Presenting Author: Nicholas A Pullen
, Associate Professor and MBS Coordinator at Univ. of Northern Colorado
Abstract:
FcεRI is typically associated with type 2 effectors such as mast cells (MC). The unique expression profile of FcεRI and evidence from pre-clinical and clinical settings have led us to study MC as potential therapeutic targets in breast cancer. Our work with the 4T1 model in vivo identified MC interacting with tumor cells, but this was complicated by a surprising finding that tumor cells intrinsically expressed FcεRI. Here we further study the expression and function of FcεRI in breast cancer cells in vitro. 4T1 cells express FcεRI similar to mouse BMMC. Two established cultures derived from human T-47D cells, estrogen dependent (E3) and estrogen withdrawn (EWD8), also express FcεRI: EWD8 cells are strong FcεRI expressers while E3 are modest, compared to LAD2 cells, a human MC line. Expression (mRNA) of all FcεRI subunits (α, β, γ) was confirmed. IgE-mediated antigen stimulation does not elicit classic Ca2+ flux in breast cancer cells as seen in respective species MC; however, it can stimulate IL-6 production from them. Preliminary analysis of primary breast cancer datasets using R2 is ongoing and discordant with our in vitro work: FcεRI mRNA abundance declines in metastatic cancers compared to non-cancerous breast tissue. We report a previously unidentified, immunologically substantive difference between breast cancer models and human primary tumors. Investigators pursuing FcεRI-relevant therapeutics in this context should be aware of this potential translational barrier.
Unexpected expression and function of Fc epsilon RI in breast cancer cells.
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Poster
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Date: May 5 Presentation Time: 03:15 PM to 04:30 PM Room: Exhibit Hall F1