IGFBP2 (Insulin-like growth factor binding protein 2)

The cells in the IBP1 and IBP2 hydrogels with enhanced cell-cell interactions demonstrated higher resistance to docetaxel (DTX). Thus, our results indicate that these bioactive hydrogels can serve as a promising platform for in vitro assessment of cancer mechanisms and drug screening.

Importantly, combinatorial blockade of IGFBP2 and CD47 synergistically suppressed tumor growth and prolonged survival in orthotopic GBM models. Together, our findings uncovered the hypoxia-exosomal IGFBP2-CD47 axis in GBM immune evasion and provided a compelling rationale for combination therapy to improve immunotherapy efficacy in GBM.

The downregulation profile suggests impairment of the host's immunothrombotic defense, whereas the upregulated proteins may represent early compensatory mechanisms aimed at preserving homeostasis. Together, these findings provide insights into systemic responses during profound cytopenias and highlight candidate proteins that may mediate early adaptations to hematopoietic and tissue injury in patients undergoing intensive chemotherapy.

SPP1 may be a potential marker for the differentiation between benign and malignant ovarian masses, while IGFBP2 can differentiate between healthy females and females with ovarian masses. Combining SPP1 with CA125 or TSP1 provides high sensitivity and specificity for the detection of EOC patients.

The framework and nomogram provide valuable insights into the roles of CAFs and key genes in GBM progression and immunity, and extend beyond classification by offering promising avenues for deciphering tumor mutations, mapping immune landscapes, refining drug predictions, and forecasting the efficacy of immunotherapeutic interventions. These findings have the potential to significantly improve personalized treatment strategies and patient outcomes.

Networks of microRNAs regulated by insulin-like growth factor 1 (IGF-1) that impede GB's response to temozolomide (TMZ)...IGFBP-2 augments the expression of CD144 and MMP2, promoting the development of vasculogenic mimicry (VM) in GB cells. Recent investigations have revealed a crucial signaling mechanism that is vital for the survival of GB patients.

Moreover, the chemical drug ONC201 was shown to effectively impede ESCC progression induced by the hyperactive IRF2BPL-IGFBP2 axis in tumor cells. Collectively, our findings verified that the IRF2BPL-IGFBP2 axis plays a critical role in enhancing ESCC progression by increasing the malignancy of ESCC cells and fostering an immune-deficient tumor microenvironment. Targeting the IRF2BPL-IGFBP2 axis may represent a promising therapeutic strategy for ESCC.

The proliferative lesions were also dependent on IGFBP2-mTOR-cyclin D1 pathway signalling, in which inhibition of either IGFBP2 or mTOR suppressed proliferation and tumorigenesis. Therefore, we propose that zonal identity dictates hepatocyte susceptibility to WNT-driven tumorigenesis and that escaping WNT-induced differentiation is essential for liver cancer.

Proteomic analysis of VS patient plasma identified several disease-classifying biomarkers. Hepcidin warrants further investigation into its role in VS progression.

Collectively, these findings indicate that IL-35 is a promising therapeutic target whose blockade not only suppresses PSC activation and stromal fibrosis, but also enhances the efficacy of standard chemotherapies (gemcitabine and gemcitabine/nab-paclitaxel). This provides a strong rationale for its clinical development as a combinatorial strategy in PDAC treatment.

YTHDF1 and IGFBP2 were independent risk factors for poor prognosis of PC patients. They may be involved in the progression of prostate cancer, and serve as potential biomarkers for evaluating the prognosis of patients. However, its clinical translation value needs to be further verified by large sample and multi-center studies.