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      Detection of gene mutations in gastric cancer tissues using a commercial sequencing panel

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          Abstract

          Predicting malignancy is important for adequate adjuvant therapy in patients with cancer. Due to cancer being a genetic disease, the detection of gene mutations could be helpful in predicting the prognosis and efficacy of drugs. Gastric cancer is the fifth most common cancer and is the third leading cause of cancer associated mortality worldwide. Mutations in genes may correlate with clinical information in patients with gastric cancer after surgery and, therefore, may be useful for predicting the prognosis of this disease. In the present study, to assess the usefulness of a commercial sequencing panel, TruSeq ® Amplicon-Cancer Panel (Illumina), using a next-generation sequencer (Illumina MiSeq), mutation analysis of fresh as well as formalin-fixed paraffin-embedded (FFPE) gastric cancer tissues was performed retrospectively. The study group comprised of 4 patients who underwent gastrectomy for gastric cancer. Cancer and normal stomach tissues were collected immediately following surgical removal. Thereafter, the specimens were fixed in 10% neutral formalin for 24–72 h. Normal and FFPE cancer tissues were histologically examined and confirmed. A total of 3 mutations were identified in the driver genes ( KRAS, TP53 and APC) in cancer tissues from 2 of the 4 patients, using fresh samples. In addition, FFPE samples were analysed for the same tissues and the same results were obtained by setting the threshold for the percentage of the mutation rate to avoid detection of pseudo-positive mutations. In conclusion, the sequencing analysis using FFPE-derived DNA samples was successfully performed.

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          Five-year outcomes of a randomized phase III trial comparing adjuvant chemotherapy with S-1 versus surgery alone in stage II or III gastric cancer.

          Mitsuru Sasako, Shinichi Sakuramoto, Hitoshi Katai … (2011)
          The first planned interim analysis (median follow-up, 3 years) of the Adjuvant Chemotherapy Trial of S-1 for Gastric Cancer confirmed that the oral fluoropyrimidine derivative S-1 significantly improved overall survival, the primary end point. The results were therefore opened at the recommendation of an independent data and safety monitoring committee. We report 5-year follow-up data on patients enrolled onto the ACTS-GC study. Patients with histologically confirmed stage II or III gastric cancer who underwent gastrectomy with D2 lymphadenectomy were randomly assigned to receive S-1 after surgery or surgery only. S-1 (80 to 120 mg per day) was given for 4 weeks, followed by 2 weeks of rest. This 6-week cycle was repeated for 1 year. The primary end point was overall survival, and the secondary end points were relapse-free survival and safety. The overall survival rate at 5 years was 71.7% in the S-1 group and 61.1% in the surgery-only group (hazard ratio [HR], 0.669; 95% CI, 0.540 to 0.828). The relapse-free survival rate at 5 years was 65.4% in the S-1 group and 53.1% in the surgery-only group (HR, 0.653; 95% CI, 0.537 to 0.793). Subgroup analyses according to principal demographic factors such as sex, age, disease stage, and histologic type showed no interaction between treatment and any characteristic. On the basis of 5-year follow-up data, postoperative adjuvant therapy with S-1 was confirmed to improve overall survival and relapse-free survival in patients with stage II or III gastric cancer who had undergone D2 gastrectomy.
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            Gastric adenocarcinoma

            Jaffer A Ajani, Jeeyun Lee, Takeshi Sano … (2017)
            Gastric cancers, with gastric adenocarcinoma (GAC) as the most common histological type, impose a considerable global health burden. Although the screening strategies for early detection have been shown to be successful in Japan and South Korea, they are either not implemented or not feasible in most of the world, leading to late diagnosis in most patients. Helicobacter pylori infection contributes to the development of many endemic GACs, and pre-emptive eradication or early treatment of this bacterial infection might provide effective primary prevention. GACs are phenotypically and genotypically heterogeneous. Localized (clinical stage I) GAC is best treated either endoscopically or with limited surgical resection, but clinical stage II or stage III tumours require multidisciplinary adjunctive approaches in addition to surgery. Although GAC is highly treatable in its early stages, advanced (clinical stage IV) GAC has a median survival of just ∼9-10 months. However, detailed molecular and immune profiling of GAC is yielding promise; early studies with immune checkpoint inhibitors suggest that GAC is amenable to immune modulation. Molecular studies have yielded a vast quantity of new information for potential exploitation. Nevertheless, advances against GACs have lagged compared with other tumours of similar incidence, and more research is necessary to overcome the obstacles to prolong survival.
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              Association of the APC tumor suppressor protein with catenins.

              W Kinzler, Bert Vogelstein, L. Su (1993)
              Mutations of APC appear to initiate sporadic and inherited forms of human colorectal cancer. Although these mutations have been well characterized, little is known about the function of the APC gene product. Two cellular proteins that associate with APC were identified by nucleotide sequence analysis and peptide mapping as the E-cadherin-associated proteins alpha- and beta-catenin. A 27-residue fragment of APC containing a 15-amino acid repeat was sufficient for the interaction with the catenins. These results suggest an important link between tumor initiation and cell adhesion.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Clin Oncol
                Journal ID (iso-abbrev): Mol Clin Oncol
                Journal ID (publisher-id): MCO
                Title: Molecular and Clinical Oncology
                Publisher: D.A. Spandidos
                ISSN (Print): 2049-9450
                ISSN (Electronic): 2049-9469
                Publication date (Print): November 2019
                Publication date (Electronic): 24 September 2019
                Publication date PMC-release: 24 September 2019
                Volume: 11
                Issue: 5
                Pages: 455-460
                Affiliations
                [1 ]Department of Surgery, Juntendo University Shizuoka Hospital, Juntendo University School of Medicine, Shizuoka 410-2295, Japan
                [2 ]DNA Chip Research Inc., Tokyo 105-0022, Japan
                [3 ]Department of Pathology, Juntendo University Shizuoka Hospital, Juntendo University School of Medicine, Shizuoka 410-2295, Japan
                Author notes
                Correspondence to: Dr Tomoaki Ito, Department of Surgery, Juntendo University Shizuoka Hospital, Juntendo University School of Medicine, 1129 Nagaoka, Izunokuni-shi, Shizuoka 410-2295, Japan, E-mail: tomo-ito@ 123456juntendo.ac.jp
                Article
                Publisher ID: MCO-0-0-1926
                DOI: 10.3892/mco.2019.1926
                PMC ID: 6787944
                SO-VID: 674650f9-9460-4517-ac7f-edc88b7bf6cb
                Copyright © Copyright: © Ito et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 20 March 2019
                Date accepted : 26 August 2019
                Categories
                Subject: Articles

                Keywords: gastric cancer,sequencing panel,cancer panel,next-generation sequencing,mutation,formalin-fixed paraffin-embedded,adenomatous polyposis coli,v-ki-ras2 kirsten rat sarcoma viral oncogene homolog,tumor protein 53 function loss
                Data availability:
                Keywords: gastric cancer, sequencing panel, cancer panel, next-generation sequencing, mutation, formalin-fixed paraffin-embedded, adenomatous polyposis coli, v-ki-ras2 kirsten rat sarcoma viral oncogene homolog, tumor protein 53 function loss

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