Evidence map›Paper›PMID 19201693›Full record

ArticleCancer research2009

Arginase I-producing myeloid-derived suppressor cells in renal cell carcinoma are a subpopulation of activated granulocytes.

Paulo C Rodriguez, Marc S Ernstoff, Claudia Hernandez, Michael Atkins, Jovanny Zabaleta, Rosa Sierra, Augusto C Ochoa

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 445 papers.

0numbers the graph read from it
0cells of the map it votes in
445citing papers in PubMed
15.8field-weighted citation impact, top 1% 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

445 citing papers in PubMed, 749 citations in OpenAlex.

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  8. The role of neutrophils in the pathogenesis of abdominal aortic aneurysms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  19. Metastasis-promoting functions of myeloid cells.Cancer metastasis reviews · 2025
    Review
  20. Article

385 more citing papers are in PubMed but not listed here.

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

7 authors at 4 institutions in 2 countries.

Paulo C RodriguezDepartment of Microbiology, Stanley S Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112, USA.
Marc S Ernstoff
Claudia Hernandez
Michael Atkins
Jovanny Zabaleta
Rosa Sierra
Augusto C Ochoa
Bipar · FRDana-Farber/Harvard Cancer Center · USDartmouth College · USLouisiana State University Health Sciences Center New Orleans · US

Funding

TUMOR MICROENVIRONMENT AND B CELL LYMPHOMASP20RR021970 · NCRR · LSU HEALTH SCIENCES CENTER · PI ZABALETA, JOVANNY · 2005 to 2011
$14.1M
Arginase Production in Cancer: Evading Immune ResponseR01CA107974 · NCI · LSU HEALTH SCIENCES CENTER · PI OCHOA, AUGUSTO C. · 2004 to 2015
$3.6M
INDUCTION OF ANERGY AND ALTERED SIGNAL TRANSDUCTIONR01CA082689 · NCI · LSU HEALTH SCIENCES CENTER · PI OCHOA, AUGUSTO C. · 1999 to 2013
$3.1M
NCI NIH HHS CA107974NCI NIH HHS CA82689NCI NIH HHS R01 CA082689NCI NIH HHS R01 CA107974NCRR NIH HHS P20 RR021970
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSC) producing arginase I are increased in the peripheral blood of patients with renal cell carcinoma (RCC). MDSC inhibit T-cell function by reducing the availability of L-arginine and are therefore considered an important tumor escape mechanism. We aimed to determine the origin of arginase I-producing MDSC in RCC patients and to identify the mechanisms used to deplete extracellular L-arginine. The results show that human MDSC are a subpopulation of activated polymorphonuclear (PMN) cells expressing high levels of CD66b, CD11b, and VEGFR1 and low levels of CD62L and CD16. In contrast to murine MDSC, human MDSC do not deplete L-arginine by increasing its uptake but instead release arginase I into the circulation. Activation of normal PMN induces phenotypic and functional changes similar to MDSC and also promotes the release of arginase I from intracellular granules. Interestingly, although activation of normal PMN usually ends with apoptosis, MDSC showed no increase in apoptosis compared with autologous PMN or PMN obtained from normal controls. High levels of VEGF have been shown to increase suppressor immature myeloid dendritic cells in cancer patients. Treatment of RCC patients with anti-VEGF antibody bevacizumab, however, did not reduce the accumulation of MDSC in peripheral blood. In contrast, the addition of interleukin-2 to the treatment increased the number of MDSC in peripheral blood and the plasma levels of arginase I. These results may provide new insights on the mechanisms of tumor-induced anergy/tolerance and may help explain why some immunotherapies fail to induce an antitumor response.

Indexed as

Angiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntigens, CDArginaseArginineBevacizumabCarcinoma, Renal CellFemaleGranulocytesHumansImmunotherapyKidney NeoplasmsMaleMiceAngiogenesis InhibitorsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntigens, CDArginaseArginineBevacizumabRNA, Messenger

Identifiers

PMID19201693
PMCPMC2900845
OpenAlexW2054246680

What OpenQuestion holds

Textmetadata
LicenceTDM
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.