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      A Catalog of 5’ Fusion Partners in ROS1-Positive NSCLC Circa 2020

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          Abstract

          ROS1 fusion–positive ( ROS1+) NSCLC was discovered in 2007, the same year as the discovery of ALK-positive ( ALK+) NSCLC but has trailed ALK+ NSCLC in terms of development. There seems to be a differential response to ROS1 inhibitors, which depend on fusion partners (CD74, SLC34A2, or SDC4); thus, knowledge of the fusion partners in ROS1+ NSCLC is important. To date (end of February 2020), we have identified 24 unique 5’ fusion partners of ROS1 in ROS1+ NSCLC from published literature and congress proceedings. Thus, we published this catalog for easy reference.

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          Comprehensive molecular profiling of lung adenocarcinoma

          Nikolaus Schultz (2015)
          Adenocarcinoma of the lung is the leading cause of cancer death worldwide. Here we report molecular profiling of 230 resected lung adenocarcinomas using messenger RNA, microRNA and DNA sequencing integrated with copy number, methylation and proteomic analyses. High rates of somatic mutation were seen (mean 8.9 mutations per megabase). Eighteen genes were statistically significantly mutated, including RIT1 activating mutations and newly described loss-of-function MGA mutations which are mutually exclusive with focal MYC amplification. EGFR mutations were more frequent in female patients, whereas mutations in RBM10 were more common in males. Aberrations in NF1, MET, ERBB2 and RIT1 occurred in 13% of cases and were enriched in samples otherwise lacking an activated oncogene, suggesting a driver role for these events in certain tumours. DNA and mRNA sequence from the same tumour highlighted splicing alterations driven by somatic genomic changes, including exon 14 skipping in MET mRNA in 4% of cases. MAPK and PI(3)K pathway activity, when measured at the protein level, was explained by known mutations in only a fraction of cases, suggesting additional, unexplained mechanisms of pathway activation. These data establish a foundation for classification and further investigations of lung adenocarcinoma molecular pathogenesis.
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            Mutational Landscape of Metastatic Cancer Revealed from Prospective Clinical Sequencing of 10,000 Patients

            Ahmet Zehir, Ryma Benayed, Ronak H Shah … (2017)
            Tumor molecular profiling is a fundamental component of precision oncology, enabling the identification of genomic alterations in genes and pathways that can be targeted therapeutically. The existence of recurrent targetable alterations across distinct histologically-defined tumor types, coupled with an expanding portfolio of molecularly-targeted therapies, demands flexible and comprehensive approaches to profile clinically significant genes across the full spectrum of cancers. We established a large-scale, prospective clinical sequencing initiative utilizing a comprehensive assay, MSK-IMPACT, through which we have compiled matched tumor and normal sequence data from a unique cohort of more than 10,000 patients with advanced cancer and available pathological and clinical annotations. Using these data, we identified clinically relevant somatic mutations, novel non-coding alterations, and mutational signatures that were shared among common and rare tumor types. Patients were enrolled on genomically matched clinical trials at a rate of 11%. To enable discovery of novel biomarkers and deeper investigation into rare alterations and tumor types, all results are publicly accessible.
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              Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer.

              Klarisa Rikova, Ailan Guo, Qingfu Zeng … (2008)
              Despite the success of tyrosine kinase-based cancer therapeutics, for most solid tumors the tyrosine kinases that drive disease remain unknown, limiting our ability to identify drug targets and predict response. Here we present the first large-scale survey of tyrosine kinase activity in lung cancer. Using a phosphoproteomic approach, we characterize tyrosine kinase signaling across 41 non-small cell lung cancer (NSCLC) cell lines and over 150 NSCLC tumors. Profiles of phosphotyrosine signaling are generated and analyzed to identify known oncogenic kinases such as EGFR and c-Met as well as novel ALK and ROS fusion proteins. Other activated tyrosine kinases such as PDGFRalpha and DDR1 not previously implicated in the genesis of NSCLC are also identified. By focusing on activated cell circuitry, the approach outlined here provides insight into cancer biology not available at the chromosomal and transcriptional levels and can be applied broadly across all human cancers.
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                Author and article information

                Contributors
                Sai-Hong Ignatius Ou
                Journal
                Journal ID (nlm-ta): JTO Clin Res Rep
                Journal ID (iso-abbrev): JTO Clin Res Rep
                Title: JTO Clinical and Research Reports
                Publisher: Elsevier
                ISSN (Electronic): 2666-3643
                Publication date PMC-release: 28 April 2020
                Publication date Collection: September 2020
                Publication date (Electronic): 28 April 2020
                Volume: 1
                Issue: 3
                Electronic Location Identifier: 100048
                Affiliations
                [a ]Chao Family Comprehensive Cancer Center, Department of Medicine, Division of Hematology-Oncology, University of California Irvine School of Medicine, Orange, California
                [b ]Department of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan
                [c ]Department of Neurology, St. Marianna University Graduate School of Medicine, Kawasaki, Japan
                Author notes
                [∗ ]Corresponding author. Address for correspondence: Sai-Hong Ignatius Ou, MD, PhD, Chao Family Comprehensive Cancer Center, Department of Medicine, Division of Hematology-Oncology, University of California Irvine School of Medicine, 200 South Manchester Avenue, Suite 400, Room 407, Orange, CA 92868-3298. siou@ 123456hs.uci.edu
                Article
                Publisher Item ID: S2666-3643(20)30053-9 Publisher ID: 100048
                DOI: 10.1016/j.jtocrr.2020.100048
                PMC ID: 8474457
                PubMed ID: 34589944
                SO-VID: a320afa3-90ea-4aa9-88ee-f8d9f1384d0f
                Copyright © © 2020 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 18 March 2020
                Date revision received : 13 April 2020
                Date accepted : 22 April 2020
                Categories
                Subject: Review Article

                Keywords: ros1 fusion partner,next-generation sequencing,ros1-positive nsclc
                Data availability:
                Keywords: ros1 fusion partner, next-generation sequencing, ros1-positive nsclc

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