Evidence map›Paper›PMID 25816016›Full record

ArticlePloS one2015

Folate receptor-α (FOLR1) expression and function in triple negative tumors.

Brian M Necela, Jennifer A Crozier, Cathy A Andorfer, Laura Lewis-Tuffin, Jennifer M Kachergus, Xochiquetzal J Geiger, Krishna R Kalari, Daniel J Serie, Zhifu Sun, Alvaro Moreno-Aspitia and 9 more

Erratum issuedAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing 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

67 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. The plasma proteome and breast cancer risk.Breast cancer research : BCR · 2025
    Article
  5. Review
  6. Review
  7. Preparation and preclinical evaluation ofEJNMMI radiopharmacy and chemistry · 2025
    Article
  8. Emerging Targets in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2024
    Review
  9. Article
  10. Folate Receptor Alpha-A Novel Approach to Cancer Therapy.International journal of molecular sciences · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors.

Brian M NecelaDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida, United Sates of America.
Jennifer A CrozierDepartment of Hematology and Oncology, Mayo Clinic, Jacksonville, Florida, United States of America.
Cathy A AndorferDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida, United Sates of America.
Laura Lewis-TuffinDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida, United Sates of America.
Jennifer M KachergusDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida, United Sates of America.
Xochiquetzal J GeigerDepartment of Pathology and Laboratory Medicine, Mayo Clinic, Jacksonville, Florida, United States of America.
Krishna R KalariDepartment of Health Sciences Research, Mayo Clinic, Rochester, Minnesota, United States of America.
Daniel J SerieDepartment of Health Sciences Research, Mayo Clinic, Jacksonville, Florida United States of America.
Zhifu SunDepartment of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota, United States of America.
Alvaro Moreno-AspitiaDepartment of Hematology and Oncology, Mayo Clinic, Jacksonville, Florida, United States of America.
Alvaro Moreno Aspita
Daniel J O'ShannessyDepartment of Translational Medicine and Diagnostics, Morphotek, Exton, Pennsylvania, United States of America.
Julia D MaltzmanDepartment of Clinical Development, Morphotek, Exton, Pennsylvania, United States of America.
Ann E McCulloughDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Scottsdale, Arizona, United States of America.
Barbara A PockajDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Scottsdale, Arizona, United States of America.
Heather E CunliffeDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Karla V BallmanDepartment of Biomedical Statistics and Informatics, Mayo Clinic, Rochester, Minnesota, United States of America.
E Aubrey ThompsonDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida, United Sates of America.
Edith A PerezDepartment of Cancer Biology, Mayo Clinic, Jacksonville, Florida, United Sates of America.

Funding

Women's Cancer ProgramP30CA015083 · NCI · MAYO CLINIC ROCHESTER · PI Felicity Enders · 1985 to 2026
$151.3M
NCI NIH HHS P30 CA015083NCI NIH HHS P30 CA15083
6 · The paper itself

Abstract

Folate receptor alpha (FOLR1) has been identified as a potential prognostic and therapeutic target in a number of cancers. A correlation has been shown between intense overexpression of FOLR1 in breast tumors and poor prognosis, yet there is limited examination of the distribution of FOLR1 across clinically relevant breast cancer subtypes. To explore this further, we used RNA-seq data from multiple patient cohorts to analyze the distribution of FOLR1 mRNA across breast cancer subtypes comprised of estrogen receptor positive (ER+), human epidermal growth factor receptor positive (HER2+), and triple negative (TNBC) tumors. FOLR1 expression varied within breast tumor subtypes; triple negative/basal tumors were significantly associated with increased expression of FOLR1 mRNA, compared to ER+ and HER2+ tumors. However, subsets of high level FOLR1 expressing tumors were observed in all clinical subtypes. These observations were supported by immunohistochemical analysis of tissue microarrays, with the largest number of 3+ positive tumors and highest H-scores of any subtype represented by triple negatives, and lowest by ER+ tumors. FOLR1 expression did not correlate to common clinicopathological parameters such as tumor stage and nodal status. To delineate the importance of FOLR1 overexpression in triple negative cancers, RNA-interference was used to deplete FOLR1 in overexpressing triple negative cell breast lines. Loss of FOLR1 resulted in growth inhibition, whereas FOLR1 overexpression promoted folate uptake and growth advantage in low folate conditions. Taken together, our data suggests patients with triple negative cancers expressing high FOLR1 expression represent an important population of patients that may benefit from targeted anti-FOLR1 therapy. This may prove particularly helpful for a large number of patients who would typically be classified as triple negative and who to this point have been left without any targeted treatment options.

Indexed as

Cell Line, TumorFemaleFolate Receptor 1HumansRNA, MessengerTriple Negative Breast NeoplasmsUp-RegulationFolate Receptor 1FOLR1 protein, humanRNA, Messenger

Identifiers

PMID25816016
PMCPMC4376802

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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.