Evidence map›Paper›PMID 37444617›Full record

ReviewCancers2023

Polarization of Cancer-Associated Macrophages Maneuver Neoplastic Attributes of Pancreatic Ductal Adenocarcinoma.

Huey-Jen Lin, Yingguang Liu, Kailey Caroland, Jiayuh Lin

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. 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

4 authors at 3 institutions in 1 country.

Huey-Jen LinDepartment of Medical & Molecular Sciences, University of Delaware, Willard Hall Education Building, 16 West Main Street, Newark, DE 19716, USA.ORCID 0000-0003-1726-6385
Yingguang LiuDepartment of Molecular and Cellular Sciences, College of Osteopathic Medicine, Liberty University, 306 Liberty View Lane, Lynchburg, VA 24502, USA.ORCID 0000-0002-2114-3997
Kailey CarolandDepartment of Biochemistry and Molecular Biology, Molecular Medicine Graduate Program, Greenebaum Comprehensive Cancer Center, School of Medicine, University of Maryland, 108 N. Greene Street, Baltimore, MD 21201, USA.ORCID 0009-0003-8195-8615
Jiayuh LinDepartment of Biochemistry and Molecular Biology, Molecular Medicine Graduate Program, Greenebaum Comprehensive Cancer Center, School of Medicine, University of Maryland, 108 N. Greene Street, Baltimore, MD 21201, USA.
University of Maryland, Baltimore · USLiberty University · USUniversity of Delaware · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mounting evidence links the phenomenon of enhanced recruitment of tumor-associated macrophages towards cancer bulks to neoplastic growth, invasion, metastasis, immune escape, matrix remodeling, and therapeutic resistance. In the context of cancer progression, naïve macrophages are polarized into M1 or M2 subtypes according to their differentiation status, gene signatures, and functional roles. While the former render proinflammatory and anticancer effects, the latter subpopulation elicits an opposite impact on pancreatic ductal adenocarcinoma. M2 macrophages have gained increasing attention as they are largely responsible for molding an immune-suppressive landscape. Through positive feedback circuits involving a paracrine manner, M2 macrophages can be amplified by and synergized with neighboring neoplastic cells, fibroblasts, endothelial cells, and non-cell autonomous constituents in the microenvironmental niche to promote an advanced disease state. This review delineates the molecular cues expanding M2 populations that subsequently convey notorious clinical outcomes. Future therapeutic regimens shall comprise protocols attempting to abolish environmental niches favoring M2 polarization; weaken cancer growth typically assisted by M2; promote the recruitment of tumoricidal CD8

Indexed as

angiogenesischemoresistanceepithelial–mesenchymal transitionextracellular matrixgemcitabinehypoxiaimmune checkpoint blockadesimmune suppressionKrasmetastasispancreatic ductal adenocarcinomatumor-associated macrophagestumor-infiltrating lymphocytestumor microenvironment

Identifiers

PMID37444617
PMCPMC10340421
OpenAlexW4383346210

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.