Evidence map›Paper›PMID 40809351›Full record

ArticleHemaSphere2025

3D Tumor microenvironment interaction reveals AP-1 complex regulation and contact-mediated reprogramming of bone marrow stromal cells in chronic lymphocytic leukemia.

Jana Lindacher, Anne Hartebrodt, Janin Dingfelder, Pascal Lukas, Laeschkir Würthner, Simon Völkl, David B Blumenthal, Frederik Graw, Kerstin Amann, Manuela Krumbholz and 4 more

Abstract read
In one paragraph

Article in HemaSphere, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

14 authors.

Jana LindacherDepartment of Internal Medicine 5, Hematology and Oncology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
Anne HartebrodtDepartment of Artificial Intelligence in Biomedical Engineering (AIBE) Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
Janin DingfelderDepartment of Internal Medicine 5, Hematology and Oncology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
Pascal LukasDepartment of Internal Medicine 5, Hematology and Oncology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.ORCID https://orcid.org/0009-0009-7028-2887
Laeschkir WürthnerDepartment of Internal Medicine 5, Hematology and Oncology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
Simon VölklDepartment of Internal Medicine 5, Hematology and Oncology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
David B BlumenthalDepartment of Artificial Intelligence in Biomedical Engineering (AIBE) Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
Frederik GrawDepartment of Internal Medicine 5, Hematology and Oncology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
Kerstin AmannDepartment of Nephropathology, Institute of Pathology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
Manuela KrumbholzBavarian Cancer Research Center (BZKF) Erlangen Germany.
Martina HaibachMedical Care Center for Internal Medicine Oncology and Haematology Erlangen Germany.
Jochen WilkeMedical Care Center Oncology and Haematology Fürth Germany.
Andreas MackensenDepartment of Internal Medicine 5, Hematology and Oncology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.
Gloria Lutzny-GeierDepartment of Internal Medicine 5, Hematology and Oncology Universitätsklinikum Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU) Erlangen Germany.ORCID https://orcid.org/0000-0002-9648-2635

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic lymphocytic leukemia (CLL) cells actively reprogram their tumor microenvironment (TME) to promote drug resistance and tumor progression. Tumor cell survival critically depends on heterotypic communication with benign cells in the microenvironment, particularly bone marrow-derived stromal cells (BMSCs). Our three-dimensional (3D) approach allows us to investigate spatially defined, mutual direct cell-cell interactions between CLL B cells, autologous T cells, and BMSCs, forming complex scaffold-like structures reminiscent of in vivo conditions. Here, we observe that CLL B cells localized in the core regions of 3D structures upregulate the AP-1 transcription factor complex, which confers significant protection against therapy-induced cell death. Additionally, regulatory T cells (T

Identifiers

PMID40809351
PMCPMC12348881

What OpenQuestion holds

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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.