Molecular Pathways: ROS1 Fusion Proteins in Cancer
Genetic alterations that lead to constitutive activation of kinases are frequently observed in cancer. In many cases, the growth and survival of tumor cells rely upon an activated kinase such that inhibition of its activity is an effective anticancer therapy. ROS1 is a receptor tyrosine kinase that...
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| Published in | Clinical cancer research Vol. 19; no. 15; pp. 4040 - 4045 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
Philadelphia, PA
American Association for Cancer Research
01.08.2013
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Genetic alterations that lead to constitutive activation of kinases are frequently observed in cancer. In many cases, the growth and survival of tumor cells rely upon an activated kinase such that inhibition of its activity is an effective anticancer therapy. ROS1 is a receptor tyrosine kinase that has recently been shown to undergo genetic rearrangements in a variety of human cancers, including glioblastoma, non-small cell lung cancer (NSCLC), cholangiocarcinoma, ovarian cancer, gastric adenocarcinoma, colorectal cancer, inflammatory myofibroblastic tumor, angiosarcoma, and epithelioid hemangioendothelioma. These rearrangements create fusion proteins in which the kinase domain of ROS1 becomes constitutively active and drives cellular proliferation. Targeting ROS1 fusion proteins with the small-molecule inhibitor crizotinib is showing promise as an effective therapy in patients with NSCLC whose tumors are positive for these genetic abnormalities. This review discusses the recent preclinical and clinical findings on ROS1 gene fusions in cancer. |
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| AbstractList | Genetic alterations that lead to constitutive activation of kinases are frequently observed in cancer. In many cases, the growth and survival of tumor cells rely upon an activated kinase such that inhibition of its activity is an effective anticancer therapy. ROS1 is a receptor tyrosine kinase that has recently been shown to undergo genetic rearrangements in a variety of human cancers, including glioblastoma, non-small cell lung cancer (NSCLC), cholangiocarcinoma, ovarian cancer, gastric adenocarcinoma, colorectal cancer, inflammatory myofibroblastic tumor, angiosarcoma, and epithelioid hemangioendothelioma. These rearrangements create fusion proteins in which the kinase domain of ROS1 becomes constitutively active and drives cellular proliferation. Targeting ROS1 fusion proteins with the small-molecule inhibitor crizotinib is showing promise as an effective therapy in patients with NSCLC whose tumors are positive for these genetic abnormalities. This review discusses the recent preclinical and clinical findings on ROS1 gene fusions in cancer. Genetic alterations that lead to constitutive activation of kinases are frequently observed in cancer. In many cases, the growth and survival of tumor cells relies upon an activated kinase such that inhibition of its activity is an effective anti-cancer therapy. ROS1 is a receptor tyrosine kinase that has recently been demonstrated to undergo genetic rearrangements in a variety of human cancers including glioblastoma, non-small cell lung cancer (NSCLC), cholangiocarcinoma, ovarian cancer, gastric adenocarcinoma, colorectal cancer, inflammatory myofibroblastic tumor, angiosarcoma, and epithelioid hemangioendothelioma. These rearrangements create fusion proteins in which the kinase domain of ROS1 becomes constitutively active and drives cellular proliferation. Targeting ROS1 fusion proteins with the small molecule inhibitor crizotinib is showing promise as an effective therapy in NSCLC patients whose tumors are positive for these genetic abnormalities. This review will discuss the recent preclinical and clinical findings on ROS1 gene fusions in cancer. Abstract Genetic alterations that lead to constitutive activation of kinases are frequently observed in cancer. In many cases, the growth and survival of tumor cells rely upon an activated kinase such that inhibition of its activity is an effective anticancer therapy. ROS1 is a receptor tyrosine kinase that has recently been shown to undergo genetic rearrangements in a variety of human cancers, including glioblastoma, non–small cell lung cancer (NSCLC), cholangiocarcinoma, ovarian cancer, gastric adenocarcinoma, colorectal cancer, inflammatory myofibroblastic tumor, angiosarcoma, and epithelioid hemangioendothelioma. These rearrangements create fusion proteins in which the kinase domain of ROS1 becomes constitutively active and drives cellular proliferation. Targeting ROS1 fusion proteins with the small-molecule inhibitor crizotinib is showing promise as an effective therapy in patients with NSCLC whose tumors are positive for these genetic abnormalities. This review discusses the recent preclinical and clinical findings on ROS1 gene fusions in cancer. Clin Cancer Res; 19(15); 4040–5. ©2013 AACR. |
| Author | DOEBELE, Robert C DAVIES, Kurtis D |
| AuthorAffiliation | 1 Department of Medicine, Division of Medical Oncology, University of Colorado – Anschutz Medical Campus, Aurora Colorado |
| AuthorAffiliation_xml | – name: 1 Department of Medicine, Division of Medical Oncology, University of Colorado – Anschutz Medical Campus, Aurora Colorado |
| Author_xml | – sequence: 1 givenname: Kurtis D surname: DAVIES fullname: DAVIES, Kurtis D organization: Division of Medical Oncology, Department of Medicine, University of Colorado ― Anschutz Medical Campus, Aurora, Colorado, United States – sequence: 2 givenname: Robert C surname: DOEBELE fullname: DOEBELE, Robert C organization: Division of Medical Oncology, Department of Medicine, University of Colorado ― Anschutz Medical Campus, Aurora, Colorado, United States |
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| References | Yoshida (2022061023465323400_bib41) 2013; 37 Chan (2022061023465323400_bib36) 1997; 272 Camidge (2022061023465323400_bib44) 2012; 13 Charest (2022061023465323400_bib26) 2003; 100 Birch (2022061023465323400_bib16) 2011; 6 Camidge (2022061023465323400_bib35) 2012; 9 Shaw (2022061023465323400_bib40) 2011; 17 Biskup (2022061023465323400_bib11) 2004; 117 Lee (2022061023465323400_bib22) 2013; 119 Li (2022061023465323400_bib38) 2011; 6 Anjum (2022061023465323400_bib45) 2012 Matsushime (2022061023465323400_bib1) 1986; 6 Lee (2022061023465323400_bib37) 2013; 20 Weickhardt (2022061023465323400_bib23) 2013; 31 Acquaviva (2022061023465323400_bib4) 2009; 1795 Seo (2022061023465323400_bib21) 2012; 22 Rimkunas (2022061023465323400_bib5) 2012; 18 Gu (2022061023465323400_bib15) 2011; 6 Zeng (2022061023465323400_bib10) 2000; 20 Birchmeier (2022061023465323400_bib2) 1986; 6 Bergethon (2022061023465323400_bib32) 2012; 30 Jemal (2022061023465323400_bib39) 2011; 61 Xiong (2022061023465323400_bib8) 1996; 16 Lovly (2022061023465323400_bib24) 2013; 31 Giacomini (2022061023465323400_bib25) 2013; 9 Birchmeier (2022061023465323400_bib13) 1987; 84 El-Deeb (2022061023465323400_bib6) 2010; 31 Jun (2022061023465323400_bib27) 2012; 72 Charest (2022061023465323400_bib29) 2006; 66 Nguyen (2022061023465323400_bib12) 2002; 277 Arai (2022061023465323400_bib30) 2013; 8 Sonnenberg-Riethmacher (2022061023465323400_bib7) 1996; 10 Ou (2022061023465323400_bib42) 2012; 23 Yasuda (2022061023465323400_bib33) 2012; 7 Zong (2022061023465323400_bib9) 1998; 273 Lovly (2022061023465323400_bib34) 2011; 71 Suehara (2022061023465323400_bib17) 2012; 18 Robinson (2022061023465323400_bib3) 2000; 19 Takeuchi (2022061023465323400_bib19) 2012; 18 Rikova (2022061023465323400_bib18) 2007; 131 Davies (2022061023465323400_bib28) 2012; 18 Hammerman (2022061023465323400_bib47) 2009; 15 Govindan (2022061023465323400_bib20) 2012; 150 McDermott (2022061023465323400_bib31) 2008; 68 Charest (2022061023465323400_bib14) 2003; 37 Pao (2022061023465323400_bib43) 2010; 10 Sang (2022061023465323400_bib46) 2013; 3 |
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| Snippet | Genetic alterations that lead to constitutive activation of kinases are frequently observed in cancer. In many cases, the growth and survival of tumor cells... Abstract Genetic alterations that lead to constitutive activation of kinases are frequently observed in cancer. In many cases, the growth and survival of tumor... |
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| SubjectTerms | Antineoplastic agents Biological and medical sciences Cell Proliferation Crizotinib Humans Medical sciences Molecular Targeted Therapy Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Mutation Neoplasms - drug therapy Neoplasms - genetics Neoplasms - pathology Oncogene Proteins, Fusion - genetics Oncogene Proteins, Fusion - metabolism Pharmacology. Drug treatments Protein Kinase Inhibitors - therapeutic use Protein-Tyrosine Kinases - genetics Protein-Tyrosine Kinases - metabolism Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Pyrazoles - therapeutic use Pyridines - therapeutic use Tumors |
| Title | Molecular Pathways: ROS1 Fusion Proteins in Cancer |
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