FISH Analysis of Crizotinib Target Genes ROS1/ALK/MET in Malignant Mesothelioma Sandra Salvi, PhD, Serena Varesano, PhD, Simona Boccardo, PhD, Jean Louis.

Slides:

Advertisements

Similar presentations

Naomi Fujioka, MD, Christopher A. French, MD, Michael J

Advertisements

Is Cytology Reliable for Epidermal Growth Factor Receptor Gene Evaluation in Non- small Cell Lung Cancer? Cecilia Bozzetti, PhD, Marcello Tiseo, MD, Costanza.

Droplet Digital PCR for Absolute Quantification of EML4-ALK Gene Rearrangement in Lung Adenocarcinoma Qiushi Wang, Xin Yang, Yong He, Qiang Ma, Li Lin,

Detection of ALK Gene Rearrangement in Non-small Cell Lung Cancer: A Comparison of Fluorescence In Situ Hybridization and Chromogenic In Situ Hybridization.

New Methods for ALK Status Diagnosis in Non–Small-Cell Lung Cancer: An Improved ALK Immunohistochemical Assay and a New, Brightfield, Dual ALK IHC–In.

Detection of Rearrangements and Transcriptional Up-Regulation of ALK in FFPE Lung Cancer Specimens Using a Novel, Sensitive, Quantitative Reverse Transcription.

Malignant Pleural Mesothelioma Harboring Both G719C and S768I Mutations of EGFR Successfully Treated with Afatinib Nobukazu Agatsuma, MD Journal of.

EGFR Status in Mesothelioma: Possible Implications for the Efficacy of Anti-EGFR and Anti-MET Therapies Sandra Salvi, PhD, Serena Varesano, PhD, Simona.

Malignant Pleural Mesothelioma Harboring Both G719C and S768I Mutations of EGFR Successfully Treated with Afatinib Nobukazu Agatsuma, MD Journal of.

Next-Generation Sequencing Identifies and Immunohistochemistry Confirms a Novel Crizotinib-Sensitive ALK Rearrangement in a Patient with Metastatic Non–Small-Cell.

ALK FISH and IHC: You Cannot Have One without the Other

Cases of ALK-Rearranged Lung Cancer with 5-Year Progression-Free Survival with Crizotinib as Initial Precision Therapy Deepa Rangachari, MD, Xiuning.

Heterogeneity of Anaplastic Lymphoma Kinase Gene Rearrangement in Non–Small-Cell Lung Carcinomas: A Comparative Study Between Small Biopsy and Excision.

Jessica J. Lin, MD, Lauren L. Ritterhouse, MD, PhD, Siraj M

Transformation to Sarcomatoid Carcinoma in ALK-Rearranged Adenocarcinoma, Which Developed Acquired Resistance to Crizotinib and Received Subsequent Chemotherapies

Dramatic Response to Combination Erlotinib and Crizotinib in a Patient with Advanced, EGFR-Mutant Lung Cancer Harboring De Novo MET Amplification Justin.

Clinical and Translational Implications of RET Rearrangements in Non–Small Cell Lung Cancer Roberto Ferrara, MD, Nathalie Auger, MD, Edouard Auclin,

Clinicopathologic Analysis of ROS1-Rearranged Non–Small-Cell Lung Cancer and Proposal of a Diagnostic Algorithm Heounjeong Go, MD, PhD, Dong-Wan Kim,

A Sensitive ALK Immunohistochemistry Companion Diagnostic Test Identifies Patients Eligible for Treatment with Crizotinib Trish Thorne-Nuzzo, BS, Crystal.

The Unique Characteristics of MET Exon 14 Mutation in Chinese Patients with NSCLC Si-Yang Liu, MD, Lan-Ying Gou, MD, An-Na Li, MD, Na-Na Lou, MMed, Hong-Fei.

Responses to Crizotinib Can Occur in High-Level MET-Amplified Non–Small Cell Lung Cancer Independent of MET Exon 14 Alterations Rafael Caparica, MD,

Increased ALK Gene Copy Number and Amplification are Frequent in Non-small Cell Lung Cancer Marta Salido, MSc, Lara Pijuan, MD, PhD, Luz Martínez-Avilés,

Bob T. Li, M. B. B. S. , MPH, Dara S. Ross, MD, Dara L

A Validation Study for the Use of ROS1 Immunohistochemical Staining in Screening for ROS1 Translocations in Lung Cancer Patrizia Viola, MD, Manisha Maurya,

MET and EGFR Mutations Identified in ALK-Rearranged Pulmonary Adenocarcinoma: Molecular Analysis of 25 ALK-Positive Cases Jennifer M. Boland, MD, Jin.

Bright-Field Dual-Color Chromogenic In Situ Hybridization for Diagnosing Echinoderm Microtubule-Associated Protein-Like 4-Anaplastic Lymphoma Kinase-Positive.

High-Dose Crizotinib for Brain Metastases Refractory to Standard-Dose Crizotinib Young Hak Kim, MD, Hiroaki Ozasa, MD, Hiroki Nagai, MD, Yuichi Sakamori,

A Case of Large-Cell Neuroendocrine Carcinoma Harboring an EML4–ALK Rearrangement with Resistance to the ALK Inhibitor Crizotinib Naoki Omachi, MD, Shigeki.

Multiple Acquired Resistance Mutations of the ALK Tyrosine Kinase Domain after Sequential Use of ALK Inhibitors Hsin-Yi Wang, MD Journal of Thoracic.

Circulating Tumor DNA Identifies EGFR Coamplification as a Mechanism of Resistance to Crizotinib in a Patient with Advanced MET-Amplified Lung Adenocarcinoma

Acquired Resistance to Crizotinib in NSCLC with MET Exon 14 Skipping

Comprehensive Hybrid Capture–Based Next-Generation Sequencing Identifies a Double ALK Gene Fusion in a Patient Previously Identified to Be False-Negative.

ALK and NRG1 Fusions Coexist in a Patient with Signet Ring Cell Lung Adenocarcinoma Lucia Anna Muscarella, PhD, Domenico Trombetta, PhD, Federico Pio.

A Case of Squamous Cell Carcinoma Harboring an EML4-ALK Rearrangement that Was Unsuccessfully Treated with the ALK Inhibitor Alectinib Akihiro Tamiya,

Dual IHC and FISH Testing for ALK Gene Rearrangement in Lung Adenocarcinomas in a Routine Practice: A French Study Anne McLeer-Florin, PhD, Denis Moro-Sibilot,

Combined Use of ALK Immunohistochemistry and FISH for Optimal Detection of ALK- Rearranged Lung Adenocarcinomas Lynette M. Sholl, MD, Stanislawa Weremowicz,

ALK/EML4 Fusion Gene May Be Found in Pure Squamous Carcinoma of the Lung Anna Caliò, MD, Alessia Nottegar, MD, Eliana Gilioli, MD, Emilio Bria, MD, Sara.

A Sensitive ALK Immunohistochemistry Companion Diagnostic Test Identifies Patients Eligible for Treatment with Crizotinib Trish Thorne-Nuzzo, BS, Crystal.

Combinational Analysis of FISH and Immunohistochemistry Reveals Rare Genomic Events in ALK Fusion Patterns in NSCLC that Responds to Crizotinib Treatment

Reliability Assurance of Detection of EML4-ALK Rearrangement in Non–Small Cell Lung Cancer: The Results of Proficiency Testing in China Yulong Li, MD,

ALK Rearrangement Detected in a Focus of Pulmonary Atypical Adenomatous Hyperplasia Filippo Lococo, MD, Alessandra Bisagni, MD, Maria Cecilia Mengoli,

Searching for ROS1 Rearrangements in Lung Cancer by Fluorescent In Situ Hybridization: The Importance of Probe Design Arnaud Uguen, MD, Pascale Marcorelles,

A Novel EML4-ALK Variant: Exon 6 of EML4 Fused to Exon 19 of ALK

MET Gene Status in Malignant Mesothelioma Using Fluorescent In Situ Hybridization Serena Varesano, PhD, Sandra Salvi, PhD, Simona Boccardo, PhD, Jean.

Parallel FISH and Immunohistochemical Studies of ALK Status in 3244 Non–Small-Cell Lung Cancers Reveal Major Discordances Florian Cabillic, PharMD, PhD,

Response to Crizotinib Observed in Lung Adenocarcinoma with MET Copy Number Gain but without a High-Level MET/CEP7 Ratio, MET Overexpression, or Exon.

Erratum Journal of Thoracic Oncology

Arnaud Uguen, MD, PhD Journal of Thoracic Oncology

A Case of ALK-Rearranged Adenocarcinoma with Small Cell Carcinoma-Like Transformation and Resistance to Crizotinib Yoon Jin Cha, MD, PhD, Byoung Chul.

High MET Receptor Expression But Not Gene Amplification in ALK 2p23 Rearrangement Positive Non–Small-Cell Lung Cancer Yan Feng, MD, Eugen C. Minca, MD,

Loss of p16INK4A Expression and Homozygous CDKN2A Deletion Are Associated with Worse Outcome and Younger Age in Thymic Carcinomas Scott W. Aesif, MD,

Amplification of MET in a Patient with Malignant Pleural Mesothelioma

Detection of ALK-Positive Non–Small-Cell Lung Cancers on Cytological Specimens: High Accuracy of Immunocytochemistry with the 5A4 Clone Spasenija Savic,

ALK Translocation in Non-small Cell Lung Cancer with Adenocarcinoma and Squamous Cell Carcinoma Markers Samuel J. Klempner, MD, David W. Cohen, MD, Daniel.

Expanded Circulating Tumor Cells from a Patient with ALK-Positive Lung Cancer Present with EML4-ALK Rearrangement Along with Resistance Mutation and Enable.

Daniel B. Costa, MD, PhD, Susumu Kobayashi, MD, PhD

Nivolumab-Induced Granulomatous Inflammation of the Pleura

Atypical Negative ALK Break-Apart FISH Harboring a Crizotinib-Responsive ALK Rearrangement in Non–Small-Cell Lung Cancer Shengxiang Ren, MD, PhD, Fred.

Toni-Maree Rogers, BMLS, Prudence A

Immunohistochemistry is a Reliable Screening Tool for Identification of ALK Rearrangement in Non–Small-Cell Lung Carcinoma and is Antibody Dependent

BIRC6-ALK, a Novel Fusion Gene in ALK Break-Apart FISH-Negative Lung Adenocarcinoma, Responds to Crizotinib Ling Shan, PhD, Peidi Jiang, MD, Feng Xu,

Concomitant Epidermal Growth Factor Receptor Mutation and EML4-ALK Fusion in a Patient with Multifocal Lung Adenocarcinomas Jun Fan, MD Journal of Thoracic.

Clinical Implications of Variant ALK FISH Rearrangement Patterns

A Dramatic Response to Crizotinib in a Non–Small-Cell Lung Cancer Patient with IHC- Positive and FISH-Negative ALK Jong-Mu Sun, MD, PhD, Yoon-La Choi,

Clinicopathologic Features of NSCLC Diagnosed During Pregnancy or the Peripartum Period in the Era of Molecular Genotyping Ibiayi Dagogo-Jack, MD, Justin.

ALK Status Testing in Non–Small-Cell Lung Carcinoma by FISH on ThinPrep Slides with Cytology Material Eugen C. Minca, MD, PhD, Christopher P. Lanigan,

Waxing and Waning of MET Amplification in EGFR-Mutated NSCLC in Response to the Presence and Absence of Erlotinib Selection Pressure Joel P. Womack,

ALK Gene Rearrangements: A New Therapeutic Target in a Molecularly Defined Subset of Non-small Cell Lung Cancer Benjamin Solomon, MBBS, PhD, Marileila.

Circulating Tumor DNA Identifies EGFR Coamplification as a Mechanism of Resistance to Crizotinib in a Patient with Advanced MET-Amplified Lung Adenocarcinoma

The Current Role of Whole Brain Radiation Therapy in Non–Small Cell Lung Cancer Patients Gokoulakrichenane Loganadane, MD, Lizza Hendriks, MD, PhD, Cécile.

Presentation transcript:

FISH Analysis of Crizotinib Target Genes ROS1/ALK/MET in Malignant Mesothelioma Sandra Salvi, PhD, Serena Varesano, PhD, Simona Boccardo, PhD, Jean Louis Ravetti, MD Journal of Thoracic Oncology Volume 12, Issue 8, Pages e116-e118 (August 2017) DOI: 10.1016/j.jtho.2017.03.015 Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions

Figure 1 ROS1, anaplastic lymphoma receptor tyrosine kinase gene (ALK), and MNNG HOS Transforming gene (MET) status in malignant pleural mesothelioma (MPM). ROS1 gene rearrangement was investigated by fluorescence in situ hybridization (FISH) with a Spectrum Green Probe (Abbott Molecular, Des Plaines, IL) and Vysis 6q22 ROS1 Break Apart FISH Probe (Abbott Molecular). ALK gene rearrangement was investigated by FISH with a Vysis LSI ALK Dual-Color Break Apart Rearrangement Probe (Abbott Molecular). A cell with normal expression of ROS1 or ALK shows fused red and green signals as a unique yellow signal or as two red and green distinct signals close to each other. In contrast, in the case of translocation of ALK (ROS1), the signals are separated by a gap. White arrows indicate the spot signals in the nucleus for ROS1 or ALK gene, respectively. (A and B) Epthelioid mesothelioma without ROS1 chromosomal translocation. (C and D) Epthelioid mesothelioma without ALK chromosomal translocation. (E and F) Positive control NSCLC with ROS1 chromosomal translocation. (G and H) Positive control NSCLC with ALK translocation. (A, C, E, and G) FISH gene (original magnification, ×100). (B, D, F, and H) Hematoxylin and eosin (original magnification, ×20). Journal of Thoracic Oncology 2017 12, e116-e118DOI: (10.1016/j.jtho.2017.03.015) Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions