TEST:

nCounter® Tumor Signaling 360 Panel

After transformation, tFL samples showed a reduction in T follicular helper cells (p=0.008) and an increase in immunosuppressive M2-like macrophages and neutrophils (p<0.001 and p=0.028, respectively). By elucidating the distinct molecular and immune landscapes of FL at the time of diagnosis and transformation, this study underscores the importance of immune microenvironment in FL transformation and patient outcome.

After transformation, tFL samples showed a reduction in T follicular helper cells (p = 0.008) and an increase in immunosuppressive M2-like macrophages and neutrophils (p < 0.001 and p = 0.028, respectively). By elucidating the distinct molecular and immune landscapes of FL at the time of diagnosis and transformation, this study underscores the importance of immune microenvironment in FL transformation and patient outcome.

Our findings implicate a putative role for dysregulation in glucose metabolism, TGF-β and HIF1 signaling in the pathogenesis of both WD/DDLPS suggesting a possible proinflammatory tumor environment within WDLPS and subsequent activation of the TGF-β signaling pathway. Additional studies are warranted to understand the role of these pathways in the pathogenesis of WD/DDLPS.

with validation in a large series of cases. The currenty study has evolved a panel of biomarkers, namely PRDX6, MLANA and AR to be potentially useful in identifying high-risk OSMF patients with an increased risk of OSCC development.

Type A and B3 thymomas and thymic carcinomas harbor clinically relevant, differentially expressed genes. Furthermore, a subset of these genes appears to be uniquely differentially expressed by TET subtype, which may be useful in distinguishing these entities. Further analysis to correlate gene expression with clinical features, outcome, and available target therapies will be performed.

Genes differentially expressed (<8 genes per patient) in multifocal disease were all upregulated in LDT-treated tumors from pathways involving epithelial mesenchymal transition, extracellular matrix remodeling, and/or inflammation potentially implicating intrahepatic metastases. Incomplete response to LDT may drive expression patterns that inhibit an effective anti-tumoral response through immune exclusion and induce intrahepatic spread.

mRNA gene expression profiles between HCC tumors are remarkably similar . LDT history and radiographic characteristics of the lesions did not impact mRNA expression in genes for common cancer pathways and those involved in immune evasion and antitumoral immunity . The high overlap in mRNA expression profile of multifocal patients suggests intrahepatic spread as opposed to de novo HCC generation .

Conclusions Utilizing multi-platform immune profiling approaches, we observed a distinct relationship between the TT and immune signatures. Understanding underlying immune signatures underpinning the biology of thick versus thin MPM tumors provides insights to potential responsiveness to immune-based therapies and may inform on the design for future novel strategies relative to the disease extent based on TT.

mRNA gene expression profiles between HCC tumors are remarkably similar. LDT history and radiographic characteristics of the lesions did not impact mRNA expression in genes for common cancer pathways and those involved in immune evasion and antitumoral immunity. The high overlap in mRNA expression profile of multifocal patients suggests intrahepatic spread as opposed to de novo HCC generation.