Evidence map›Paper›PMID 27376091›Full record

ArticleJournal of immunology research2016

Monocyte Differentiation towards Protumor Activity Does Not Correlate with M1 or M2 Phenotypes.

G Karina Chimal-Ramírez, Nancy Adriana Espinoza-Sánchez, Luis Chávez-Sánchez, Lourdes Arriaga-Pizano, Ezequiel M Fuentes-Pananá

Abstract read
In one paragraph

Article in Journal of immunology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Reactive Oxygen Species Imaging in U937 Cells.Frontiers in physiology · 2020
    Article
  16. Article
  17. Article
  18. An obligatory anaerobicOncology letters · 2018
    Article
  19. Article
  20. 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

5 authors.

G Karina Chimal-RamírezUnidad de Investigación en Virología y Cáncer, Hospital Infantil de México Federico Gómez, Dr. Márquez 162, Colonia Doctores, 06720 Ciudad de México, DF, Mexico.
Nancy Adriana Espinoza-SánchezUnidad de Investigación en Virología y Cáncer, Hospital Infantil de México Federico Gómez, Dr. Márquez 162, Colonia Doctores, 06720 Ciudad de México, DF, Mexico; Programa de Doctorado en Ciencias Biomédicas, Universidad Nacional Autónoma de México (UNAM), 04510 Ciudad de México, DF, Mexico.
Luis Chávez-SánchezUIM en Inmunología, Hospital de Pediatría, CMN Siglo XXI, IMSS, 06720 Ciudad de México, DF, Mexico.
Lourdes Arriaga-PizanoUIM en Inmunoquímica, Hospital de Especialidades, CMN Siglo XXI, IMSS, 06720 Ciudad de México, DF, Mexico.
Ezequiel M Fuentes-PananáUnidad de Investigación en Virología y Cáncer, Hospital Infantil de México Federico Gómez, Dr. Márquez 162, Colonia Doctores, 06720 Ciudad de México, DF, Mexico.ORCID 0000-0003-2872-0459

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages facilitate breast cancer progression. Macrophages were initially classified as M1 or M2 based on their distinct metabolic programs and then expanded to include antitumoral (M1) and protumoral (M2) activities. However, it is still uncertain what markers define the pro- and antitumoral phenotypes and what conditions lead to their formation. In this study, monocytic cell lines and primary monocytes were subjected to commonly reported protocols of M1/M2 polarization and conditions known to engage monocytes into protumoral functions. The results showed that only IDO enzyme and CD86 M1 markers were upregulated correlating with M1 polarization. TNF-α, CCR7, IL-10, arginase I, CD36, and CD163 were expressed indistinguishably from M1 or M2 polarization. Similarly, protumoral engaging resulted in upregulation of both M1 and M2 markers, with conditioned media from the most aggressive breast cancer cell line promoting the greatest changes. In spite of the mixed phenotype, M1-polarized macrophages exhibited the highest expression/secretion of inflammatory mediators, many of which have previously been associated with breast cancer aggressiveness. These data argue that although the existence of protumoral macrophages is unquestionable, their associated phenotypes and the precise conditions driving their formation are still unclear, and those conditions may need both M1 and M2 stimuli.

Indexed as

Cell DifferentiationArginaseB7-2 AntigenCD30 LigandCD36 AntigensCell Line, TumorCells, CulturedCytokinesFemaleFlow CytometryHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukin-10MacrophagesMonocytesPhenotypeArginaseB7-2 AntigenCCR7 protein, humanCD30 LigandCD36 AntigensCD86 protein, humanCytokinesIDO1 protein, humanIL10 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukin-10Receptors, CCR7Tumor Necrosis Factor-alpha

Identifiers

PMID27376091
PMCPMC4916292

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.