IGF1R (Insulin-like growth factor 1 receptor)

IGF-1R expression could potentially serve as a better predictor of PD-1/PD-L1 inhibitor response rate in patients with HPSCC compared to p16 status. Combination therapy using IGF-1R inhibitors and PD-1/PD-L1 blockade may prove to be an effective treatment approach for patients with p16+ HPSCC.

Structural analysis reveals that the mutation causes conformational changes in key conserved regions, particularly in the activation loop, compromising IGF1R's structural integrity and function. Additionally, the roles of residues Y987 and K1033 in regulating IGF1R functions were examined.

Immune profiling shows P2 as immunosuppressive, characterized by LGALS9 and M2 macrophages. Our proteogenomic analyses provide a molecular landscape of LMS, revealing biological insights, patient outcome stratification, and therapeutic targets.

Our findings suggest that the inhibition of the IGF1R-promoted, DNA-PKcs-dependent non-homologous end joining (NHEJ) repair mode is a promising strategy to prevent the activation of HSCs. To the best of our knowledge, the present study is pioneering in its exploration of the mechanism by which IGF1R mediates radiation-induced activation of HSCs by regulating DNA-PKcs.

This study represents the first report of CCND1, FGF19, and IGF1R gene amplification in a breast neuroendocrine carcinoma. These findings provide new insights into the molecular profile of this entity and may contribute to future studies on precision oncology.

The findings suggest that RTK/RAS (FGFR4, IGF1R), PI3K (INPP4B), and TGF-Beta (TGFBR2) pathway alterations may play a distinct role in HCC among H/L patients, while their prognostic significance in NHW patients remains unclear. These insights emphasize the importance of incorporating ethnicity-specific molecular profiling into precision medicine approaches to improve early detection, targeted therapies, and clinical outcomes in HCC, particularly for underrepresented populations.

These findings indicate that BYHWD may facilitate post-stroke white matter repair by modulating TREM2-dependent microglia-oligodendrocyte interactions, supporting its potential as a therapeutic approach for TREM2-associated white matter injury.

During 10-year follow-up, tumor recurrence was an important cause of death, accounting for approximately half of follow-up mortality despite the benign grading of meningiomas. This ambitious, prospective observational study failed to identify expression of GHr, Igf1r, CD34, EGFR, caspase 3 and VEGF as clinically relevant biomarkers.

Importantly, we observed that simvastatin synergised with cisplatin in reducing tumour cell proliferation. Collectively, these data suggest that simvastatin is a potential anticancer drug capable of counteracting LCT growth, and it could be proposed as an adjuvant for chemotherapy in LCT treatment.

In vivo, tumors derived from Brachy-overexpressing clones exhibited faster growth compared to those derived from IGF1R-overexpressing clones. Taken together, our results indicate that Brachy promotes EMT, leading to a more aggressive phenotype, while IGF1R favors epithelial features and reduces proliferation, suggesting opposing roles for Brachy and IGF1R in thyroid tumor biology.

A final diagnosis can be made based on all clinical and paraclinical data. The prognosis after the treatment is dependent on the pathological diagnosis, disease location and resection completeness, presence of ganglion-like cells, nuclear atypia, mitotic index, and necrosis. Not only neoplastic but also reactive lesions can recur. The presence of gene rearrangements and necrosis can have diagnostic value.

Moreover, in vivo inhibition of IGF1R reversed the armored & cold TME, thereby enhancing anti-PD-1 therapy. In conclusion, this study identified IGF1R as a novel therapeutic target for the immuno-collagenic subtype, and combining IGF1R inhibition with anti-PD-1 therapy provides a promising foundation for a novel combination immunotherapy regimen for TNBC.