Evidence map›Paper›PMID 28507152›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Embryonic transcription factor SOX9 drives breast cancer endocrine resistance.

Rinath Jeselsohn, MacIntosh Cornwell, Matthew Pun, Gilles Buchwalter, Mai Nguyen, Clyde Bango, Ying Huang, Yanan Kuang, Cloud Paweletz, Xiaoyong Fu and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
11.5field-weighted citation impact, top 1% of its field
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

68 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
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  4. Review
  5. Review
  6. Article
  7. SOX9: an important factor in regulating breast cancer.European journal of medical research · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
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  14. HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  15. Article
  16. Article
  17. Article
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  19. Review
  20. Article

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

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

23 authors at 7 institutions in 2 countries.

Rinath JeselsohnDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215; myles_brown@dfci.harvard.edu rinath_jeselsohn@dfci.harvard.edu.
MacIntosh CornwellDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Matthew PunDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Gilles BuchwalterDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Mai NguyenDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Clyde BangoDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Ying HuangDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Yanan KuangBelfer Center for Applied Cancer Science, Dana Farber Cancer Institute, Boston, MA 02215.
Cloud PaweletzBelfer Center for Applied Cancer Science, Dana Farber Cancer Institute, Boston, MA 02215.
Xiaoyong FuLester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030.
Agostina NardoneLester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030.
Carmine De AngelisLester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030.
Simone DetreRalph Lauren Centre for Breast Cancer Research, Royal Marsden Hospital, London, SW3 6JB, United Kingdom.
Andrew DodsonRalph Lauren Centre for Breast Cancer Research, Royal Marsden Hospital, London, SW3 6JB, United Kingdom.
Hisham MohammedNuclear Transcription Factor Laboratory, Cancer Research UK, Cambridge Institute, Cambridge University, Li Ka Shing Centre, Cambridge, CB2 0RE, United Kingdom.
Jason S CarrollNuclear Transcription Factor Laboratory, Cancer Research UK, Cambridge Institute, Cambridge University, Li Ka Shing Centre, Cambridge, CB2 0RE, United Kingdom.
Michaela BowdenDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Prakash RaoDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Henry W LongDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Fugen LiDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215.
Mitchell DowsettRalph Lauren Centre for Breast Cancer Research, Royal Marsden Hospital, London, SW3 6JB, United Kingdom.
Rachel SchiffLester and Sue Smith Breast Center, Baylor College of Medicine, Houston, TX 77030.
Myles BrownDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215; myles_brown@dfci.harvard.edu rinath_jeselsohn@dfci.harvard.edu.
Dana-Farber Cancer Institute · USBaylor College of Medicine · USBreast Cancer Now · GBChildren's Cancer Center · USCancer Research UK · GBRoyal Marsden Hospital · GBUniversity of Cambridge · GB

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Tissue and Pathology CoreP50CA168504 · NCI · DANA-FARBER CANCER INST · PI MYLES A BROWN · 2013 to 2026
$30.1M
Cancer Research UK 20411NCI NIH HHS P30 CA125123NCI NIH HHS P50 CA168504
6 · The paper itself

Abstract

The estrogen receptor (ER) drives the growth of most luminal breast cancers and is the primary target of endocrine therapy. Although ER blockade with drugs such as tamoxifen is very effective, a major clinical limitation is the development of endocrine resistance especially in the setting of metastatic disease. Preclinical and clinical observations suggest that even following the development of endocrine resistance, ER signaling continues to exert a pivotal role in tumor progression in the majority of cases. Through the analysis of the ER cistrome in tamoxifen-resistant breast cancer cells, we have uncovered a role for an RUNX2-ER complex that stimulates the transcription of a set of genes, including most notably the stem cell factor SOX9, that promote proliferation and a metastatic phenotype. We show that up-regulation of SOX9 is sufficient to cause relative endocrine resistance. The gain of SOX9 as an ER-regulated gene associated with tamoxifen resistance was validated in a unique set of clinical samples supporting the need for the development of improved ER antagonists.

Indexed as

Antineoplastic Agents, HormonalBreastBreast NeoplasmsCell ProliferationChromatinDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleHumansMCF-7 CellsReceptors, EstrogenSOX9 Transcription FactorTamoxifenAntineoplastic Agents, HormonalChromatinReceptors, EstrogenSOX9 protein, humanSOX9 Transcription FactorTamoxifenbreast cancercistromeendocrine resistanceestrogen receptorSOX9

Identifiers

PMID28507152
PMCPMC5465894
OpenAlexW2614254014

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.