Evidence map›Paper›PMID 40674249›Full record

ArticleMolecular oncology2025

Exploring the role of cyclin D1 in the pathogenesis of multiple myeloma beyond cell cycle regulation.

Ignacio J Cardona-Benavides, Sara Cristobal-Vargas, Cristina De Ramón, Elizabeta A Rojas, Irena Misiewicz-Krzeminska, Isabel Isidro, José Juan Pérez, Bruno Paiva, Noemi Puig, Miguel Alcoceba and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Ignacio J Cardona-BenavidesHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.ORCID 0000-0001-6772-6859
Sara Cristobal-VargasHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
Cristina De RamónHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
Elizabeta A RojasHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
Irena Misiewicz-KrzeminskaDepartment of Experimental Hematology, Institute of Hematology and Transfusion Medicine, Warsaw, Poland.
Isabel IsidroHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
José Juan PérezHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
Bruno PaivaClínica Universidad de Navarra, Centro de Investigaciones Biomédicas Aplicadas (CIMA), Instituto de Investigación Sanitaria de Navarra (IdiSNA), Pamplona, Spain.
Noemi PuigHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
Miguel AlcocebaHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
María-Victoria MateosHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
Luis A CorcheteKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center, Boston, MA, USA.
Myriam CuadradoHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.
Norma C GutiérrezHematology Department, Institute of Biomedical Research of Salamanca (IBSAL), University Hospital of Salamanca, Spain.

Funding

Fundación Científica Asociación Española Contra el Cáncer PROYE20047GUTIInstituto de Salud Carlos III CEI10-1-0010Instituto de Salud Carlos III FI20/00226Instituto de Salud Carlos III PI19/00674Instituto de Salud Carlos III PI23/00319Junta de Castilla y León GRS1654/A/17Junta de Castilla y León GRS1849/A/18Junta de Castilla y León GRS2058/A/19
6 · The paper itself

Abstract

Cyclins D could be a unifying event in multiple myeloma (MM), even though MM is not typically considered a proliferative disease. In this study, we hypothesized that cyclins D might have additional roles in the pathogenesis of MM beyond cell cycle control. We showed that overexpression of CCND1 and CCND2 in MM cell lines lacking these proteins revealed a mutually exclusive expression pattern, with both cyclins D localized in the cytoplasm and no impact on proliferation. To investigate non-canonical roles of cyclin D1, we performed transcriptome analysis and multidimensional flow cytometry. Cyclin D1 overexpression led to upregulation of several key cell adhesion pathway proteins, including STAT1 and ZO-1, along with alterations in the actin cytoskeleton and decreased adhesion to certain matrices. Immunophenotypic analysis showed a significant reduction in CD56 expression following cyclin D1 overexpression, validated in a cohort of 85 MM patients, in which 73% with high cyclin D1 were CD56-negative. High cyclin D1 was also associated with increased circulating tumor cells (CTCs) (P < 0.001). Overall, we revealed novel functions of cyclin D1 in MM pathogenesis, particularly in cell adhesion and dissemination.

Indexed as

Cell Cycle CheckpointsCyclin D1Multiple MyelomaCell AdhesionCell Line, TumorCell ProliferationCyclin D2FemaleGene Expression Regulation, NeoplasticHumansNeoplastic Cells, CirculatingCCND1 protein, humanCyclin D1Cyclin D2adhesionCD56CTCcyclin D1multiple myeloma

Identifiers

PMID40674249
PMCPMC12591315

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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.