Evidence map›Paper›PMID 40488800›Full record

Trial reportBreast cancer research and treatment2025

Tumoral pSMAD2 as a prognostic biomarker in early-stage breast cancer: insights from the randomized SweBCG91RT trial.

Axel Stenmark Tullberg, Viktoria Thurfjell, Anikó Kovács, Patrick Micke, Aristidis Moustakas, Fredrika Killander, Emma Niméus, Erik Holmberg, Per Karlsson, Carina Strell

Abstract readRandomized Controlled Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report 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. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Axel Stenmark Tullberg *Department of Oncology, Institute of Clinical Sciences, University of Gothenburg, Sahlgrenska University Hospital, 41345, Gothenburg, Sweden.
Viktoria Thurfjell *Department of Immunology, Genetics and Pathology, Uppsala University, Dag Hammarskjölds V 20, 751 85, Uppsala, Sweden.
Anikó KovácsDepartment of Clinical Pathology, Sahlgrenska University Hospital, Gothenburg, Sweden.
Patrick MickeDepartment of Immunology, Genetics and Pathology, Uppsala University, Dag Hammarskjölds V 20, 751 85, Uppsala, Sweden.
Aristidis MoustakasDepartment of Medical Biochemistry and Microbiology, Science for Life Laboratory, Biomedical Center, Uppsala University, Uppsala, Sweden.
Fredrika KillanderDivision of Oncology, Department of Clinical Sciences, Lund, Lund University, Skåne University Hospital, Lund, Sweden.
Emma NiméusDivision of Surgery and Oncology, Department of Clinical Sciences, Lund University, Lund, Sweden.
Erik HolmbergDepartment of Oncology, Institute of Clinical Sciences, University of Gothenburg, Sahlgrenska University Hospital, 41345, Gothenburg, Sweden.
Per Karlsson *Department of Oncology, Institute of Clinical Sciences, University of Gothenburg, Sahlgrenska University Hospital, 41345, Gothenburg, Sweden. per.karlsson@oncology.gu.se.
Carina Strell *Department of Immunology, Genetics and Pathology, Uppsala University, Dag Hammarskjölds V 20, 751 85, Uppsala, Sweden. carina.strell@igp.uu.se.

Funding

Bröstcancerförbundet, Sweden FM 2023; FM2024-0017Cancerfonden 2019/0081Cancerfonden 21 1749PjStiftelsen Konung Gustaf V:s Jubileumsfond 2019:248Trond Mohn stiftelse TMS2022STG01Vetenskapsrådet 2022-01151
6 · The paper itself

Abstract

BACKGROUND/

aimThe TGF-β pathway can influence breast cancer progression and therapy efficacy, exhibiting both pro- and anti-tumoral effects. This study examined the impact of active TGF-β signaling on recurrence and radiotherapy (RT) benefit in early-stage breast cancer, using nuclear phosphorylated Smad2 (pSMAD2) as a marker for pathway activation.

methodsTissue-microarrays from 1178 stage I-IIA breast cancer patients in the SweBCG91RT trial (randomized to breast-conserving surgery with or without RT) were analyzed. pSMAD2 immunohistochemistry was scored as the mean percentage of tumor cells with nuclear staining. Recurrence risk and RT benefit were evaluated.

resultspSMAD2 scores were heavily skewed, with 45% of tumors demonstrating high staining (≥ 80% tumor cells), 38% medium (21-79%), and 17% low (≤ 20%). Low pSMAD2 tumors were associated with higher grade and larger size but not with subtype. Medium pSMAD2 tumors had a significantly increased ipsilateral breast tumor recurrence risk than high pSMAD2 tumors (HR

conclusionMedium pSMAD2 levels were linked to an increased recurrence risk compared to high levels, suggesting a tumor-suppressive role of TGF-β in early breast tumorigenesis. However, no significant differences were noted for low pSMAD2 levels. In Luminal tumors, TGF-β signaling was negatively associated with TILs. These findings indicate that therapeutic targeting of TGF-β warrants careful consideration of tumor stage and subtype.

Indexed as

Biomarkers, TumorBreast NeoplasmsSmad2 ProteinAdultAgedFemaleHumansImmunohistochemistryMiddle AgedNeoplasm Recurrence, LocalNeoplasm StagingPhosphorylationPrognosisTransforming Growth Factor betaBiomarkers, TumorSmad2 ProteinSMAD2 protein, humanTransforming Growth Factor betaBreast cancerImmune cellsPrognosisRadiotherapySMAD2TGF-β signaling

Identifiers

PMID40488800
PMCPMC12208964

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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.