Prognostic biomarker study in patients with clinical stage I esophageal squamous cell carcinoma: JCOG0502‐A1

We undertook genomic analyses of Japanese patients with stage I esophageal squamous cell carcinoma (ESCC) to investigate the frequency of genomic alterations and the association with survival outcomes. Biomarker analysis was carried out for patients with clinical stage T1bN0M0 ESCC enrolled in JCOG0...

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Veröffentlicht in:Cancer science 2022-03, Vol.113 (3), p.1018-1027
Hauptverfasser: Oshima, Kotoe, Kato, Ken, Ito, Yoshinori, Daiko, Hiroyuki, Nozaki, Isao, Nakagawa, Satoru, Shibuya, Yuichi, Kojima, Takashi, Toh, Yasushi, Okada, Morihito, Hironaka, Shuichi, Akiyama, Yuji, Komatsu, Yoshito, Maejima, Kazuhiro, Nakagawa, Hidewaki, Onuki, Ritsuko, Nagai, Momoko, Kato, Mamoru, Kanato, Keisuke, Kuchiba, Aya, Nakamura, Kenichi, Kitagawa, Yuko
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container_issue 3
container_start_page 1018
container_title Cancer science
container_volume 113
creator Oshima, Kotoe
Kato, Ken
Ito, Yoshinori
Daiko, Hiroyuki
Nozaki, Isao
Nakagawa, Satoru
Shibuya, Yuichi
Kojima, Takashi
Toh, Yasushi
Okada, Morihito
Hironaka, Shuichi
Akiyama, Yuji
Komatsu, Yoshito
Maejima, Kazuhiro
Nakagawa, Hidewaki
Onuki, Ritsuko
Nagai, Momoko
Kato, Mamoru
Kanato, Keisuke
Kuchiba, Aya
Nakamura, Kenichi
Kitagawa, Yuko
description We undertook genomic analyses of Japanese patients with stage I esophageal squamous cell carcinoma (ESCC) to investigate the frequency of genomic alterations and the association with survival outcomes. Biomarker analysis was carried out for patients with clinical stage T1bN0M0 ESCC enrolled in JCOG0502 (UMIN000000551). Whole‐exome sequencing (WES) was performed using DNA extracted from formalin‐fixed, paraffin‐embedded tissue of ESCC and normal tissue or blood sample. Single nucleotide variants (SNVs), insertions/deletions (indels), and copy number alterations (CNAs) were identified. We then evaluated the associations between each gene alteration with a frequency of 10% or more and progression‐free survival (PFS) using a Cox regression model. We controlled for family‐wise errors at 0.05 using the Bonferroni method. Among the 379 patients who were enrolled in JCOG0502, 127 patients were successfully analyzed using WES. The median patient age was 63 years (interquartile range, 57‐67 years), and 78.0% of the patients ultimately underwent surgery. The 3‐year PFS probability was 76.3%. We detected 20 genes with SNVs, indels, or amplifications with a frequency of 10% or more. Genomic alterations in FGF19 showed the strongest association with PFS with a borderline level of statistical significance of P = .00252 (Bonferroni‐adjusted significance level is .0025). Genomic alterations in FGF4, MYEOV, CTTN, and ORAOV1 showed a marginal association with PFS (P 
doi_str_mv 10.1111/cas.15251
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Biomarker analysis was carried out for patients with clinical stage T1bN0M0 ESCC enrolled in JCOG0502 (UMIN000000551). Whole‐exome sequencing (WES) was performed using DNA extracted from formalin‐fixed, paraffin‐embedded tissue of ESCC and normal tissue or blood sample. Single nucleotide variants (SNVs), insertions/deletions (indels), and copy number alterations (CNAs) were identified. We then evaluated the associations between each gene alteration with a frequency of 10% or more and progression‐free survival (PFS) using a Cox regression model. We controlled for family‐wise errors at 0.05 using the Bonferroni method. Among the 379 patients who were enrolled in JCOG0502, 127 patients were successfully analyzed using WES. The median patient age was 63 years (interquartile range, 57‐67 years), and 78.0% of the patients ultimately underwent surgery. The 3‐year PFS probability was 76.3%. We detected 20 genes with SNVs, indels, or amplifications with a frequency of 10% or more. Genomic alterations in FGF19 showed the strongest association with PFS with a borderline level of statistical significance of P = .00252 (Bonferroni‐adjusted significance level is .0025). Genomic alterations in FGF4, MYEOV, CTTN, and ORAOV1 showed a marginal association with PFS (P &lt; .05). These genomic alterations were all CNAs at chromosome 11q13.3. We have identified new genomic alterations associated with the poor efficacy of ESCC (T1bN0M0). These findings open avenues for the development of new potential treatments for patients with ESCC. According to whole‐exome sequencing of patients with stage I esophageal squamous cell carcinoma, amplification of FGF19 showed the strongest association with progression‐free survival.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.15251</identifier><identifier>PMID: 34962019</identifier><language>eng</language><publisher>England: John Wiley &amp; Sons, Inc</publisher><subject>Aged ; Biobanks ; Biomarkers ; Biomarkers, Tumor - genetics ; Biopsy ; Cancer therapies ; Chromosome 11 ; Clinical trials ; Copy number ; Dehydrogenases ; DNA Copy Number Variations ; DNA sequencing ; Esophageal cancer ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; Esophageal Neoplasms - therapy ; esophageal squamous cell carcinoma ; Esophageal Squamous Cell Carcinoma - genetics ; Esophageal Squamous Cell Carcinoma - pathology ; Esophageal Squamous Cell Carcinoma - therapy ; Esophagus ; Fibroblast growth factor 4 ; Fibroblasts ; Genes ; Genomic analysis ; Growth factors ; Humans ; Medical prognosis ; Middle Aged ; Mutation ; Neoplasm Staging ; Original ; Paraffin ; Patients ; Prognosis ; prognostic factor ; Progression-Free Survival ; Squamous cell carcinoma ; stage I ; Surgery ; tumor mutation burden ; Whole Exome Sequencing</subject><ispartof>Cancer science, 2022-03, Vol.113 (3), p.1018-1027</ispartof><rights>2021 The Authors. published by John Wiley &amp; Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2021 The Authors. Cancer Science published by John Wiley &amp; Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2022. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). 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Biomarker analysis was carried out for patients with clinical stage T1bN0M0 ESCC enrolled in JCOG0502 (UMIN000000551). Whole‐exome sequencing (WES) was performed using DNA extracted from formalin‐fixed, paraffin‐embedded tissue of ESCC and normal tissue or blood sample. Single nucleotide variants (SNVs), insertions/deletions (indels), and copy number alterations (CNAs) were identified. We then evaluated the associations between each gene alteration with a frequency of 10% or more and progression‐free survival (PFS) using a Cox regression model. We controlled for family‐wise errors at 0.05 using the Bonferroni method. Among the 379 patients who were enrolled in JCOG0502, 127 patients were successfully analyzed using WES. The median patient age was 63 years (interquartile range, 57‐67 years), and 78.0% of the patients ultimately underwent surgery. The 3‐year PFS probability was 76.3%. We detected 20 genes with SNVs, indels, or amplifications with a frequency of 10% or more. Genomic alterations in FGF19 showed the strongest association with PFS with a borderline level of statistical significance of P = .00252 (Bonferroni‐adjusted significance level is .0025). Genomic alterations in FGF4, MYEOV, CTTN, and ORAOV1 showed a marginal association with PFS (P &lt; .05). These genomic alterations were all CNAs at chromosome 11q13.3. We have identified new genomic alterations associated with the poor efficacy of ESCC (T1bN0M0). These findings open avenues for the development of new potential treatments for patients with ESCC. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oshima, Kotoe</au><au>Kato, Ken</au><au>Ito, Yoshinori</au><au>Daiko, Hiroyuki</au><au>Nozaki, Isao</au><au>Nakagawa, Satoru</au><au>Shibuya, Yuichi</au><au>Kojima, Takashi</au><au>Toh, Yasushi</au><au>Okada, Morihito</au><au>Hironaka, Shuichi</au><au>Akiyama, Yuji</au><au>Komatsu, Yoshito</au><au>Maejima, Kazuhiro</au><au>Nakagawa, Hidewaki</au><au>Onuki, Ritsuko</au><au>Nagai, Momoko</au><au>Kato, Mamoru</au><au>Kanato, Keisuke</au><au>Kuchiba, Aya</au><au>Nakamura, Kenichi</au><au>Kitagawa, Yuko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prognostic biomarker study in patients with clinical stage I esophageal squamous cell carcinoma: JCOG0502‐A1</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2022-03</date><risdate>2022</risdate><volume>113</volume><issue>3</issue><spage>1018</spage><epage>1027</epage><pages>1018-1027</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>We undertook genomic analyses of Japanese patients with stage I esophageal squamous cell carcinoma (ESCC) to investigate the frequency of genomic alterations and the association with survival outcomes. Biomarker analysis was carried out for patients with clinical stage T1bN0M0 ESCC enrolled in JCOG0502 (UMIN000000551). Whole‐exome sequencing (WES) was performed using DNA extracted from formalin‐fixed, paraffin‐embedded tissue of ESCC and normal tissue or blood sample. Single nucleotide variants (SNVs), insertions/deletions (indels), and copy number alterations (CNAs) were identified. We then evaluated the associations between each gene alteration with a frequency of 10% or more and progression‐free survival (PFS) using a Cox regression model. We controlled for family‐wise errors at 0.05 using the Bonferroni method. Among the 379 patients who were enrolled in JCOG0502, 127 patients were successfully analyzed using WES. The median patient age was 63 years (interquartile range, 57‐67 years), and 78.0% of the patients ultimately underwent surgery. The 3‐year PFS probability was 76.3%. We detected 20 genes with SNVs, indels, or amplifications with a frequency of 10% or more. Genomic alterations in FGF19 showed the strongest association with PFS with a borderline level of statistical significance of P = .00252 (Bonferroni‐adjusted significance level is .0025). Genomic alterations in FGF4, MYEOV, CTTN, and ORAOV1 showed a marginal association with PFS (P &lt; .05). These genomic alterations were all CNAs at chromosome 11q13.3. We have identified new genomic alterations associated with the poor efficacy of ESCC (T1bN0M0). These findings open avenues for the development of new potential treatments for patients with ESCC. According to whole‐exome sequencing of patients with stage I esophageal squamous cell carcinoma, amplification of FGF19 showed the strongest association with progression‐free survival.</abstract><cop>England</cop><pub>John Wiley &amp; Sons, Inc</pub><pmid>34962019</pmid><doi>10.1111/cas.15251</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0001-9714-231X</orcidid><orcidid>https://orcid.org/0000-0003-1807-772X</orcidid><orcidid>https://orcid.org/0000-0002-1570-6802</orcidid><orcidid>https://orcid.org/0000-0002-1733-5072</orcidid><orcidid>https://orcid.org/0000-0002-2554-8334</orcidid><oa>free_for_read</oa></addata></record>
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identifier ISSN: 1347-9032
ispartof Cancer science, 2022-03, Vol.113 (3), p.1018-1027
issn 1347-9032
1349-7006
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8898710
source MEDLINE; DOAJ Directory of Open Access Journals; Access via Wiley Online Library; Wiley Online Library Open Access; PubMed Central
subjects Aged
Biobanks
Biomarkers
Biomarkers, Tumor - genetics
Biopsy
Cancer therapies
Chromosome 11
Clinical trials
Copy number
Dehydrogenases
DNA Copy Number Variations
DNA sequencing
Esophageal cancer
Esophageal Neoplasms - genetics
Esophageal Neoplasms - pathology
Esophageal Neoplasms - therapy
esophageal squamous cell carcinoma
Esophageal Squamous Cell Carcinoma - genetics
Esophageal Squamous Cell Carcinoma - pathology
Esophageal Squamous Cell Carcinoma - therapy
Esophagus
Fibroblast growth factor 4
Fibroblasts
Genes
Genomic analysis
Growth factors
Humans
Medical prognosis
Middle Aged
Mutation
Neoplasm Staging
Original
Paraffin
Patients
Prognosis
prognostic factor
Progression-Free Survival
Squamous cell carcinoma
stage I
Surgery
tumor mutation burden
Whole Exome Sequencing
title Prognostic biomarker study in patients with clinical stage I esophageal squamous cell carcinoma: JCOG0502‐A1
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