifies GPRC5A as a potential biomarker for the early diagnosis of gastric cancer. These findings enhance our understanding of metabolic reprogramming in gastric cancer and provide support for targeting the glycolytic pathway in therapeutic interventions.
6 months ago
Journal
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CLDN1 (Claudin 1) • IFNAR2 (Interferon Alpha And Beta Receptor Subunit 2) • CLDN3 (Claudin 3) • GPRC5A (G Protein-Coupled Receptor Class C Group 5 Member A) • PGK1 (Phosphoglycerate Kinase 1) • PLEK2 (Pleckstrin 2)
High expression of nucleotide synthetic enzyme thymidylate synthase (TYMS) is responsible for the resistance to fluorouracil (FU) treatment and worse survival in colorectal cancer (CRC)...PLEK2 inhibition is sufficient to ameliorate the progression of AOM/DSS-induced CRC. Together, our study identified PLEK2 as a key regulator for the progress of CRC via the regulation of TYMS expression, and demonstrated that PLEK2 is a novel therapeutic target for CRC.
We established a novel DCRS with robust prognostic and predictive value in LUAD. This work highlights the pivotal role of dendritic cell programs in shaping the tumor microenvironment and provides potential targets for improving precision immunotherapy.
Cyclosporin A also markedly reduced JAK2 mutated erythroid and myeloid proliferation in an induced pluripotent stem cell-derived human bone marrow organoid model. Our findings revealed PPIL2 as a critical component of the PLEK2 signalosome in driving MPN pathogenesis through negatively regulating p53, thus providing a target and an opportunity for drug repurposing by using cyclosporin A to treat MPNs.
In conclusion, the DAMPscore is a promising prognostic biomarker for PAAD, surpassing traditional models in various datasets. This study emphasizes the role of DAMP-related pathways in influencing tumor biology and highlights the importance of immune modulation in PAAD prognosis, suggesting that therapeutic strategies targeting DAMP signaling could improve patient outcomes.
Additionally, PLEK2 identified as a miR-138-5p target gene. The potential regulatory role of circCNKSR2 in NSCLC progression and Warburg effect via the miR-138-5p/PLEK2 pathway was demonstrated.
PLEK2 is upregulated in UVM and correlates with poor patient prognosis, likely influencing the calcium signaling pathway. PLEK2 represents a promising prognostic biomarker and therapeutic target for UVM.
Compounds like Navitoclax were also identified as potential PLEK2 inhibitors. In conclusion, PLEK2 played a multifaceted role in cancer progression and immune response modulation. Targeting PLEK2 might suppress tumor growth and overcome immunotherapy resistance, offering a promising biomarker and therapeutic target to improve cancer treatment outcomes.
over 1 year ago
Journal • PD(L)-1 Biomarker • IO biomarker • Pan tumor
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CD8 (cluster of differentiation 8) • PLEK2 (Pleckstrin 2)
Overall, the present study suggests that PLEK2 may play a tumor-promoting role in PDAC. These findings provide valuable insights into the molecular mechanisms of pancreatic cancer and highlight the potential of PLEK2 as a therapeutic target.