FSTL1 (Follistatin Like 1)

Furthermore, increased FSTL1 expression has been found in the inflammatory synovial tissues of patients with osteoarthritis and it contributes to nucleus pulposus cell inflammation. In conclusion, the distinctive structural features and widespread expression of FSTL1 position it as a key target for understanding the mechanisms underlying inflammation, senescence and tumourigenesis, providing potential options for novel diagnostic and therapeutic strategies for these conditions.

Reduced circulating FSTL-1 levels were independently associated with sarcopenia in patients with cancer-related malnutrition. These results indicate that FSTL-1 may act as a biomarker of impaired muscle quality and mass, as reflected by AI-assisted ultrasound and bioimpedance parameters.

Our findings indicate that elevated FSTL1 levels may contribute to advanced clinical characteristics and worse outcomes in DLBCL. FSTL1 contributes to drug resistance likely through DIP2a/ICAM-1-mediated adhesion mechanism.

These results highlight the potential of network-informed machine learning to identify subtle proteomic patterns and pathway-level dysregulation prior to clinical diagnosis. This proof-of-concept study supports further development of GNN approaches for early ovarian cancer detection and warrants validation in larger, independent cohorts.

In summary, the findings of the study indicate that elevated FSTL1 expression could serve as a prognostic biomarker for unfavorable outcomes in colorectal cancer (CRC) diagnosis and may also identify potential targets for immunotherapy in CRC.

These data suggest that high baseline levels of both FSTL1 and DIP2A+ cells in peripheral blood are significant poor prognostic factors for nivolumab therapy for advanced GC. Targeting the FSTL1-DIP2A axis may be a promising strategy to improve clinical outcomes in GC as a biomarker to predict anti-PD1/PDL1 therapeutic efficacy more accurately.

These findings indicate that circulating CTRP3, CTRP9, and FSTL1 concentrations are affected by exercise intensity during endurance exercise, increasing only after high-intensity exercise.

CTRP6 levels were found to be higher in obese children than in the healthy control group, while FSLT1 and FAM19A5 levels were found to be lower. Changes in the levels of these adipokines may play important roles in obesity and related conditions.

Furthermore, FSTL1 intensifies the inflammatory response at osteolytic sites, also contributing to the progression of osteolysis. Our findings indicate that FSTL1 may represent a promising therapeutic target for the treatment of periprosthetic osteolysis.

Both proteins participate in multiple important signaling pathways, and understanding their diagnostic and therapeutic potential holds great scientific interest. Their complex nature requires careful evaluation of safety concerns and translation to clinical practice.

The changes identified indicate a complex reprogramming of transcriptional activity affecting cell cycle processes, DNA repair, metabolism, and the epithelial-mesenchymal transition. The findings expand our understanding of the molecular mechanisms of trastuzumab resistance and open prospects for the development of novel therapeutic strategies to overcome drug resistance in HER2-positive breast cancer.

This study deepens the understanding of GBM by pinpointing critical genetic markers and elucidating their influence on the tumor immune microenvironment (TME) as well as treatment response. The risk model developed in this study holds promise for enhancing prognostic accuracy and facilitating the personalization of GBM therapy.