Evidence map›Paper›PMID 37256148›Full record

ArticleFrontiers in immunology2023

Serum immune mediators as novel predictors of response to anti-PD-1/PD-L1 therapy in non-small cell lung cancer patients with high tissue-PD-L1 expression.

Afsheen Raza, Reyad Mohsen, Aladdin Kanbour, Abdul Rehman Zar Gul, Anite Philip, Suma Vijayakumar, Shereena Hydrose, Kirti S Prabhu, Aisha Khamis Al-Suwaidi, Varghese Philipose Inchakalody and 13 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. 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

23 authors.

Afsheen RazaDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Reyad MohsenDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Aladdin KanbourDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Abdul Rehman Zar GulDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Anite PhilipDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Suma VijayakumarDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Shereena HydroseDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Kirti S PrabhuTranslational Research Institute (TRI), Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Aisha Khamis Al-SuwaidiDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Varghese Philipose InchakalodyDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Maysaloun MerhiDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Dina M Abo El-EllaDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Melissa Annrose TauroDepartment of Human Genetics, Sidra Medical and Research Center, Doha, Qatar.
Shayista AkbarCollege of Health and Life Sciences, Hamad Bin Khalifa University, Doha, Qatar.
Issam Al-BozomDepartment of Laboratory Medicine and Pathology, Hamad Medical Corporation, Doha, Qatar.
Wafa AbualaininDiagnostic Genomic Division , Department of Laboratory Medicine and Pathology, Hamad Medical Corporation, Doha, Qatar.
Rajaa Al-AbdullaDepartment of Laboratory Medicine and Pathology, Hamad Medical Corporation, Doha, Qatar.
Shaza Abu SirriyaDiagnostic Genomic Division , Department of Laboratory Medicine and Pathology, Hamad Medical Corporation, Doha, Qatar.
Suparna HassnadDepartment of Radiation Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Shahab UddinTranslational Research Institute and Dermatology Institute, Academic Health System, Hamad, Medical Corporation, Doha, Qatar.
Mohamed Izham Mohamed IbrahimClinical Pharmacy and Practice Department, College of Pharmacy, Qatar University (QU) Health, Qatar University, Doha, Qatar.
Ussama Al HomsiDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
Said DemimeDepartment of Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related morbidity and mortality worldwide. Immune checkpoint inhibitors (ICIs) including anti-PD-1 and anti-PD-L1 antibodies, have significantly changed the treatment outcomes with better overall survival, but only 15-40% of the patients respond to ICIs therapy. The search for predictive biomarkers of responses is warranted for better clinical outcomes. We aim here to identify pre-treatment soluble immune molecules as surrogate biomarkers for tissue PD-L1 (TPD-L1) status and as predictors of response to anti-PD-1/PD-L1 therapy in NSCLC patients. Sera from 31 metastatic NSCLC patients, eligible for anti-PD-1/PD-L1 or combined chemoimmunotherapy, were collected prior to treatment. Analysis of soluble biomarkers with TPD-L1 status showed significant up/down regulation of the immune inhibitory checkpoint markers (sSiglec7, sSiglec9, sULBP4 and sPD-L2) in patients with higher TPD-L1 (TPD-L1 >50%) expression. Moreover, correlation analysis showed significant positive linear correlation of soluble PD-L1 (sPD-L1) with higher TPD-L1 expression. Interestingly, only responders in the TPD-L1 >50% group showed significant down regulation of the immune inhibitory markers (sPD-L2, sTIMD4, sNectin2 and CEA). When responders vs. non-responders were compared, significant down regulation of other immune inhibitory biomarkers (sCD80, sTIMD4 and CEA) was recorded only in responding patients. In this, the optimal cut-off values of CD80 <91.7 pg/ml and CEA <1614 pg/ml were found to be significantly associated with better progression free survival (PFS). Indeed, multivariate analysis identified the cutoff-value of CEA <1614 pg/ml as an independent predictor of response in our patients. We identified here novel immune inhibitory/stimulatory soluble mediators as potential surrogate/predictive biomarkers for TPD-L1 status, treatment response and PFS in NSCLC patients treated with anti-PD-1/PD-L1 therapy.

Indexed as

Antineoplastic Agents, ImmunologicalCarcinoma, Non-Small-Cell LungLung NeoplasmsHumansImmunologic FactorsProgression-Free SurvivalTreatment OutcomeAntineoplastic Agents, ImmunologicalImmunologic Factorsanti-PD-1anti-PD-L1CEAnon-small cell lung cancerpredictive soluble biomarkerstissue PD-L1

Identifiers

PMID37256148
PMCPMC10225547

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.