CD163 (CD163 Molecule)

Furthermore, we also used Kaplan-Meier curves, multivariate analysis and penalized Cox regression model to identify six genes (C2CD5, CD163, JADE3, BIRC3, TMEM200A, and LINC00877) related to the prognosis of DLBCL. In conclusion, we developed a machine learning model integrating clinical characteristics and gene expression profiles, providing a reliable decision-support tool for DLBCL prognosis and treatment selection.

This review highlights a need for further research of the TME in each fusion subtype. This will improve our understanding of how the fusion gene drives malignancy and ultimately aids in the development of novel treatment strategies.

MPL is frequently misdiagnosed as malignancy. MetaPath can reliably detect pathogens in archival tissue and guide targeted antimicrobial therapy, representing a valuable adjunct to conventional culture.

In luminal cells, EIF1A knockdown and the translation inhibitor homoharringtonine (HHT) both suppress HIF-1α translation and tumor growth, while promoting infiltration of anticancer immune cells including PD-1- T cells and CD163- macrophages...Collectively, this work defines conserved molecular features across PCa subtypes, providing promising insights for clinical management. This study was registered at Clinicaltrials.gov (NCT06834321).

We found multiple immune suppressive markers were enriched in the endosteum, including Foxp3, CD163, CD27, Pd-1, and Pd-l1, while proliferation markers were enriched in tumor cells in the marrow, including p38 Mapk, pan-Ras, Mek1, and phospho-Erk1/2. These findings shed light on the niche-specific proteins and pathways that are activated in breast cancer bone metastases and establish a user-friendly highly multiplexed approach for spatial proteomics in pre-clinical models of bone metastasis.

MAdCAM-1 and TNF-α expression was positively correlated with inflammatory cell infiltration. This exploratory study provided the first histological evidence that MAdCAM-1 and TNF-α could be upregulated in pediatric pouchitis and associated with disease severity, highlighting the pathological relevance of adult UC therapeutic targets in this setting.

To investigate the molecular and spatial determinants of this heterogeneity, we analyzed five metastatic sites (colon, liver, peritoneum, left ovary, and right ovary) from a dMMR CRC patient treated with pembrolizumab using bulk and single-cell RNA sequencing combined with multiplex immunohistochemistry...In contrast, resistant lesions demonstrated reduced effector cell presence and were enriched in immunosuppressive programs, including SPP1+ and CD163+ macrophages, noncanonical WNT5A/B signaling, and TGF-β-mediated matrix remodeling. Collectively, these findings highlight the importance of spatial immune architecture and macrophage polarization in shaping ICI responses in dMMR CRC and underscore the need for spatial profiling to guide immunotherapy strategies in metastatic disease.

The presence of anaplastic features poses a high risk of misdiagnosis as a sarcoma or carcinoma, potentially leading to overly aggressive therapy. Therefore, we advocate for the inclusion of this entity in the differential diagnosis of adrenal neoplasms and recommend routine ALK testing in similar challenging cases to guide precise management and avoid therapeutic errors.

Together, immune subtyping and the simplified macrophage-based risk model represent complementary strategies, with the latter providing a practical tool for prognostic stratification. Targeting DOK3 offers a promising therapeutic strategy to reprogram the TME and improve clinical outcomes in patients with GBM.

These findings imply that the pathomic properties of TAMs mirror their functional aberrations. Through validation and generalization via molecular pathological examinations, this approach has the potential to unveil and understand functional aberrations in histopathological assessments.

These results indicate that an increased diversity of immune-cell subtypes influences VS tumor size. Thus, novel diagnostic and therapeutic options could be developed by targeting the tumor-associated immune-cell populations in VSs.

Drug sensitivity analysis suggested a role for KRTCAP2 in chemoresistance, with targeted inhibition enhancing glioma cell responsiveness to temozolomide (TMZ). Our findings identify KRTCAP2 as a novel prognostic biomarker in glioma, with potential utility in predicting immunotherapy response. The study highlights its clinical significance and multifaceted role in shaping an immunosuppressive glioma microenvironment, underscoring KRTCAP2 as a promising therapeutic target.