Evidence map›Paper›PMID 35385924›Full record

ArticleHaematologica2022

Iron- and erythropoietin-resistant anemia in a spontaneous breast cancer mouse model.

Nuria Fabregas Bregolat, Maja Ruetten, Milene Costa Da Silva, Mostafa A Aboouf, Hyrije Ademi, Nadine von Büren, Julia Armbruster, Martina Stirn, Sandro Altamura, Oriana Marques and 7 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
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

17 authors at 5 institutions in 4 countries.

Nuria Fabregas BregolatInstitute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, Zurich.
Maja RuettenPathoVet AG, Pathology Diagnostic Laboratory, Tagelswangen ZH.
Milene Costa Da SilvaDepartment of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg.
Mostafa A AbooufInstitute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Departement of Biochemistry, Faculty of Pharmacy, Ain Shams University, Cairo.
Hyrije AdemiInstitute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, Zurich.
Nadine von BürenInstitute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, Zurich.
Julia ArmbrusterInstitute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, Zurich.
Martina StirnClinical Laboratory, Department of Clinical Diagnostics and Services, Vetsuisse Faculty, University of Zurich, Zurich.
Sandro AltamuraDepartment of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg, Germany; Molecular Medicine Partnership Unit, Heidelberg.
Oriana MarquesDepartment of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg, Germany; Molecular Medicine Partnership Unit, Heidelberg.
Josep M Monné RodriguezLaboratory for Animal Model Pathology, Institute of Veterinary Pathology, Vetsuisse Faculty, University of Zurich, Zurich.
Victor J SamillanUniversidad Le Cordon Bleu, School of Human Nutrition, Lima.
Rashim Pal SinghInstitute of Clinical Chemistry and Laboratory Medicine, Carl Gustav Carus, TU Dresden.
Ben WielockxInstitute of Clinical Chemistry and Laboratory Medicine, Carl Gustav Carus, TU Dresden.
Martina U MuckenthalerDepartment of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, Heidelberg, Germany; 7Molecular Medicine Partnership Unit, Heidelberg, Germany; Translational Lung Research Center Heidelberg (TLRC), German Center for Lung Research (DZL), University of Heidelberg, Germany; German Centre for Cardiovascular Research, Partner Site.
Max GassmannInstitute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich.
Markus ThierschInstitute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Center for Clinical Studies, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland; Zurich Center for Integrative Human Physiology (ZIHP), University of Zurich, Zurich. markus.thiersch@uzh.ch.
University of Zurich · CHHeidelberg University · DEUniversity Hospital Carl Gustav Carus · DEGerman Centre for Cardiovascular Research · DELe Cordon Bleu College of Culinary Arts · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anemia of cancer (AoC) with its multifactorial etiology and complex pathology is a poor prognostic indicator for cancer patients. One of the main causes of AoC is cancer-associated inflammation that activates mechanisms, commonly observed in anemia of inflammation, whereby functional iron deficiency and iron-restricted erythropoiesis are induced by increased hepcidin levels in response to raised levels of interleukin-6. So far only a few AoC mouse models have been described, and most of them did not fully recapitulate the interplay of anemia, increased hepcidin levels and functional iron deficiency in human patients. To test if the selection and the complexity of AoC mouse models dictates the pathology or if AoC in mice per se develops independently of iron deficiency, we characterized AoC in Trp53floxWapCre mice that spontaneously develop breast cancer. These mice developed AoC associated with high levels of interleukin-6 and iron deficiency. However, hepcidin levels were not increased and hypoferremia coincided with anemia rather than causing it. Instead, an early shift in the commitment of common myeloid progenitors from the erythroid to the myeloid lineage resulted in increased myelopoiesis and in the excessive production of neutrophils that accumulate in necrotic tumor regions. This process could not be prevented by either iron or erythropoietin treatment. Trp53floxWapCre mice are the first mouse model in which erythropoietin-resistant anemia is described and may serve as a disease model to test therapeutic approaches for a subpopulation of human cancer patients with normal or corrected iron levels who do not respond to erythropoietin.

Indexed as

AnemiaBreast NeoplasmsErythropoietinIron DeficienciesAnimalsErythropoiesisFemaleHepcidinsHumansInflammationInterleukin-6IronMiceErythropoietinHepcidinsInterleukin-6Iron

Identifiers

PMID35385924
PMCPMC9521231
OpenAlexW4225491339

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.