Evidence map›Paper›PMID 30134604›Full record

ArticleCancers2018

Expression Analysis of Autophagy Related Markers LC3B, p62 and HMGB1 Indicate an Autophagy-Independent Negative Prognostic Impact of High p62 Expression in Pulmonary Squamous Cell Carcinomas.

Rupert Langer, Christina Neppl, Manuel D Keller, Ralph A Schmid, Mario P Tschan, Sabina Berezowska

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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  15. [Lung cancer under stress].Der Pathologe · 2018
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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

6 authors at 1 institution in 1 country.

Rupert LangerInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland. rupert.langer@pathology.unibe.ch.ORCID 0000-0001-9491-3609
Christina NepplInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland. christina.neppl@pathology.unibe.ch.
Manuel D KellerInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland. manuel.keller@students.unibe.ch.
Ralph A SchmidDivision of General Thoracic Surgery, Inselspital University Hospital Bern, 3010 Bern, Switzerland. ralph.schmid@insel.ch.
Mario P TschanInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland. mario.tschan@pathology.unibe.ch.ORCID 0000-0001-5897-3647
Sabina BerezowskaInstitute of Pathology, University of Bern, Murtenstrasse 31, 3008 Bern, Switzerland. sabina.berezowska@pathology.unibe.ch.ORCID 0000-0001-5442-9791
University of Bern · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is involved in maintaining cellular homeostasis under stress conditions. It also plays an important role in various diseases including cancer. Pulmonary squamous cell carcinomas (pSQCC) at present lack targetable molecular alterations, and demand alternative therapeutic options. We assessed the expression levels of autophagy related proteins LC3B, p62, and HMGB1 in 271 primary resected pSQCC by immunohistochemistry, in correlation with clinical and pathological parameters, as a rationale for a potential autophagy directed therapy. LC3B, p62, and HMGB1 staining showed various patterns. LC3B

Indexed as

autophagyHMGB1LC3BLung cancerp62squamous cell carcinoma

Identifiers

PMID30134604
PMCPMC6162479
OpenAlexW2887998261

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.