Evidence map›Paper›PMID 38822093›Full record

ArticleScientific reports2024

PIK3CA mutations in endocrine-resistant breast cancer.

Caroline Schagerholm, Stephanie Robertson, Hosein Toosi, Emmanouil G Sifakis, Johan Hartman

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Article
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  4. Enhanced efficacy of a next-generation EEEV self-replicating RNA platform for combination cancer immunotherapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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  10. Analysis ofFrontiers in oncology · 2026
    Article
  11. ESR1 fusions in breast cancer: functions, mechanisms and therapeutic opportunities.Translational breast cancer research : a journal focusing on translational research in breast cancer · 2026
    Review
  12. Review
  13. Article
  14. Pathologica · 2025
    Article
  15. Review
  16. Review
  17. Article
  18. Article
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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

5 authors.

Caroline SchagerholmDepartment of Oncology-Pathology, Karolinska Institutet, Bioclinicum, Stockholm, Sweden. caroline.schagerholm@ki.se.
Stephanie RobertsonDepartment of Oncology-Pathology, Karolinska Institutet, Bioclinicum, Stockholm, Sweden.
Hosein ToosiDivision of Computational Science and Technology, KTH Royal Institute of Technology and Science for Life Laboratory, Stockholm, Sweden.
Emmanouil G SifakisDepartment of Oncology-Pathology, Karolinska Institutet, Bioclinicum, Stockholm, Sweden.
Johan HartmanDepartment of Oncology-Pathology, Karolinska Institutet, Bioclinicum, Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Around 75% of breast cancer (BC) patients have tumors expressing the predictive biomarker estrogen receptor α (ER) and are offered endocrine therapy. One-third eventually develop endocrine resistance, a majority with retained ER expression. Mutations in the phosphatidylinositol bisphosphate 3-kinase (PI3K) catalytic subunit encoded by PIK3CA is a proposed resistance mechanism and a pharmacological target in the clinical setting. Here we explore the frequency of PIK3CA mutations in endocrine-resistant BC before and during treatment and correlate to clinical features. Patients with ER-positive (ER +), human epidermal growth factor receptor 2 (HER2)-negative primary BC with an ER + relapse within 5 years of ongoing endocrine therapy were retrospectively assessed. Tissue was collected from primary tumors (n = 58), relapse tumors (n = 54), and tumor-free lymph nodes (germline controls, n = 62). Extracted DNA was analyzed through panel sequencing. Somatic mutations were observed in 50% (31/62) of the patients, of which 29% occurred outside hotspot regions. The presence of PIK3CA mutations was significantly associated with nodal involvement and mutations were more frequent in relapse than primary tumors. Our study shows the different PIK3CA mutations in endocrine-resistant BC and their fluctuations during therapy. These results may aid investigations of response prediction, facilitating research deciphering the mechanisms of endocrine resistance.

Indexed as

Breast NeoplasmsClass I Phosphatidylinositol 3-KinasesDrug Resistance, NeoplasmMutationAdultAgedAged, 80 and overAntineoplastic Agents, HormonalErb-b2 Receptor Tyrosine KinasesEstrogen Receptor alphaFemaleHumansMiddle AgedNeoplasm Recurrence, LocalRetrospective StudiesAntineoplastic Agents, HormonalClass I Phosphatidylinositol 3-KinasesErb-b2 Receptor Tyrosine KinasesEstrogen Receptor alphaPIK3CA protein, humanBreast cancerEndocrine-resistancePIK3CA

Identifiers

PMID38822093
PMCPMC11143214

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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.