Evidence map›Paper›PMID 32929519›Full record

ReviewHNO2020

[Tumor microenvironment in salivary gland carcinomas: Consequences for new therapeutic concepts].

M F Meyer, C Arolt, B A Kansy, J Doescher, A Quaas, D Beutner, S Lang, J P Klußmann

Abstract readReview
PubMed Publisher
In one paragraph

Review in HNO, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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

8 authors at 6 institutions in 1 country.

M F MeyerKlinik für Hals‑, Nasen- und Ohrenheilkunde, Universitätsklinikum Essen, Universität Duisburg-Essen, Hufelandstraße 55, 45147, Essen, Deutschland. moritz.meyer@uk-essen.de.
C AroltInstitut für Pathologie, Medizinische Fakultät und Uniklinik Köln, Universität zu Köln, Köln, Deutschland.
B A KansyKlinik für Hals‑, Nasen- und Ohrenheilkunde, Universitätsklinikum Essen, Universität Duisburg-Essen, Hufelandstraße 55, 45147, Essen, Deutschland.
J DoescherKlinik für Hals-Nasen-Ohrenheilkunde, Kopf- und Halschirurgie, Universitätsklinikum Ulm, Ulm, Deutschland.
A QuaasInstitut für Pathologie, Medizinische Fakultät und Uniklinik Köln, Universität zu Köln, Köln, Deutschland.
D BeutnerKlinik und Poliklinik für Hals‑, Nasen-, und Ohrenheilkunde, Universitätsklinik Göttingen, Göttingen, Deutschland.
S LangKlinik für Hals‑, Nasen- und Ohrenheilkunde, Universitätsklinikum Essen, Universität Duisburg-Essen, Hufelandstraße 55, 45147, Essen, Deutschland.
J P KlußmannKlinik und Poliklinik für Hals‑, Nasen- und Ohrenheilkunde, Kopf- und Halschirurgie, Medizinische Fakultät und Uniklinik Köln, Universität zu Köln, Köln, Deutschland.
Essen University Hospital · DEUniversity Hospital Cologne · DEKlinik und Poliklinik für Hals-, Nasen-, Ohrenheilkunde · DEUniversity Hospital Ulm · DEUniversity of Cologne · DEUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionSalivary gland carcinomas (SGCs) are rare tumors which represent a challenge for diagnosis and therapy due to their histological diversity and the different disease courses depending on the respective subtype. Little is known about the composition of the tumor microenvironment in SGCs. A more comprehensive understanding of the relevant molecular changes and immunological processes of the tumor and surrounding stroma could help to improve therapeutic efficiency, for example by adjuvant immunomodulation.

methodsThis manuscript highlights recent studies analyzing the composition of the tumor microenvironment in salivary gland carcinomas.

resultsThe tumor microenvironment displays a significant diversity in the composition of immune cells among different tumor entities. In one third of the SGCs, an expression of cell surface molecule LAG3 on tumor infiltrating lymphocytes could be observed. LAG3-similar to CTLA‑4 and PD-1-inhibits cellular proliferation, activation, and homeostasis of antitumor-effective T cells. Especially, prognostically less favorable entities such as salivary duct carcinomas and adenocarcinomas NOS (not otherwise specified) yielded higher expressions.

conclusionsLAG3 is particularly detectable in aggressive entities and advanced tumors. Hence, LAG3 inhibition poses a potential targeted therapy for advanced and metastatic SGCs.

Indexed as

CarcinomaSalivary Gland NeoplasmsBiomarkers, TumorHumansLymphocytes, Tumor-InfiltratingSalivary GlandsTumor MicroenvironmentBiomarkers, TumorHead and neck neoplasmsImmunity, cellularImmunotherapyPD‑1Tumor escape

Identifiers

PMID32929519
OpenAlexW3084793365

What OpenQuestion holds

Textmetadata
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.