bleomycin

This study showed that tumor-bearing status elicits proinflammatory activation in endothelial cells and inflammatory cell infiltration into the lungs that aggravates DILD caused by BLM.

The combination of PFD, MET, and BM-MSCs offered superior therapeutic efficacy in treating BLM-induced pulmonary fibrosis compared to individual treatments. This multimodal approach effectively targets oxidative stress, inflammation, apoptosis, and fibrosis, suggesting strong potential for future clinical application.

P=N/A, N=160, Recruiting, Sahlgrenska University Hospital

P=N/A, N=10, Active, not recruiting, University Medical Centre Ljubljana | Terminated --> Active, not recruiting | Phase classification: P1 --> PN/A | Trial completion date: Mar 2021 --> May 2026

Extragonadal penile localization of endodermal sinus tumor is rare but has a favorable prognosis when treated with conservative management and chemotherapy. aFP is a useful marker for both diagnosis and follow-up.

Importantly, the therapeutic effects of HA-Wm were abolished in Fpr2-deficient mice, confirming an FPR2-dependent mechanism of action. Collectively, these results demonstrate that topical treatment of HA-Wm alleviates skin fibrosis and inflammation via an FPR2-dependent pathway, representing a promising noninvasive therapeutic avenue for fibrotic skin disorders such as systemic sclerosis.

Using DDX41 knockout (KO) cells, we found that these cells were sensitive to bleomycin, camptothecin, and UV...Moreover, increased and prolonged RPA and reduced RAD51 foci were found in DDX41 KO and DDX41-R525H expressing cells, indicating a defect in the transition from end resection to RAD51 filament assembly. Overall, our results suggest that DDX41 utilizes its unwinding activity to resolve R-loops, which may play a key role in HR-based repair, and dysregulation of this pathway may lead to MDS/AML.

Crizotinib could inhibit the PI3K/AKT/mTOR, STAT3 and ERK signaling pathways. Crizotinib might be an emerging medication choice for patients with IPF.

P2, N=13, Recruiting, Institute of Oncology Ljubljana

P3, N=1334, Completed, Takeda | Active, not recruiting --> Completed

Further, treatment of mice with bleomycin-induced lung injury using CSP7, an anti-IL-17A antibody, or an IL-17RA blocking antibody attenuates total lung hydroxyproline and soluble collagen content, as well as levels of profibrogenic markers. These observations support the role of IL-17A/IL-17RA signaling in lung injury and post-injury remodeling.

AA (50 μg/animal) and LXA4 improved the antioxidant status and upregulated anti-inflammatory and anti-apoptotic genes IκB and Bcl2. These results suggest AA and LXA4 can prevent bleomycin-induced dysfunction of pancreatic β cells.