Evidence map›Paper›PMID 38760444›Full record

ArticleBritish journal of cancer2024

Epigenetic activation of SOX11 is associated with recurrence and progression of ductal carcinoma in situ to invasive breast cancer.

Warapen Treekitkarnmongkol, Vandna Shah, Kazuharu Kai, Hiroshi Katayama, Justin Wong, Farah A Ladha, Tristian Nguyen, Brian Menegaz, Wei Lu, Fei Yang and 11 more

Abstract read
In one paragraph

Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

21 authors.

Warapen TreekitkarnmongkolDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0000-0002-7542-5201
Vandna ShahSchool of Cancer and Pharmaceutical Sciences, Faculty of Life Sciences and Medicine, Guy's Cancer Centre, King's College London, London, UK.ORCID 0009-0008-8827-6912
Kazuharu KaiDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Hiroshi KatayamaDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Justin WongDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0000-0002-6803-1060
Farah A LadhaDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Tristian NguyenDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0009-0000-4565-1534
Brian MenegazDan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA.
Wei LuDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Fei YangDepartment of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Barbara MinoDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Ximing TangDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Mihai GageaDepartment of Veterinary Medicine & Surgery, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Harsh BatraDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Maria Gabriela RasoDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.ORCID 0000-0003-2105-5556
Ignacio I WistubaDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Savitri KrishnamurthyDepartment of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Sarah E PinderSchool of Cancer and Pharmaceutical Sciences, Faculty of Life Sciences and Medicine, Guy's Cancer Centre, King's College London, London, UK.ORCID 0000-0003-4167-8910
Elinor J SawyerSchool of Cancer and Pharmaceutical Sciences, Faculty of Life Sciences and Medicine, Guy's Cancer Centre, King's College London, London, UK.ORCID 0000-0001-8285-4111
Alastair M ThompsonDan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX, USA. Alastair.Thompson@bcm.edu.ORCID 0000-0003-0604-7267
Subrata SenDepartment of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. ssen@mdanderson.org.ORCID 0000-0001-6884-6246

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Fabien Delerue · 1985 to 2026
$290.8M
Translational Genomics and Precision Medicine in Cancer Training ProgramT32CA217789 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Subrata Sen · 2018 to 2026
$2.2M
Breast Cancer Now TAP379Cancer Research UK (CRUK) C38317/A24043NCI NIH HHS P30 CA016672NCI NIH HHS T32 CA217789
6 · The paper itself

Abstract

backgroundRisk of recurrence and progression of ductal carcinoma in situ (DCIS) to invasive cancer remains uncertain, emphasizing the need for developing predictive biomarkers of aggressive DCIS.

methodsHuman cell lines and mouse models of disease progression were analyzed for candidate risk predictive biomarkers identified and validated in two independent DCIS cohorts.

resultsRNA profiling of normal mammary and DCIS tissues (n = 48) revealed that elevated SOX11 expression correlates with MKI67, EZH2, and DCIS recurrence score. The 21T human cell line model of DCIS progression to invasive cancer and two mouse models developing mammary intraepithelial neoplasia confirmed the findings. AKT activation correlated with chromatin accessibility and EZH2 enrichment upregulating SOX11 expression. AKT and HER2 inhibitors decreased SOX11 expression along with diminished mammosphere formation. SOX11 was upregulated in HER2+ and basal-like subtypes (P < 0.001). Longitudinal DCIS cohort (n = 194) revealed shorter recurrence-free survival in SOX11+ than SOX11- patients (P = 0.0056 in all DCIS; P < 0.0001 in HER2+ subtype) associated with increased risk of ipsilateral breast event/IBE (HR = 1.9, 95%CI = 1.2-2.9; P = 0.003). DISCUSSION: Epigenetic activation of SOX11 drives recurrence of DCIS and progression to invasive cancer, suggesting SOX11 as a predictive biomarker of IBE.

Indexed as

Breast NeoplasmsCarcinoma, Intraductal, NoninfiltratingDisease ProgressionEpigenesis, GeneticNeoplasm Recurrence, LocalSOXC Transcription FactorsAnimalsBiomarkers, TumorCell Line, TumorEnhancer of Zeste Homolog 2 ProteinErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessBiomarkers, TumorEnhancer of Zeste Homolog 2 ProteinERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesEZH2 protein, humanSOX11 protein, humanSOXC Transcription Factors

Identifiers

PMID38760444
PMCPMC11231151

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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.