plerixafor

We established and validated a CSC-related prognostic model that was closely associated with macrophage polarization and clinical outcomes in STAD. CXCR4 was identified as the key gene in this model, which unregulated lactate secretion to drive M2 macrophage polarization and maintain CSC properties in STAD, and may serve as a putative regulatory factor in STAD progression. The CXCR4 inhibitor AMD3100 exerted significant anti-tumor effects in vitro, suggesting that CXCR4 may serve as a promising prognostic biomarker and a candidate target for STAD.

Collectively, these findings identify IL-1β and CXCL12 as potential critical mediators of the inflammatory crosstalk between adipocytes and PanNET cells. Targeting this signalling axis may therefore represent a promising therapeutic strategy for PanNETs.

Plerixafor on day 4 appears to enhance PBSC collection efficiency and reduce the need for multiple apheresis sessions compared with conventional day-5 administration. These findings support consideration of earlier plerixafor use in mobilization protocols, though larger studies are warranted to confirm clinical and cost-effectiveness.

Agonists induced transient heteromerization coupled to receptor internalization, while antagonists, especially plerixafor together with maraviroc, stabilized persistent surface-associated complexes. Molecular dynamics simulations in asymmetric bilayers resembling MDA-MB-231 and MCF-10A membranes identified cholesterol-enriched receptor interfaces that prolong CXCR4-CCR5 dimer lifetimes in MDA-like membranes. These results show that GPCR heteromerization is not an intrinsic fixed property of receptor pairs, but an emergent behavior shaped by cell state, lipid environment, and ligand input.

Mobilizing peripheral blood stem cells in lymphoma patients with a single high-dose of etoposide combined with mecapegfilgrastim is effective, safe and cost-effective.

P2, N=74, Not yet recruiting, National Cancer Institute (NCI)

P1, N=12, Not yet recruiting, St. Jude Children's Research Hospital

P1, N=66, Active, not recruiting, Stanford University | Recruiting --> Active, not recruiting | Trial completion date: Nov 2027 --> May 2028 | Trial primary completion date: Nov 2027 --> May 2028

In our cohort, the incorporation of ASCT into multimodality therapy was feasible with resource-adapted strategies; however, this did not translate into a meaningful improvement in survival outcomes when compared with our historical non-transplant cohort.

Preclinical studies demonstrate that CXCR4 antagonists (e.g., plerixafor, LY2510924) suppress metastasis and, when combined with immune checkpoint inhibitors, can reverse the "cold" immune phenotype of microsatellite-stable CRC. We also discuss recent advances in the regulation of CXCL12/CXCR4 expression, the role of related receptors such as CXCR7, and emerging strategies targeting this axis for therapeutic intervention. Collectively, current evidence supports the CXCL12/CXCR4 axis as a promising biomarker and therapeutic target in metastatic CRC, and further elucidation of its regulatory network may facilitate the development of more effective precision treatment strategies.

P1/2, N=8, Active, not recruiting, City of Hope Medical Center | Trial completion date: Feb 2026 --> Feb 2027

P=N/A, N=10, Recruiting, Northwell Health | Initiation date: Oct 2025 --> Jun 2026