Evaluation of Serum Glycoprotein Biomarker Candidates for Detection of Esophageal Adenocarcinoma and Surveillance of Barrett's Esophagus
This paper reports independent cohort validation of previously discovered esophageal adenocarcinoma (EAC) serum diagnostic glycoprotein biomarker candidates. To demonstrate their potential clinical application in evaluating patients during endoscopy-biopsy surveillance, we developed a panel of 10 bi...
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| Published in | Molecular & cellular proteomics Vol. 17; no. 12; pp. 2324 - 2334 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
01.12.2018
The American Society for Biochemistry and Molecular Biology |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1535-9476 1535-9484 1535-9484 |
| DOI | 10.1074/mcp.RA118.000734 |
Cover
| Abstract | This paper reports independent cohort validation of previously discovered esophageal adenocarcinoma (EAC) serum diagnostic glycoprotein biomarker candidates. To demonstrate their potential clinical application in evaluating patients during endoscopy-biopsy surveillance, we developed a panel of 10 biomarker candidates (AUC 0.93) to discriminate Barrett's esophagus (BE) patients not requiring intervention [BE+/− low-grade dysplasia] from those requiring intervention [BE with high-grade dysplasia or EAC]. Complement pathway proteins appear to be dysregulated during EAC, with C9 detected in BE and EAC tissue.
[Display omitted]
Highlights
•C9, GSN, PON1, and PON3 validated as serum biomarker candidates of EAC.•Multimarker panel with AUROC of 0.93 to aid current endoscopy surveillance of BE.•Induction of tissue C9 in BE, dysplastic BE and EAC.•Alteration of complement pathway glycoproteins during BE-EAC pathogenesis.
Esophageal adenocarcinoma (EAC) is thought to develop from asymptomatic Barrett's esophagus (BE) with a low annual rate of conversion. Current endoscopy surveillance of BE patients is probably not cost-effective. Previously, we discovered serum glycoprotein biomarker candidates which could discriminate BE patients from EAC. Here, we aimed to validate candidate serum glycoprotein biomarkers in independent cohorts, and to develop a biomarker candidate panel for BE surveillance. Serum glycoprotein biomarker candidates were measured in 301 serum samples collected from Australia (4 states) and the United States (1 clinic) using previously established lectin magnetic bead array (LeMBA) coupled multiple reaction monitoring mass spectrometry (MRM-MS) tier 3 assay. The area under receiver operating characteristic curve (AUROC) was calculated as a measure of discrimination, and multivariate recursive partitioning was used to formulate a multi-marker panel for BE surveillance. Complement C9 (C9), gelsolin (GSN), serum paraoxonase/arylesterase 1 (PON1) and serum paraoxonase/lactonase 3 (PON3) were validated as diagnostic glycoprotein biomarkers in lectin pull-down samples for EAC across both cohorts. A panel of 10 serum glycoprotein biomarker candidates discriminated BE patients not requiring intervention (BE± low grade dysplasia) from those requiring intervention (BE with high grade dysplasia (BE-HGD) or EAC) with an AUROC value of 0.93. Tissue expression of C9 was found to be induced in BE, dysplastic BE and EAC. In longitudinal samples from subjects that have progressed toward EAC, levels of serum C9 were significantly (p < 0.05) increased with disease progression in EPHA (erythroagglutinin from Phaseolus vulgaris) and NPL (Narcissus pseudonarcissus lectin) pull-down samples. The results confirm alteration of complement pathway glycoproteins during BE-EAC pathogenesis. Further prospective clinical validation of the confirmed biomarker candidates in a large cohort is warranted, prior to development of a first-line BE surveillance blood test. |
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| AbstractList | Esophageal adenocarcinoma (EAC) is thought to develop from asymptomatic Barrett's esophagus (BE) with a low annual rate of conversion. Current endoscopy surveillance of BE patients is probably not cost-effective. Previously, we discovered serum glycoprotein biomarker candidates which could discriminate BE patients from EAC. Here, we aimed to validate candidate serum glycoprotein biomarkers in independent cohorts, and to develop a biomarker candidate panel for BE surveillance. Serum glycoprotein biomarker candidates were measured in 301 serum samples collected from Australia (4 states) and the United States (1 clinic) using previously established lectin magnetic bead array (LeMBA) coupled multiple reaction monitoring mass spectrometry (MRM-MS) tier 3 assay. The area under receiver operating characteristic curve (AUROC) was calculated as a measure of discrimination, and multivariate recursive partitioning was used to formulate a multi-marker panel for BE surveillance. Complement C9 (C9), gelsolin (GSN), serum paraoxonase/arylesterase 1 (PON1) and serum paraoxonase/lactonase 3 (PON3) were validated as diagnostic glycoprotein biomarkers in lectin pull-down samples for EAC across both cohorts. A panel of 10 serum glycoprotein biomarker candidates discriminated BE patients not requiring intervention (BE± low grade dysplasia) from those requiring intervention (BE with high grade dysplasia (BE-HGD) or EAC) with an AUROC value of 0.93. Tissue expression of C9 was found to be induced in BE, dysplastic BE and EAC. In longitudinal samples from subjects that have progressed toward EAC, levels of serum C9 were significantly (
< 0.05) increased with disease progression in EPHA (erythroagglutinin from
) and NPL (
lectin) pull-down samples. The results confirm alteration of complement pathway glycoproteins during BE-EAC pathogenesis. Further prospective clinical validation of the confirmed biomarker candidates in a large cohort is warranted, prior to development of a first-line BE surveillance blood test. This paper reports independent cohort validation of previously discovered esophageal adenocarcinoma (EAC) serum diagnostic glycoprotein biomarker candidates. To demonstrate their potential clinical application in evaluating patients during endoscopy-biopsy surveillance, we developed a panel of 10 biomarker candidates (AUC 0.93) to discriminate Barrett’s esophagus (BE) patients not requiring intervention [BE+/− low-grade dysplasia] from those requiring intervention [BE with high-grade dysplasia or EAC]. Complement pathway proteins appear to be dysregulated during EAC, with C9 detected in BE and EAC tissue. Highlights C9, GSN, PON1, and PON3 validated as serum biomarker candidates of EAC. Multimarker panel with AUROC of 0.93 to aid current endoscopy surveillance of BE. Induction of tissue C9 in BE, dysplastic BE and EAC. Alteration of complement pathway glycoproteins during BE-EAC pathogenesis. Esophageal adenocarcinoma (EAC) is thought to develop from asymptomatic Barrett's esophagus (BE) with a low annual rate of conversion. Current endoscopy surveillance of BE patients is probably not cost-effective. Previously, we discovered serum glycoprotein biomarker candidates which could discriminate BE patients from EAC. Here, we aimed to validate candidate serum glycoprotein biomarkers in independent cohorts, and to develop a biomarker candidate panel for BE surveillance. Serum glycoprotein biomarker candidates were measured in 301 serum samples collected from Australia (4 states) and the United States (1 clinic) using previously established lectin magnetic bead array (LeMBA) coupled multiple reaction monitoring mass spectrometry (MRM-MS) tier 3 assay. The area under receiver operating characteristic curve (AUROC) was calculated as a measure of discrimination, and multivariate recursive partitioning was used to formulate a multi-marker panel for BE surveillance. Complement C9 (C9), gelsolin (GSN), serum paraoxonase/arylesterase 1 (PON1) and serum paraoxonase/lactonase 3 (PON3) were validated as diagnostic glycoprotein biomarkers in lectin pull-down samples for EAC across both cohorts. A panel of 10 serum glycoprotein biomarker candidates discriminated BE patients not requiring intervention (BE± low grade dysplasia) from those requiring intervention (BE with high grade dysplasia (BE-HGD) or EAC) with an AUROC value of 0.93. Tissue expression of C9 was found to be induced in BE, dysplastic BE and EAC. In longitudinal samples from subjects that have progressed toward EAC, levels of serum C9 were significantly ( p < 0.05) increased with disease progression in EPHA (erythroagglutinin from Phaseolus vulgaris ) and NPL ( Narcissus pseudonarcissus lectin) pull-down samples. The results confirm alteration of complement pathway glycoproteins during BE-EAC pathogenesis. Further prospective clinical validation of the confirmed biomarker candidates in a large cohort is warranted, prior to development of a first-line BE surveillance blood test. This paper reports independent cohort validation of previously discovered esophageal adenocarcinoma (EAC) serum diagnostic glycoprotein biomarker candidates. To demonstrate their potential clinical application in evaluating patients during endoscopy-biopsy surveillance, we developed a panel of 10 biomarker candidates (AUC 0.93) to discriminate Barrett's esophagus (BE) patients not requiring intervention [BE+/− low-grade dysplasia] from those requiring intervention [BE with high-grade dysplasia or EAC]. Complement pathway proteins appear to be dysregulated during EAC, with C9 detected in BE and EAC tissue. [Display omitted] Highlights •C9, GSN, PON1, and PON3 validated as serum biomarker candidates of EAC.•Multimarker panel with AUROC of 0.93 to aid current endoscopy surveillance of BE.•Induction of tissue C9 in BE, dysplastic BE and EAC.•Alteration of complement pathway glycoproteins during BE-EAC pathogenesis. Esophageal adenocarcinoma (EAC) is thought to develop from asymptomatic Barrett's esophagus (BE) with a low annual rate of conversion. Current endoscopy surveillance of BE patients is probably not cost-effective. Previously, we discovered serum glycoprotein biomarker candidates which could discriminate BE patients from EAC. Here, we aimed to validate candidate serum glycoprotein biomarkers in independent cohorts, and to develop a biomarker candidate panel for BE surveillance. Serum glycoprotein biomarker candidates were measured in 301 serum samples collected from Australia (4 states) and the United States (1 clinic) using previously established lectin magnetic bead array (LeMBA) coupled multiple reaction monitoring mass spectrometry (MRM-MS) tier 3 assay. The area under receiver operating characteristic curve (AUROC) was calculated as a measure of discrimination, and multivariate recursive partitioning was used to formulate a multi-marker panel for BE surveillance. Complement C9 (C9), gelsolin (GSN), serum paraoxonase/arylesterase 1 (PON1) and serum paraoxonase/lactonase 3 (PON3) were validated as diagnostic glycoprotein biomarkers in lectin pull-down samples for EAC across both cohorts. A panel of 10 serum glycoprotein biomarker candidates discriminated BE patients not requiring intervention (BE± low grade dysplasia) from those requiring intervention (BE with high grade dysplasia (BE-HGD) or EAC) with an AUROC value of 0.93. Tissue expression of C9 was found to be induced in BE, dysplastic BE and EAC. In longitudinal samples from subjects that have progressed toward EAC, levels of serum C9 were significantly (p < 0.05) increased with disease progression in EPHA (erythroagglutinin from Phaseolus vulgaris) and NPL (Narcissus pseudonarcissus lectin) pull-down samples. The results confirm alteration of complement pathway glycoproteins during BE-EAC pathogenesis. Further prospective clinical validation of the confirmed biomarker candidates in a large cohort is warranted, prior to development of a first-line BE surveillance blood test. Esophageal adenocarcinoma (EAC) is thought to develop from asymptomatic Barrett's esophagus (BE) with a low annual rate of conversion. Current endoscopy surveillance of BE patients is probably not cost-effective. Previously, we discovered serum glycoprotein biomarker candidates which could discriminate BE patients from EAC. Here, we aimed to validate candidate serum glycoprotein biomarkers in independent cohorts, and to develop a biomarker candidate panel for BE surveillance. Serum glycoprotein biomarker candidates were measured in 301 serum samples collected from Australia (4 states) and the United States (1 clinic) using previously established lectin magnetic bead array (LeMBA) coupled multiple reaction monitoring mass spectrometry (MRM-MS) tier 3 assay. The area under receiver operating characteristic curve (AUROC) was calculated as a measure of discrimination, and multivariate recursive partitioning was used to formulate a multi-marker panel for BE surveillance. Complement C9 (C9), gelsolin (GSN), serum paraoxonase/arylesterase 1 (PON1) and serum paraoxonase/lactonase 3 (PON3) were validated as diagnostic glycoprotein biomarkers in lectin pull-down samples for EAC across both cohorts. A panel of 10 serum glycoprotein biomarker candidates discriminated BE patients not requiring intervention (BE± low grade dysplasia) from those requiring intervention (BE with high grade dysplasia (BE-HGD) or EAC) with an AUROC value of 0.93. Tissue expression of C9 was found to be induced in BE, dysplastic BE and EAC. In longitudinal samples from subjects that have progressed toward EAC, levels of serum C9 were significantly (p < 0.05) increased with disease progression in EPHA (erythroagglutinin from Phaseolus vulgaris) and NPL (Narcissus pseudonarcissus lectin) pull-down samples. The results confirm alteration of complement pathway glycoproteins during BE-EAC pathogenesis. Further prospective clinical validation of the confirmed biomarker candidates in a large cohort is warranted, prior to development of a first-line BE surveillance blood test.Esophageal adenocarcinoma (EAC) is thought to develop from asymptomatic Barrett's esophagus (BE) with a low annual rate of conversion. Current endoscopy surveillance of BE patients is probably not cost-effective. Previously, we discovered serum glycoprotein biomarker candidates which could discriminate BE patients from EAC. Here, we aimed to validate candidate serum glycoprotein biomarkers in independent cohorts, and to develop a biomarker candidate panel for BE surveillance. Serum glycoprotein biomarker candidates were measured in 301 serum samples collected from Australia (4 states) and the United States (1 clinic) using previously established lectin magnetic bead array (LeMBA) coupled multiple reaction monitoring mass spectrometry (MRM-MS) tier 3 assay. The area under receiver operating characteristic curve (AUROC) was calculated as a measure of discrimination, and multivariate recursive partitioning was used to formulate a multi-marker panel for BE surveillance. Complement C9 (C9), gelsolin (GSN), serum paraoxonase/arylesterase 1 (PON1) and serum paraoxonase/lactonase 3 (PON3) were validated as diagnostic glycoprotein biomarkers in lectin pull-down samples for EAC across both cohorts. A panel of 10 serum glycoprotein biomarker candidates discriminated BE patients not requiring intervention (BE± low grade dysplasia) from those requiring intervention (BE with high grade dysplasia (BE-HGD) or EAC) with an AUROC value of 0.93. Tissue expression of C9 was found to be induced in BE, dysplastic BE and EAC. In longitudinal samples from subjects that have progressed toward EAC, levels of serum C9 were significantly (p < 0.05) increased with disease progression in EPHA (erythroagglutinin from Phaseolus vulgaris) and NPL (Narcissus pseudonarcissus lectin) pull-down samples. The results confirm alteration of complement pathway glycoproteins during BE-EAC pathogenesis. Further prospective clinical validation of the confirmed biomarker candidates in a large cohort is warranted, prior to development of a first-line BE surveillance blood test. |
| Author | Spicer, Bradley A. Watson, David I. Brown, Ian Barbour, Andrew P. Phillips, Wayne A. Winterford, Clay Hartel, Gunter Shah, Alok K. Na, Renhua Joshi, Virendra Hill, Michelle M. Dunstone, Michelle A. Whiteman, David C. Cao, Kim-Anh Lê Lord, Reginald V. |
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| Keywords | Targeted mass spectrometry Multiple reaction monitoring Barrett's esophagus Glycoproteins Cancer biomarker(s) Complement pathway Biomarker: Diagnostic Esophageal adenocarcinoma Gastrointestinal disease Serum/Plasma |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author contributions: A.K.S., M.A.D., and M.M.H. designed research; A.K.S., C.W., and B.A.S. performed research; A.K.S., G.H., and R.N. analyzed data; A.K.S., G.H., D.C.W., and M.M.H. wrote the paper; G.H., K.-A.L.C., B.A.S., and M.A.D. contributed new reagents/analytic tools; I.B. evaluated and scored immunohistochemistry slides; R.N. patient sample selection for the study; W.A.P., R.V.L., A.P.B., and D.I.W. contributed to sample collection; V.J. contributed to sample collection and selection; D.C.W. contributed to sample collection and selection. |
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| Snippet | This paper reports independent cohort validation of previously discovered esophageal adenocarcinoma (EAC) serum diagnostic glycoprotein biomarker candidates.... Esophageal adenocarcinoma (EAC) is thought to develop from asymptomatic Barrett's esophagus (BE) with a low annual rate of conversion. Current endoscopy... |
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| SubjectTerms | Adenocarcinoma - blood Adenocarcinoma - diagnosis Adenocarcinoma - etiology Adenocarcinoma - pathology Aged Area Under Curve Aryldialkylphosphatase - blood Australia Barrett Esophagus - blood Barrett Esophagus - complications Barrett Esophagus - diagnosis Barrett Esophagus - pathology Barrett's esophagus Biomarker: Diagnostic Biomarkers - blood Biopsy Cancer biomarker(s) Cohort Studies Complement C9 - analysis Complement pathway Diagnosis, Differential Esophageal adenocarcinoma Esophageal Neoplasms - blood Esophageal Neoplasms - diagnosis Esophageal Neoplasms - etiology Esophageal Neoplasms - pathology Female Gastrointestinal disease Gelsolin - blood Glycoproteins Humans Male Mass Spectrometry - methods Middle Aged Multiple reaction monitoring Multivariate Analysis Public Health Surveillance Serum/Plasma Targeted mass spectrometry United States |
| Title | Evaluation of Serum Glycoprotein Biomarker Candidates for Detection of Esophageal Adenocarcinoma and Surveillance of Barrett's Esophagus |
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