Presentation is loading. Please wait.

Presentation is loading. Please wait.

ALK and ROS1 Double-Rearranged Lung Squamous Cell Carcinoma Responding to Crizotinib Treatment: A Case Report  Qiong Li, MD, Jian Wu, MD, PhD, Li-Xu Yan,

Published byLenard Logan Modified over 5 years ago

Similar presentations

Presentation on theme: "ALK and ROS1 Double-Rearranged Lung Squamous Cell Carcinoma Responding to Crizotinib Treatment: A Case Report  Qiong Li, MD, Jian Wu, MD, PhD, Li-Xu Yan,"— Presentation transcript:

1 ALK and ROS1 Double-Rearranged Lung Squamous Cell Carcinoma Responding to Crizotinib Treatment: A Case Report  Qiong Li, MD, Jian Wu, MD, PhD, Li-Xu Yan, MD, PhD, Jun-Wei Huang, MD, Zhou Zhang, PhD, Jin-E Zhang, MD, Xing-Lin Gao, MD, PhD, Ze-Ru Luo, MD, Jing Liu, PhD, Shi-Fang Yang, MD, PhD, Yan-Hui Liu, MD, PhD  Journal of Thoracic Oncology  Volume 12, Issue 12, Pages e193-e197 (December 2017) DOI: /j.jtho Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions

2 Figure 1 Histopathological and immunohistological findings of the primary lung (A–C) and metastatic pleural (D and E) tumor tissue samples. (A and D) Hematoxylin and eosin staining showed a moderately differentiated squamous cell carcinoma (original magnification, ×400). (B, C, E, and F) Immunostaining for p63 and anaplastic lymphoma kinase. (B and E) The tumor was strongly positive for p63 (N/A rabbit immunoglobulin G [Biocare Medical, Concord, CA]) (400X). (C and F) ALK receptor tyrosine kinase gene (ALK) rearrangement was suggested by positive immunostaining using ALK (D5F3) CDx assay (Ventana Medical Systems, Tucson, AZ) (original magnification, ×400). Expression of CK5/6 and p40 and no expression of thyroid transcription factor-1, napsin A, or neuroendocrine markers was observed (staining not shown). Journal of Thoracic Oncology  , e193-e197DOI: ( /j.jtho ) Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions

3 Figure 2 Next-generation sequencing (NGS) findings of testing of the primary lung and metastatic pleural tumor tissue samples. (A) The Integrative Genomics Viewer screenshots show that chimeric reads by NGS indicate ALK receptor tyrosine kinase gene (ALK) and ROS1 double rearrangement. ROS1 genes were rearranged with two partners, with 5′ of ROS1 joined to 16 kilobases upstream of regulatory factor X6 gene (RFX6) and 3′ of ROS1 joined to 4 kilobases downstream of G protein–coupled receptor class C group 6 member A gene (GPRC6A). (B) Comparison of NGS mutation profiling between the primary and the metastastic tumor. The percentages represent the mutation allele fraction. EML4, echinoderm microtubule associated protein like 4 gene; AF, allele fraction; CN, copy number; PTEN, phosphatase and tensin homolog gene; STAG2, stromal antigen 2 gene; CTNNA1, catenin alpha 1 gene; ARID2, AT-rich interaction domain 2 gene; FANC1, Fanconi anemia complementation group 1 gene; MYC, v-myc avian myelocytomatosis viral oncogene homolog gene; NFE2L2, nuclear factor erythroid 2, like 2 gene; EMSY, EMSY, BRCA interacting transcriptional repressor gene; PMS2, PMS1 homolog 2, mismatch repair system component gene; DAXX, death domain associated protein gene; PALB2, partner and localizer of BRCA2 gene. Journal of Thoracic Oncology  , e193-e197DOI: ( /j.jtho ) Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions

4 Figure 3 The dynamic evolution of the patient's primary lung tumor (A₁–E₁) and metastases (A₂–E₂) after crizotinib treatment. (A) The baseline chest computed tomography (CT) scan (November 5, 2015) showing a 6×7 cm mass in the inferior lingular segment of the left upper lobe of the lung (A₁), and showing pleural tumors in the lower lobe of the lung and small pleural effusion (A₂). (B) Positron emission tomography/CT scan after 5 weeks of crizotinib treatment (December 18, 2015). The lesion of the primary lung tumor was obviously smaller (from 6×7 cm to 2.6×2.4 cm), and there was a distinct reduction in radiopharmaceutical uptake (maximum standardized uptake decreased from 21.7 to 2.0) compared with on October 3, 2015 (B₁). The left pleural lesions disappeared and left pleura radiopharmaceutical uptake was completely absent (B₂). (C) Chest CT scan after 3 months of crizotinib treatment (February 18, 2016). The primary tumor continued to decrease (C₁). Multiple nodules occurred in the pleura of left lower lobe of the lung, with the largest one at 20×22 mm (C₂). (D) Chest CT scan after 5 months of crizotinib treatment (April 19, 2016). No obvious change in the primary tumor compared with on February 18, 2016 (D₁). Multiple nodules in the pleura of the left lower lobe progressed, with the largest one at 46×32 mm (D₂). (E) Chest CT scan before death (September 22, 2016): No change in the primary tumor (E₁). Extensive metastases including pleural and liver tumor lesions occurred in the patient (E₂). Journal of Thoracic Oncology  , e193-e197DOI: ( /j.jtho ) Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions

5 Figure 4 The clinical course of the diagnosis and treatment of the patient. On October 31, 2015, the patient's positron emission tomography/CT scan suggested a left lung tumor and left pleural metastases; On November 5, 2015, she underwent CT-guided lung biopsy. On November 11, 2015, she started crizotinib treatment. On December 18, 2015 (after 5 weeks of crizotinib treatment), positron emission tomography/CT showed a dramatic reduction in the size and the radiopharmaceutical uptake in the mass, disappearance of the pleural metastases, and partial disappearance of the mediastinal lymph nodes. On April 22, 2016, she underwent a second biopsy of the pleural metastasis in the posterior basal segment of the left lower lobe. On April 26, 2016, she underwent an ablation of the left lower pleural metastases. On May 26, 2016, she switched to gemcitabine plus paclitaxel chemotherapy for two cycles in the local hospital and died on September 30, PR, partial response; PD, progressive disease. Journal of Thoracic Oncology  , e193-e197DOI: ( /j.jtho ) Copyright © 2017 International Association for the Study of Lung Cancer Terms and Conditions

Download ppt "ALK and ROS1 Double-Rearranged Lung Squamous Cell Carcinoma Responding to Crizotinib Treatment: A Case Report  Qiong Li, MD, Jian Wu, MD, PhD, Li-Xu Yan,"

Similar presentations

Acquired C797S Mutation upon Treatment with a T790M-Specific Third-Generation EGFR Inhibitor (HM61713) in Non–Small Cell Lung Cancer  Haa-Na Song, MD,

Acquired C797S Mutation upon Treatment with a T790M-Specific Third-Generation EGFR Inhibitor (HM61713) in Non–Small Cell Lung Cancer  Haa-Na Song, MD,
A Rare STRN-ALK Fusion in Lung Adenocarcinoma Identified Using Next-Generation Sequencing–Based Circulating Tumor DNA Profiling Exhibits Excellent Response.

A Rare STRN-ALK Fusion in Lung Adenocarcinoma Identified Using Next-Generation Sequencing–Based Circulating Tumor DNA Profiling Exhibits Excellent Response.
Next Generation Sequencing Uncovers Potential Genetic Driver Mutations of Malignant Pulmonary Granular Cell Tumor  Song Xu, Qingchun Zhao, Sen Wei, Yi.

Next Generation Sequencing Uncovers Potential Genetic Driver Mutations of Malignant Pulmonary Granular Cell Tumor  Song Xu, Qingchun Zhao, Sen Wei, Yi.
Secondary Mutations at I1171 in the ALK Gene Confer Resistance to Both Crizotinib and Alectinib  Gouji Toyokawa, MD, PhD, Fumihiko Hirai, MD, PhD, Eiko.

Secondary Mutations at I1171 in the ALK Gene Confer Resistance to Both Crizotinib and Alectinib  Gouji Toyokawa, MD, PhD, Fumihiko Hirai, MD, PhD, Eiko.
PET/CT Fusion Scan in Lung Cancer: Current Recommendations and Innovations  Cristina Gámez, MD, PhD, Rafael Rosell, MD, PhD, Alejandro Fernández, MD, PhD,

PET/CT Fusion Scan in Lung Cancer: Current Recommendations and Innovations  Cristina Gámez, MD, PhD, Rafael Rosell, MD, PhD, Alejandro Fernández, MD, PhD,
Hironori Yoshida, MD, Young Hak Kim, MD  Journal of Thoracic Oncology 

Hironori Yoshida, MD, Young Hak Kim, MD  Journal of Thoracic Oncology 
Longitudinal Cell-Free DNA Analysis in Patients with Small Cell Lung Cancer Reveals Dynamic Insights into Treatment Efficacy and Disease Relapse  Karinna.

Longitudinal Cell-Free DNA Analysis in Patients with Small Cell Lung Cancer Reveals Dynamic Insights into Treatment Efficacy and Disease Relapse  Karinna.
A Higher Proportion of the EGFR T790M Mutation May Contribute to the Better Survival of Patients with Exon 19 Deletions Compared with Those with L858R 

A Higher Proportion of the EGFR T790M Mutation May Contribute to the Better Survival of Patients with Exon 19 Deletions Compared with Those with L858R 
Two Cases of Small Cell Lung Cancer Transformation from EGFR Mutant Adenocarcinoma During AZD9291 Treatment  Jun Soo Ham, MD, Seokhwi Kim, MD, Hee Kyung.

Two Cases of Small Cell Lung Cancer Transformation from EGFR Mutant Adenocarcinoma During AZD9291 Treatment  Jun Soo Ham, MD, Seokhwi Kim, MD, Hee Kyung.
Malignant Pleural Mesothelioma Harboring Both G719C and S768I Mutations of EGFR Successfully Treated with Afatinib  Nobukazu Agatsuma, MD  Journal of.

Malignant Pleural Mesothelioma Harboring Both G719C and S768I Mutations of EGFR Successfully Treated with Afatinib  Nobukazu Agatsuma, MD  Journal of.
A Rare STRN-ALK Fusion in Lung Adenocarcinoma Identified Using Next-Generation Sequencing–Based Circulating Tumor DNA Profiling Exhibits Excellent Response.

A Rare STRN-ALK Fusion in Lung Adenocarcinoma Identified Using Next-Generation Sequencing–Based Circulating Tumor DNA Profiling Exhibits Excellent Response.
Malignant Pleural Mesothelioma Harboring Both G719C and S768I Mutations of EGFR Successfully Treated with Afatinib  Nobukazu Agatsuma, MD  Journal of.

Malignant Pleural Mesothelioma Harboring Both G719C and S768I Mutations of EGFR Successfully Treated with Afatinib  Nobukazu Agatsuma, MD  Journal of.
Recent Advances in Targeting ROS1 in Lung Cancer

Recent Advances in Targeting ROS1 in Lung Cancer
Osimertinib and Cabozantinib Combinatorial Therapy in an EGFR-Mutant Lung Adenocarcinoma Patient with Multiple MET Secondary-Site Mutations after Resistance.

Osimertinib and Cabozantinib Combinatorial Therapy in an EGFR-Mutant Lung Adenocarcinoma Patient with Multiple MET Secondary-Site Mutations after Resistance.
Lung Adenocarcinoma Harboring EGFR T790M and In Trans C797S Responds to Combination Therapy of First- and Third-Generation EGFR TKIs and Shifts Allelic.

Lung Adenocarcinoma Harboring EGFR T790M and In Trans C797S Responds to Combination Therapy of First- and Third-Generation EGFR TKIs and Shifts Allelic.
Cases of ALK-Rearranged Lung Cancer with 5-Year Progression-Free Survival with Crizotinib as Initial Precision Therapy  Deepa Rangachari, MD, Xiuning.

Cases of ALK-Rearranged Lung Cancer with 5-Year Progression-Free Survival with Crizotinib as Initial Precision Therapy  Deepa Rangachari, MD, Xiuning.
Y-L Chang, MD, C-T Wu, MD, Y-C Lee, MD, PhD 

Y-L Chang, MD, C-T Wu, MD, Y-C Lee, MD, PhD 
Acquired C797S Mutation upon Treatment with a T790M-Specific Third-Generation EGFR Inhibitor (HM61713) in Non–Small Cell Lung Cancer  Haa-Na Song, MD,

Acquired C797S Mutation upon Treatment with a T790M-Specific Third-Generation EGFR Inhibitor (HM61713) in Non–Small Cell Lung Cancer  Haa-Na Song, MD,
Detection of Discrepant Driver Mutations in a Patient with Two Synchronous Primary Non–Small Cell Lung Cancers (NSCLCs) with Liquid Biopsy  Sotirios Lakis,

Detection of Discrepant Driver Mutations in a Patient with Two Synchronous Primary Non–Small Cell Lung Cancers (NSCLCs) with Liquid Biopsy  Sotirios Lakis,
Sclerosing Pneumocytoma with Lymph Node Metastasis

Sclerosing Pneumocytoma with Lymph Node Metastasis

Similar presentations

Ads by Google