Evidence map›Paper›PMID 36524315›Full record

ArticleCancer medicine2023

Arginase-1+ bone marrow myeloid cells are reduced in myeloproliferative neoplasms and correlate with clinical phenotype, fibrosis, and molecular driver.

Arturo Bonometti, Oscar Borsani, Elisa Rumi, Virginia Valeria Ferretti, Claudia Dioli, Elena Lucato, Marco Paulli, Emanuela Boveri

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 16% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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

8 authors at 3 institutions in 1 country.

Arturo BonomettiUnit of Anatomic Pathology, IRCCS San Matteo Foundation, Pavia, Italy.ORCID 0000-0003-3258-0727
Oscar BorsaniDepartment of Molecular Medicine, University of Pavia, Pavia, Italy.
Elisa RumiDepartment of Molecular Medicine, University of Pavia, Pavia, Italy.
Virginia Valeria FerrettiUnit of Clinical Epidemiology and Biostatistics, Fondazione IRCCS Policlinico San Matteo, Pavia, Italy.
Claudia DioliDepartment of Molecular Medicine, University of Pavia, Pavia, Italy.
Elena LucatoUnit of Anatomic Pathology, IRCCS San Matteo Foundation, Pavia, Italy.
Marco PaulliUnit of Anatomic Pathology, IRCCS San Matteo Foundation, Pavia, Italy.
Emanuela BoveriUnit of Anatomic Pathology, IRCCS San Matteo Foundation, Pavia, Italy.
University of Pavia · ITHumanitas University · ITPoliclinico San Matteo Fondazione · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPhiladelphia-negative myeloproliferative neoplasms (MPN) are clonal myeloid proliferative disorders characterized by sustained systemic inflammation. Despite its renowned importance, the knowledge concerning the inflammatory pathophysiology of these conditions is currently limited to studies on serum cytokines, while cellular immunity has rarely been investigated.

methodsIn the present study, we targeted Arginase-1 immunosuppressive myeloid cells in the bone marrow of MPN patients and healthy controls and investigated their clinical and prognostic significance. We demonstrated that MPN are characterized by a significant reduction of bone marrow immunosuppressive cells and that the number of these cells significantly correlates with several clinical and histopathological features of diagnostic and prognostic importance. Moreover, we identified an unreported correlation between a reduction of Arginase-1+ bone marrow cells and the presence of CALR mutations, linking tumor-promoting immunity and molecular drivers. Finally, we postulate that the reduction of bone marrow Arginase-1+ immunosuppressive cells may be due to the migration of these cells to the spleen, where they may exert systemic immunomodulatory function.

conclusionAltogether, this study preliminary investigated the contribution of cellular immunity in the pathogenesis of myeloproliferative neoplasms and identified a possible interesting therapeutic target as well as a set of new links that may contribute to unraveling the biological mechanisms behind these interesting hematological neoplasms.

Indexed as

Hematologic NeoplasmsMyeloproliferative DisordersArginaseBone MarrowFibrosisHumansMutationMyeloid CellsArginaseCALRimmune microenvironmentMDSCmyelofibrosismyeloproliferative neoplasms

Identifiers

PMID36524315
PMCPMC10134329
OpenAlexW4311675913

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.