Evidence map›Paper›PMID 28870260›Full record

ArticleBMC cancer2017

Programmed cell death ligand 1 cut-point is associated with reduced disease specific survival in resected pancreatic ductal adenocarcinoma.

Basile Tessier-Cloutier, Steve E Kalloger, Mohammad Al-Kandari, Katy Milne, Dongxia Gao, Brad H Nelson, Daniel J Renouf, Brandon S Sheffield, David F Schaeffer

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 3 pooled it
2.0field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 40 citations in OpenAlex.

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  20. UEG Week 2019 Poster Presentations.United European gastroenterology journal · 2019
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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

9 authors at 4 institutions in 1 country.

Basile Tessier-CloutierDivision of Anatomical Pathology, Vancouver General Hospital, Vancouver, British Columbia, Canada.
Steve E KallogerDepartment of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada. skalloger@mac.com.ORCID http://orcid.org/0000-0003-1332-7881
Mohammad Al-KandariDivision of Anatomical Pathology, Vancouver General Hospital, Vancouver, British Columbia, Canada.
Katy MilneDeeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia, Canada.
Dongxia GaoDivision of Medical Oncology, University of British Columbia , Vancouver, British Columbia, Canada.
Brad H NelsonDeeley Research Centre, British Columbia Cancer Agency, Victoria, British Columbia, Canada.
Daniel J RenoufDivision of Medical Oncology, University of British Columbia , Vancouver, British Columbia, Canada.
Brandon S SheffieldDepartment of Anatomical Pathology, Abbotosford Regional Hospital and Cancer Centre, Abbotsford, British Columbia, Canada.
David F SchaefferDivision of Anatomical Pathology, Vancouver General Hospital, Vancouver, British Columbia, Canada.
BC Cancer Agency · CAUniversity of British Columbia · CAAbbotsford Veterinary Clinic · CAVancouver General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgrammed cell death 1 (PD1) inhibitors have recently shown promising anti-cancer effects in a number of solid tumor types. A predictive biomarker to this class of drugs has not been clearly identified; however, overexpression of the PD1 ligand (PD-L1) has shown particular promise in lung adenocarcinoma. In this study, we explore the staining characteristics, prevalence, and clinico-molecular correlates of PD-L1 overexpression in pancreatic ductal adenocarcinoma (PDAC).

methodsA tissue microarray (TMA) was constructed from cases of resected PDAC. PD-L1 immunohistochemistry (IHC) was performed using the SP142 primary antibody. Immunohistochemical assessment for deficient mismatch repair status (MMRd), CD3 and CD8 were performed. All biomarkers were assessed independently by two anatomical pathologists and consensus achieved on all cases. Survival analysis was performed using three thresholds (> = 1%, >5% and >10%) for tumor cell membrane staining.

resultsTwo-hundred fifty-two cases were included in the TMA and evaluable by IHC. Thirty-one (12%), 17 (7%), 12(5%) cases were positive at percentage cut offs of >0, >5, and >10% respectively. Increased PD-L1 expression was associated with inferior prognosis (p = 0.0367). No statistically significant association was identified between PD-L1 status and MMR status or tumor infiltrating lymphocytes.

conclusionsThis data suggests that there is an inverse relationship between PD-L1 expression and disease specific survival times in resected PDAC. Consequently, this association may represent a phenotype where increased PD-L1 expression has an effect on tumor biology and could therefore identify a subgroup where PD1 blockade could have enhanced effectiveness.

Indexed as

Biomarkers, TumorAgedB7-H1 AntigenCarcinoma, Pancreatic DuctalChemotherapy, AdjuvantDNA Mismatch RepairFemaleGene ExpressionHumansImmunohistochemistryLymphocytes, Tumor-InfiltratingMaleMiddle AgedNeoplasm GradingNeoplasm InvasivenessNeoplasm StagingB7-H1 AntigenBiomarkers, TumorCD274 protein, humanBiomarkersDNA mismatch repairImmuno-oncologyPancreatic cancerProgrammed cell death 1 ligandTumor-infiltrating lymphocytes

Identifiers

PMID28870260
PMCPMC5584324
OpenAlexW2752101014

What OpenQuestion holds

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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.