ArticleResearch square2026
A Novel Patient-Derived Xenograft Model of Inflammatory Breast Cancer.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
18 authors.
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Abstract
Background: Few models exist for studying experimental therapeutics in inflammatory breast cancer (IBC). Our study objective was to characterize a novel patient-derived xenograft (PDX) from a HER2 positive IBC patient refractory to neoadjuvant chemotherapy. Methods: We derived a novel PDX from a patient with hormone receptor negative, HER2-positive IBC refractory to neoadjuvant chemotherapy with Docetaxel, Carboplatin, Trastuzumab, and Pertuzumab (TCHP). Tumor was implanted into NOD/SCID/γ mice (NSG) and used for serial propagation of PDX. We performed short-tandem repeat (STR) profiling, plotted tumor growth curves for mice treated with alpelisib/everolimus vs. untreated, and immunohistochemistry (IHC), and performed clinical genomic assays. Paired Student's t-tests were used to compare tumor growth curves. We used 10X Genomics for single cell transcriptome analysis of 1000 cells derived from the PDX. Results: ctDNA sequencing revealed amplifications in MYC, ERBB2 (HER2), androgen receptor (AR), PIK3CA, vMYB and loss of CDKN2A. Tumor sequencing found a H1047R mutation in PIK3CA. STR profiling showed the propagated PDX tumor matched the original tumor. The engraftment rate was 12/15 (80%) and median tumor volume doubling was 24.5 days (range 9.2-175 days) for n = 15 untreated controls. Alpelisib plus everolimus decreased tumor growth in our PDX (p = 0.006). TCHP-resistant tumor cells downregulated HER2 expression, which was re-expressed after treatment with alpelisib and everolimus. Conclusion: We established a PDX of a HER2-positive IBC tumor with a PIK3CA hotspot mutation (H1047R) refractory to TCHP. Targeting the PI3K/mTOR pathway may be useful to overcome resistance in HER2-positive IBC with a H1047R mutation in PIK3CA.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.