Anti-Human Frizzled receptor Recombinant Antibody (Vantictumab) (CAT#: TAB-880)

Nanki, Kosaku, et al. "Divergent routes toward Wnt and R-spondin niche independency during human gastric carcinogenesis." Cell 174.4 (2018): 856-869. https://doi.org/10.1016/j.jmva.2018.03.007

This study established and characterized a collection of 37 patient-derived gastric cancer (GC) organoids representing diverse histological and molecular subtypes of clinical GCs. The research revealed how genetic and epigenetic alterations affect niche factor dependencies in GC organoids. Through phenotype-genotype correlation analyses, the researchers identified that CDH1/TP53 compound mutations confer R-spondin independency, while RNF43/ZNRF3 gene alterations and epigenetic modifications contribute to Wnt niche independency. Using CRISPR-Cas9 gene editing in normal gastric organoids, they validated these findings and demonstrated that disruption of adherens junctions plays a critical role in diffuse-type GC morphological transformation. Xenograft studies further established the potential of Wnt-targeting therapy for a subset of Wnt-dependent GCs.
Creative Biolabs provided the human monoclonal anti-human Frizzled receptor antibody (OMP-18R5, CAT# TAB-880) that was instrumental in the flow cytometry analysis of Frizzled receptor expression on GC organoid surfaces. This antibody helped the researchers determine that CT mutant GC organoids gained R-spondin independency through a mechanism distinct from RNF43/ZNRF3 mutations by allowing them to assess Frizzled receptor expression levels with and without R-spondin stimulation, thus clarifying how different genetic alterations impact the Wnt signaling pathway in gastric cancer development.