Evidence map›Paper›PMID 28275576›Full record

ReviewFrontiers in oncology2017

The Unique Molecular and Cellular Microenvironment of Ovarian Cancer.

Thomas Worzfeld, Elke Pogge von Strandmann, Magdalena Huber, Till Adhikary, Uwe Wagner, Silke Reinartz, Rolf Müller

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
183citing papers in PubMed, 2 pooled it
11.4field-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

183 citing papers in PubMed, 2 syntheses or guidelines pooled it, 280 citations in OpenAlex.

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123 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 1 country.

Thomas WorzfeldInstitute of Pharmacology, Biochemical-Pharmacological Center (BPC), Philipps University, Marburg, Germany; Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
Elke Pogge von StrandmannExperimental Tumor Research, Clinic for Hematology, Oncology and Immunology, Center for Tumor Biology and Immunology, Philipps University , Marburg , Germany.
Magdalena HuberInstitute of Medical Microbiology and Hygiene, Biomedical Research Center, Philipps University , Marburg , Germany.
Till AdhikaryInstitute of Molecular Biology and Tumor Research, Center for Tumor Biology and Immunology, Philipps University , Marburg , Germany.
Uwe WagnerClinic for Gynecology, Gynecological Oncology and Gynecological Endocrinology, University Hospital of Giessen and Marburg (UKGM) , Marburg , Germany.
Silke ReinartzClinic for Gynecology, Gynecological Oncology and Gynecological Endocrinology, Center for Tumor Biology and Immunology (ZTI), Philipps University , Marburg , Germany.
Rolf MüllerInstitute of Molecular Biology and Tumor Research, Center for Tumor Biology and Immunology, Philipps University , Marburg , Germany.
Institute of Molecular Biology · DEPhilipps University of Marburg · DEInstitute of Medical Microbiology and Hygiene · DEUniversitätsklinikum Gießen und Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The reciprocal interplay of cancer cells and host cells is an indispensable prerequisite for tumor growth and progression. Cells of both the innate and adaptive immune system, in particular tumor-associated macrophages (TAMs) and T cells, as well as cancer-associated fibroblasts enter into a malicious liaison with tumor cells to create a tumor-promoting and immunosuppressive tumor microenvironment (TME). Ovarian cancer, the most lethal of all gynecological malignancies, is characterized by a unique TME that enables specific and efficient metastatic routes, impairs immune surveillance, and mediates therapy resistance. A characteristic feature of the ovarian cancer TME is the role of resident host cells, in particular activated mesothelial cells, which line the peritoneal cavity in huge numbers, as well as adipocytes of the omentum, the preferred site of metastatic lesions. Another crucial factor is the peritoneal fluid, which enables the transcoelomic spread of tumor cells to other pelvic and peritoneal organs, and occurs at more advanced stages as a malignancy-associated effusion. This ascites is rich in tumor-promoting soluble factors, extracellular vesicles and detached cancer cells as well as large numbers of T cells, TAMs, and other host cells, which cooperate with resident host cells to support tumor progression and immune evasion. In this review, we summarize and discuss our current knowledge of the cellular and molecular interactions that govern this interplay with a focus on signaling networks formed by cytokines, lipids, and extracellular vesicles; the pathophysiologial roles of TAMs and T cells; the mechanism of transcoelomic metastasis; and the cell type selective processing of signals from the TME.

Indexed as

adhesionascitesextracellular vesiclesinvasionmesothelial cellmetastasisNFκBSTATT cellT cell checkpointstumor-associated macrophagetumor microenvironment

Identifiers

PMID28275576
PMCPMC5319992
OpenAlexW2589658059

What Socratic 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 Socratic graph.