Stromal myeloid cells showed increased CD47 and PD-1 expression. Our study identified distinct epigenetic profiles in sacral chordomas, which were associated with recurrence, and revealed expression of checkpoint markers TIM3, CD47 and PD-1, warranting further investigation through functional validation.
The tumor mutational burden was low overall, varied between patients and timepoints, and tended to be higher in recurrent cases. Quantitative nuclear morphometry, integrated with immunophenotyping and genomic profiling, captures recurrence-associated phenotypic remodeling in chordoma and may provide a quantitative framework for future digital pathology or AI approaches, pending validation in larger cohorts.
The immunosuppressive chordoma TME is associated with clinical outcomes and our data suggests OV infection reverses this deleterious immunosuppressive profile. These studies provide a framework for future clinical implementation amongst chordoma patients.
In this study, we demonstrated that thyroid cancer is the most common malignancy in Turkish acromegalic patients, consistent with the results of previous studies. The increased cancer risk in acromegalic patients did not correlate with age, sex, age at diagnosis, time to diagnosing acromegaly, duration of acromegaly, or GH and IGF-1 levels at diagnosis.
These findings suggest the potential role of CHI3L1 in chordoma tumorigenesis, emphasizing its relevance as a biomarker and therapeutic target for primary tumors. Future studies are necessary to elucidate the mechanistic role of CHI3L1 in chordoma immune evasion and to explore targeted interventions that may improve patient outcomes in this aggressive cancer.
MMP13 may promote aggressive behavior in chordoma by degrading growth-inhibitory COL2-rich ECM. These data support MMP13 as a potential unfavorable prognostic marker and therapeutic target in chordoma.
FISH detection of NR4A3 gene rearrangements provides a crucial value for the diagnosis. It needs to be differentiated from myoepithelial tumors, chordomas and myxoid liposarcomas.
2 months ago
Journal
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • EWSR1 (EWS RNA Binding Protein 1) • CD34 (CD34 molecule) • NR4A3 (Nuclear receptor subfamily 4 group A member 3) • VIM (Vimentin)
MIR31 deletion upregulates LYN, enhancing stiffness perception and tipping the balance toward O-GlcNAc addition to NICD1, finally resulting in mechanoadaptation- and tumor stemness-driven recurrence. Consequently, MIR31 deletion is a potential biomarker for recurrence and patient stratification in Notch- or OGT-targeted therapies.