Evidence map›Paper›PMID 35758407›Full record

ArticleDiseases of the esophagus : official journal of the International Society for Diseases of the Esophagus2022

Development and validation of a molecular tool to predict pathologic complete response in esophageal adenocarcinoma.

David C Qian, Joel A Lefferts, Bassem I Zaki, Elizabeth B Brickley, Christopher R Jackson, Juliana Andrici, Aravindhan Sriharan, Mikhail Lisovsky

Open access · greenAbstract read
In one paragraph

Article in Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

8 authors at 3 institutions in 2 countries.

David C QianDepartment of Radiation Oncology, Winship Cancer Institute of Emory University, Atlanta, GA, USA.
Joel A LeffertsDepartment of Pathology and Laboratory Medicine, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA.
Bassem I ZakiDepartment of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, NH, USA.
Elizabeth B BrickleyDepartment of Infectious Disease Epidemiology, London School of Hygiene & Tropical Medicine, London, UK.
Christopher R JacksonDepartment of Pathology and Laboratory Medicine, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA.
Juliana AndriciDepartment of Pathology and Laboratory Medicine, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA.
Aravindhan SriharanDepartment of Pathology and Laboratory Medicine, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA.
Mikhail LisovskyDepartment of Pathology and Laboratory Medicine, Dartmouth Hitchcock Medical Center, Lebanon, NH, USA.
Dartmouth–Hitchcock Medical Center · USEmory University · USLondon School of Hygiene & Tropical Medicine · GB

Funding

Translational Engineering in Cancer (TEC)P30CA023108 · NCI · DARTMOUTH COLLEGE · PI Steven D Leach · 1985 to 2026
$91.3M
NCI NIH HHS P30 CA023108
6 · The paper itself

Abstract

Pathologic complete response (pCR) to neoadjuvant chemoradiation for locally advanced esophageal adenocarcinoma (EAC) confers significantly improved survival. The ability to infer pCR may spare esophagectomy in some patients. Currently, there are no validated biomarkers of pCR. This study sought to evaluate whether a distinct signature of DNA copy number alterations (CNA) can be predictive of pCR in EAC. Pretreatment biopsies from 38 patients with locally advanced EAC (19 with pCR and 19 with pathologic partial/poor response) were assessed for CNA using OncoScan assay. A novel technique was employed where within every cytogenetic band, the quantity of bases gained by each sample was computed as the sum of gained genomic segment lengths weighted by the surplus copy number of each segment. A threefold cross-validation was used to assess association with pCR or pathologic partial/poor response. Forty patients with locally advanced EAC from The Cancer Genome Atlas (TCGA) constituted an independent validation cohort. Gains in the chromosomal loci 14q11 and 17p11 were preferentially associated with pCR. Average area under the receiver operating characteristic curve (AUC) for predicting pCR was 0.80 among the threefold cross-validation test sets. Using 0.3 megabases as the cutoff that optimizes trade-off between sensitivity (63%) and specificity (89%) in the discovery cohort, similar prediction performance for clinical and radiographic response was demonstrated in the validation cohort from TCGA (sensitivity 61%, specificity 82%). Copy number gains in the 14q11 and 17p11 loci may be useful for prediction of pCR, and, potentially, personalization of esophagectomy in EAC.

Indexed as

AdenocarcinomaEsophageal NeoplasmsEsophagectomyHumansNeoadjuvant TherapyTreatment Outcomecopy number alterationsesophageal adenocarcinomaneoadjuvant chemoradiationpathologic complete responseThe Cancer Genome Atlas

Identifiers

PMID35758407
PMCPMC10893915
OpenAlexW4283652532

What OpenQuestion holds

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Registered trials

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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.