Accurate Prognosis Prediction of Pancreatic Ductal Adenocarcinoma Using Integrated Clinico-Genomic Data of Endoscopic Ultrasound-Guided Fine Needle Biopsy.
Accurate Prognosis Prediction of Pancreatic Ductal Adenocarcinoma Using Integrated Clinico-Genomic Data of Endoscopic Ultrasound-Guided Fine Needle Biopsy.
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DOI：
10.3390/cancers13112791
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发表时间：
2021-06-03
期刊：
影响因子：
5.2
通讯作者：
Lee KH
中科院分区：
文献类型：
--
作者：
Park JK;Kim H;Son DS;Kim NKD;Sung YK;Cho M;Lee C;Noh DH;Lee SH;Lee KT;Lee JK;Jang KT;Park WY;Lee KH
大约 10-20% 的胰腺腺癌 (PDAC) 患者接受根治性手术，但大多数患者进行内镜超声引导细针活检 (EUS-FNB) 进行病理证实。我们回顾性研究的目的是评估使用 EUS-FNB 最小样本进行靶向测序来预测 PDAC 预后的可行性。我们发现一些临床因素和遗传改变与转移和总生存显着相关，并利用临床参数和遗传改变建立了临床基因组模型来预测 PDAC 患者的预后。本研究的目的是调查从超声内镜引导细针活检 (EUS-FNB) 中获取的最小样本的临床效用，并进行靶向深度测序作为胰腺导管腺癌 (PDAC) 的预后预测工具。使用 CancerSCAN® panel 对总共 116 个经 EUS-FNB 病理证实具有 PDAC 的标本进行了测试，以进行定制的靶向深度测序。与 PDAC 生存显着相关的临床预后因素如下：分期、肿瘤块大小、肿瘤位置、转移、化疗和初始 CA19-9 水平。共有 114 名患者（98.3%）至少有一个基因改变，其中两名患者没有检测到突变，尽管他们符合靶向深度测序的条件。导致 PDAC 的主要基因突变频率为 KRAS 90%、CDKN2A 31%、TP53 77% 和 SMAD4 29%。 NF1 体细胞点突变、SMAD4 拷贝数改变和 CDKN2A 功能丧失是与总生存率显着相关的遗传因素。此外，BRCA2点突变与肝转移相关。最后，开发了一个临床基因组模型，根据影响患者生存的临床参数和基因改变来评估 PDAC 患者的预后；选择了 20 个单核苷酸变异和 3 个拷贝数变异。对最小的 PDAC 样本进行靶向深度测序，并应用于建立预后预测的临床基因组模型。
Around 10–20% of patients with pancreatic adenocarcinoma (PDAC) have a curative surgery, but most of them perform endoscopic ultrasound-guided fine-needle biopsy (EUS-FNB) for the pathologic confirmation. The aim of our retrospective study was to evaluate the feasibility of targeted sequencing using EUS-FNB minimal specimens for the prognosis prediction of PDACs. We found some clinical factors and genetic alterations significantly related to the metastasis and overall survival, and established a clinico-genomic model by using both clinical parameters and genetic alterations to predict the prognosis of patients with PDACs. The aim of this study was to investigate the clinical utility of minimal specimens acquired from endoscopic ultrasound-guided fine-needle biopsy (EUS-FNB) and perform targeted deep sequencing as a prognosis prediction tool for pancreatic ductal adenocarcinoma (PDAC). A total of 116 specimens with pathologically confirmed PDAC via EUS-FNB were tested using CancerSCAN® panel for a customized targeted deep sequencing. Clinical prognostic factors significantly associated with survival in PDACs were as follows: stage, tumor mass size, tumor location, metastasis, chemotherapy, and initial CA19-9 level. A total of 114 patients (98.3%) had at least a single genetic alteration, and no mutations were detected in two patients, although they were qualified for the targeted deep sequencing. The frequencies of major gene mutations responsible for PDACs were KRAS 90%, CDKN2A 31%, TP53 77%, and SMAD4 29%. A somatic point mutation of NF1, copy number alteration of SMAD4, and loss-of-function of CDKN2A were significantly associated genetic factors for overall survival. Moreover, BRCA2 point mutation was related to liver metastasis. Finally, a clinico-genomic model was developed to estimate the prognosis of patients with PDAC based on clinical parameters and genetic alterations affecting survival in patients; 20 single nucleotide variants and three copy number variations were selected. Targeted deep sequencing on minimal specimens of PDACs was performed, and it was applied to establish a clinico-genomic model for prognosis prediction.
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影响因子：
16.6
作者：
Shin HT;Choi YL;Yun JW;Kim NKD;Kim SY;Jeon HJ;Nam JY;Lee C;Ryu D;Kim SC;Park K;Lee E;Bae JS;Son DS;Joung JG;Lee J;Kim ST;Ahn MJ;Lee SH;Ahn JS;Lee WY;Oh BY;Park YH;Lee JE;Lee KH;Kim HC;Kim KM;Im YH;Park K;Park PJ;Park WY
通讯作者：
Park WY
影响因子：
30.8
作者：
Makohon-Moore AP;Zhang M;Reiter JG;Bozic I;Allen B;Kundu D;Chatterjee K;Wong F;Jiao Y;Kohutek ZA;Hong J;Attiyeh M;Javier B;Wood LD;Hruban RH;Nowak MA;Papadopoulos N;Kinzler KW;Vogelstein B;Iacobuzio-Donahue CA
通讯作者：
Iacobuzio-Donahue CA
影响因子：
2.3
作者：
James, Edward;Waldron-Lynch, Maeve G.;Saif, Muhammad Wasif
通讯作者：
Saif, Muhammad Wasif
影响因子：
4.8
作者：
Petrovics, Gyorgy;Price, Douglas K.;Dean, Michael
通讯作者：
Dean, Michael
影响因子：
45.3
作者：
Friess, H;Guo, XZ;Büchler, MW
通讯作者：
Büchler, MW