ArticlebioRxiv : the preprint server for biology2026
Impact of Trastuzumab and Pertuzumab on HER2 Localization and the Estrogen Receptor Cistrome in ER+/HER2+ Breast Cancer.
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Background: Although anti-HER2 monoclonal antibody therapy with trastuzumab and pertuzumab is highly effective for HER2-positive breast cancer, co-expression of estrogen receptor (ER) significantly reduces pathologic complete response rates. Objective: We investigated how HER2-targeted inhibition affects HER2 cellular localization and ER genomic binding in ER-positive, HER2-positive breast cancer. Methods: We evaluated HER2 localization in a tissue microarray of treatment-naive patients. Using cellular fractionation, immunofluorescence, chromatin immunoprecipitation, and genome-wide profiling (CUT&RUN), we evaluated HER2 localization and ER genomic binding following acute anti-HER2 treatment and in models of treatment resistance. The treatment-induced ER-bound gene signature was assessed for associations with pathologic complete response and survival in breast cancer clinical cohorts. Results: In treatment-naive primary breast tumors, nuclear HER2 inversely correlated with ER levels. In cell models, treatment with trastuzumab and pertuzumab induced nuclear and chromatin accumulation of HER2. Concurrently, acute anti-HER2 treatment displaced ER from canonical estrogen response elements at classical target genes, yet genome-wide profiling revealed redistribution of ER binding toward non-canonical zinc finger motifs adjacent to pro-survival Wnt and RAGE pathway genes ( Conclusions: Anti-HER2 targeted therapy causes dynamic cistromic reprogramming of ER from classical estrogen pathways toward alternative pro-survival networks. These findings implicate ER redistribution as a possible mediator of resistance and highlight novel therapeutic targets in ER-positive, HER2-positive breast cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.