Evidence map›Paper›PMID 31535085›Full record

ReviewCell stress2019

Myelopoiesis, metabolism and therapy: a crucial crossroads in cancer progression.

Antonio Sica, Valentina Guarneri, Alessandra Gennari

Abstract readReview
In one paragraph

Review in Cell stress, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

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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

3 authors.

Antonio SicaDepartment of Pharmaceutical Sciences, Università del Piemonte Orientale "Amedeo Avogadro", via Bovio 6, Novara, Italy.
Valentina GuarneriDepartment of Surgery, Oncology and Gastroenterology, University of Padova.
Alessandra GennariDivision of Oncology, Department of Translational Medicine, University of Eastern Piedmont, Novara, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancers promote immunological stresses that induce alterations of the myelopoietic output, defined as emergency myelopoiesis, which lead to the generation of different myeloid populations endowed with tumor-promoting activities. New evidence indicates that acquisition of this tumor-promoting phenotype by myeloid cells is the result of a multistep process, encompassing initial events originating into the bone marrow and later steps operating in the tumor microenvironment. The careful characterization of these sequential mechanisms is likely to offer new potential therapeutic opportunities. Here, we describe relevant mechanisms of myeloid cells reprogramming that instate immune dysfunctions and limit effective responses to anticancer therapy and discuss the influence that metabolic events, as well as chemotherapy, elicit on such events.

Indexed as

cancerchemotherapyemergency myelopoiesisimmune-metabolismmyeloid-derived suppressor cellstumor-associated macrophages

Identifiers

PMID31535085
PMCPMC6732213

What OpenQuestion holds

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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.