FGF2 (Fibroblast Growth Factor 2)

Notably, PET imaging revealed that [68Ga]Ga-NOTA-cRY9M exhibited significant and specific tumor uptake in FGFR1-positive NSCLC cell-derived xenograft (CDX) models and patient-derived xenograft (PDX) models. These results demonstrate that the cyclic peptide-based radiotracer [68Ga]Ga-NOTA-cRY9M serves as a potential diagnostic agent for FGFR1-expressing tumors.

FTO significantly influences cervical cancer progression, at least in part, through m6A modification of FGF2, thereby affecting downstream signaling. Targeting FTO and its downstream effectors holds potential as a therapeutic strategy for cervical cancer treatment.

The results suggest that miR-205, FGF2, and CARMA3 may serve as potential biomarkers for the identification of colorectal cancer (CRC), particularly when used in multi-marker panels to improve diagnostic accuracy. Their clinical utility should be confirmed through additional validation in larger cohorts.

The translational-level expression was analyzed using the IHC section images from the Human Protein Atlas (HPA) database. Thus, targeting these factors for therapy, diagnosis, or prognosis could be a key strategies in the field of oncology.

Genetic ablation of Trem2 or pharmacologic targeting with antisense oligonucleotides suppress paclitaxel-induced breast cancer lung metastasis in vivo. Collectively, our findings demonstrate that paclitaxel, but not nab-paclitaxel, stimulates TREM2 expression and expands TREM2+ macrophages, suggesting that TREM2 targeting could enhance paclitaxel efficacy while limiting metastasis.

FGF2 is downregulated in LUAD and inversely associated with metastatic progression and poor prognosis. The observed reduction in cancer cell motility upon FGF2 treatment in vitro, together with its expression pattern, supports a potential tumor-suppressive role and suggests that FGF2 may serve as a candidate non-invasive biomarker for monitoring LUAD metastasis.

In vivo evaluations demonstrate that Tim-AIII significantly reduces tumor growth without detectable systemic toxicity in breast cancer-bearing mice. This study not only elucidates the molecular basis of Tim-AIII's antitumor efficacy but also positions it as a potential targeted therapeutic for breast cancer, with dual action on ERS-induced apoptosis and EMT suppression.

Our results lend support to the presumption that inflammatory cytokines are important biomarkers that associate with DR severity and may represent novel targets for inhibition. The authors have no proprietary or commercial interest in any materials discussed in this article.

For example, anticancer therapies targeting vascular endothelial growth factor activity have been effective in blocking pro-angiogenic and pro-growth signals, including receptor tyrosine kinase inhibitors (e.g., Sunitinib and Sorafenib) and monoclonal antibodies (e.g., Bevacizumab). The capacity of heparin to promote the association of FGF2 with its cognate receptors (FGFRs) led to the degradation of the entire receptor-ligand complex, thereby reducing the availability of FGFRs at the cancer cell surface, which are necessary for sustained pro-oncogenic signaling. These findings highlight the potential of GLYTACs as an alternative to existing growth factor-blocking anticancer therapies and as a strategy to reshape the extracellular signaling environment of tumors.

Our data show that the high expression of IL-35 in patients with HCC is an important tumor promoter. Combined treatment with anti-IL-35 and anti-PD1 antibodies have potential therapeutic effect against HCC.

In vivo studies using the chick chorioallantoic membrane (CAM) assay confirm significant antiangiogenic activity, marked by downregulation of key angiogenic factors (VEGF, FGF2, and ANG1). Together, these results highlight a minimally invasive, NIR laser-triggered nanotherapeutic strategy with reduced systemic toxicity and establish a potential platform for TNBC treatment, warranting further preclinical validation in mammalian models.

The FGF/R axis is a key driver of SCLC metastatic spread in the YAP1-dominant subtype. These data might facilitate the development of potential future therapies targeting FGF/R signalling to prevent SCLC progression and metastasis.