PTPRD (Protein tyrosine phosphatase receptor type D)

Because PTPRD functions are pathway-specific and shaped by mini-exon usage or redundancy with other family members (PTPRS/PTPRF), domain- or ligand-selective interventions represent plausible therapeutic strategies. Elucidating its full ligand repertoire, substrate landscape, and structural basis for allosteric regulation will be critical for converting this versatile receptor from a mechanistic curiosity into a tractable target for neurodevelopmental, neuropsychiatric, and metabolic disorders.

Elevated FLI and upregulation of adipokine receptor expression highlight the potential of combining plasma-based and molecular biomarkers for EC diagnosis. However, the lack of independence from BMI and conflicting literature underscore the need for larger, standardized studies to validate these findings and determine clinical applicability.

This study indicates that PD-L1 expression levels are significantly associated with specific genomic alterations and clinical outcomes in patients with NSCLC. Particularly in evaluating the efficacy of ICI therapy, the combined biomarker of PD-L1 and TMB shows important clinical application value.

Patients with obesity and low hepatic PTPRD expression exhibit increased levels of metabolic risk factors. Our data revealed an important regulatory role of the hepatic PTPRD-STAT3 axis in maintaining glucose/lipid homeostasis, which is recapitulated in clinical manifestations of metabolic liver disease.

Hub genes PTPRD and DSCAM provide insights into potential molecular mechanisms, suggesting the potential role of Defluviitaleaceae UCG011 in modulating the initiation and progression of CRC. Further research is essential to validate these associations and delve deeper into therapeutic implications.

This interaction is proposed to suppress phosphatase activity. Our findings therefore suggest that HSPG-mediated attenuation of phosphatase activity may be involved in tumorigenic processes through PTPRD dysregulation.

According to our results, this decrease in gliogenesis resulted from a reduced number of radial glia cells at gliogenesis onset and a lower gliogenic potential in cortical neural precursors due to less activation of the JAK/STAT pathway and reduced expression of gliogenic genes. Our study shows PTPRD as a regulator of the glial/neuronal balance during cortical neurodevelopment and highlights the importance of studying glial development to understand the etiology of neurodevelopmental diseases.

Our data indicate that PTPRD may have potential as a biomarker for malignancies such as EC and GBM, further implicating asprosin as a potential metabolic regulator in these cancers. Future studies are needed to explore the potential molecular mechanisms/signalling pathways that link PTPRD and asprosin in cancer.

Our study suggested that PTPRD mutations could serve as a predictive biomarker for the sensitivity to ICIs treatment and PFS and OS in advanced NSCLC with ICIs. Our systematic nomograms showed great potential value in clinical application to predict the PFS and OS for advanced NSCLC patients with ICIs.

Our patient’s composite gene signature, recurrent rhabdomyosarcoma with unusual immunophenotype, and metastases with neuronal/neuroblastic elements suggest a closer genetic link of MEM to adult rhabdomyosarcoma. This association supports further research into the role PTPRD mutation may play in adult sarcomas and its implication for the diagnosis, tumor behavior, prognosis, and treatment of adult rhabdomyosarcoma.

PTPRD mutation could derive active immunoediting via cGAS-STING pathway and potentiate ICB therapy in TP53-mutant NSCLC. Targeting PTPRD might transform the immune tolerance status in TP53-mutant NSCLC with wild type PTPRD.

However, they differ in the presence of recurrent translocations, mutations affecting the Notch signaling pathway (NOTCH2 and less commonly NOTCH1), the transcription factors Kruppel-like factor 2 (KLF2) or the receptor-type protein tyrosine phosphatase delta (PTPRD). This review summarizes the most recent and significant advances in our understanding of the epidemiology, genetics, and biology of MZLs and outlines the current principles of the standard management of MZL at different anatomic sites.