Evidence map›Paper›PMID 39302579›Full record

ArticleBreast cancer research and treatment2025

Genomic and transcriptomic landscape of HER2-low breast cancer.

Rani Bansal, Tolulope Adeyelu, Andrew Elliott, Phillip Walker, Matias A Bustos, Estelamari Rodriguez, Melissa K Accordino, Jane Meisel, Margaret E Gatti-Mays, Emily Hsu and 6 more

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Article in Breast cancer research and treatment, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Redefining breast cancer: therapeutic opportunities in HER2-low and emerging molecular subtypes.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Rani BansalDuke Cancer Institute, Duke University Hospital, 20 Medicine Circle, Durham, NC, 27710, USA. rani.bansal@duke.edu.
Tolulope AdeyeluCaris Life Sciences, Phoenix, AZ, USA.
Andrew ElliottCaris Life Sciences, Phoenix, AZ, USA.
Phillip WalkerCaris Life Sciences, Phoenix, AZ, USA.
Matias A BustosSaint John's Cancer Institute, Santa Monica, CA, USA.
Estelamari RodriguezUniversity of Miami Sylvester Comprehensive Cancer Center, Miami, FL, USA.
Melissa K AccordinoColumbia University Herbert Irving Comprehensive Cancer Center, New York, NY, USA.
Jane MeiselEmory Winship Cancer Center, Atlanta, GA, USA.
Margaret E Gatti-MaysThe James Cancer Hospital and Solove Research Institute, The Ohio State University, Columbus, OH, USA.
Emily HsuLegorreta Cancer Center at Brown University, Providence, RI, USA.
Kate LathropUT Health San Antonio, San Antonio, TX, USA.
Virginia KaklamaniUT Health San Antonio, San Antonio, TX, USA.
Matthew OberleyCaris Life Sciences, Phoenix, AZ, USA.
George SledgeCaris Life Sciences, Phoenix, AZ, USA.
Sarah L SammonsDana Farber Cancer Institute, Boston, MA, USA.
Stephanie L GraffLegorreta Cancer Center at Brown University, Providence, RI, USA. sgraff1@lifespan.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNovel agents have expanded the traditional HER2 definitions to include HER2-Low (HER2L) Breast Cancer (BC). We sought to evaluate the distinct molecular characteristics of HER2L BC to understand potential clinical/biologic factors driving resistance and clinical outcomes.

methodsRetrospective analysis was performed on 13,613 BC samples, tested at Caris Life Sciences via NextGen DNA/RNA Sequencing. BC subtypes were defined by IHC/ISH. CODEai database was used to access clinical outcomes from insurance claims data.

resultsOverall, mutational landscape was similar between HER2L and classical subsets of HR+and HRneg cohorts. TP53 mutations were significantly higher in HRneg/HER2L group vs. HR+/HER2L tumors (p<0.001). A higher mutation rate of PIK3CA was observed in HRneg/HER2L tumors compared to TNBC subtype (p=0.016). PD-L1 positivity was elevated in HRneg/HER2L tumors compared to HR+/HER2L tumors, all p<0.01. Patients with HR+/HER2L tumors treated with CDK4/6 inhibitors had similar OS compared to pts with HR+/HER2-0 (HR=0.89, p=0.012). 27.2% of HR+/HER2L pts had activating PIK3CA mutations. Among HR+PIK3CA mutated tumors, HER2L pts treated with alpelisib showed no difference in OS vs. HER2-0 alpelisib-treated pts (HR=1.23, p=0.517). 13.9% of HER2L TNBC pts were PD-L1

conclusionOur findings expand the understanding of the molecular profile of the HER2L subgroup and comparison to the classically defined breast cancer subgroups. Genomic risk assessments after progression on novel therapeutics can be assessed to better define implications for mechanisms of resistance.

Indexed as

Biomarkers, TumorBreast NeoplasmsErb-b2 Receptor Tyrosine KinasesTranscriptomeAdultAgedB7-H1 AntigenClass I Phosphatidylinositol 3-KinasesFemaleGene Expression ProfilingGenomicsHumansMiddle AgedMutationPrognosisRetrospective StudiesB7-H1 AntigenBiomarkers, TumorClass I Phosphatidylinositol 3-KinasesERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesPIK3CA protein, humanBreast cancerGenomic profileHER2 lowHormone receptor positivePIK3CATP53Triple negative breast cancer

Identifiers

PMID39302579

What OpenQuestion holds

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Registered trials

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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.