Presentation is loading. Please wait.

Presentation is loading. Please wait.

Spatial Tumor Heterogeneity in Lung Cancer with Acquired Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Resistance: Targeting High-Level MET-Amplification.

Published byDoris Stephens Modified over 5 years ago

Similar presentations

Presentation on theme: "Spatial Tumor Heterogeneity in Lung Cancer with Acquired Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Resistance: Targeting High-Level MET-Amplification."— Presentation transcript:

1 Spatial Tumor Heterogeneity in Lung Cancer with Acquired Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Resistance: Targeting High-Level MET-Amplification and EGFR T790M Mutation Occurring at Different Sites in the Same Patient  Matthias Scheffler, MD, Sabine Merkelbach-Bruse, PhD, Marc Bos, MD, Jana Fassunke, PhD, Masyar Gardizi, MD, Sebastian Michels, MD, Laura Groneck, MD, Anne M Schultheis, MD, Florian Malchers, PhD, Frauke Leenders, PhD, Carsten Kobe, MD, Katharina König, PhD, Lukas C. Heukamp, MB, PhD, Martin L. Sos, MD, Roman K. Thomas, MD, Reinhard Büttner, MD, Jürgen Wolf, MD  Journal of Thoracic Oncology  Volume 10, Issue 6, Pages e40-e43 (June 2015) DOI: /JTO Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

2 FIGURE 1 Fluorodeoxyglucose (18F)-positron emission tomography–computed tomography results. A, October 2013: massive progression after epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor resistance and chemotherapy (lung, myocardial infiltration, liver, and soft-tissue left arm). Rebiopsy left arm: EGFRL858R, high-level METamp, TP53C277*, and TP53R110C. B, November 2013: complete metabolic response of myocard-tissue, liver-tissue, and soft-tissue metastases after 8 days of crizotinib and erlotinib. C, December 2013: ongoing metabolic response of myocard-tissue, liver-tissue, and soft-tissue metastases under crizotinib and erlotinib. D, January 2014: ongoing metabolic response of liver-tissue and soft-tissue metastases. Metabolic progression of myocard infiltrating tumor and progressive pleural effusion left. Molecular analysis of pleural effusion: EGFRL858R, EGFRT790M, TP53R110C, and low-level METamp. Peripheral blood: EGFRL858R, EGFRT790M, and TP53R110C (MET status not assessable). Stop of crizotinib and erlotinib treatment, start of AZD9291. E, March 2014: stable metabolic disease in lung tumor, tumor progression in myocard- and liver metastases, tumor control of the soft-tissue metastasis in the arm. Stop of AZD9291, restart with crizotinib. F, April 2014: complete metabolic response of liver- and myocardial metastases, ongoing tumor control of the soft-tissue metastasis. Progress of pleural effusion. Patient died after 3 weeks of crizotinib treatment. Molecular analysis of pleural effusion: EGFRL858R, EGFRT790M, TP53R110C, and no METamp. Journal of Thoracic Oncology  , e40-e43DOI: ( /JTO ) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

3 FIGURE 2 Overview of the findings in the resistance setting after erlotinib treatment (November 2011–July 2012) and afatinib/cetuximab treatment (November 2012–June 2013) with intercurrent radiation/chemotherapy. Journal of Thoracic Oncology  , e40-e43DOI: ( /JTO ) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

4 FIGURE 3 Liquid biopsy reveals epidermal growth factor receptor (EGFR) and TP53 mutations: results of the peripheral blood analysis (January 2014). A, EGFRL858R mutation with an allele frequency of 13%. B, EGFRT790M mutation with an allele frequency of 10%. C, TP53R110C mutation with an allele frequency of 9%. All identified and illustrated by integrative genome viewer. Journal of Thoracic Oncology  , e40-e43DOI: ( /JTO ) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

Download ppt "Spatial Tumor Heterogeneity in Lung Cancer with Acquired Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor Resistance: Targeting High-Level MET-Amplification."

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,
Comparison of Clinical Outcomes Following Gefitinib and Erlotinib Treatment in Non– Small-Cell Lung Cancer Patients Harboring an Epidermal Growth Factor.

Comparison of Clinical Outcomes Following Gefitinib and Erlotinib Treatment in Non– Small-Cell Lung Cancer Patients Harboring an Epidermal Growth Factor.
Phase II Study of Gefitinib, an Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor (EGFR-TKI), and Celecoxib, a Cyclooxygenase-2 (COX-2) Inhibitor,

Phase II Study of Gefitinib, an Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor (EGFR-TKI), and Celecoxib, a Cyclooxygenase-2 (COX-2) Inhibitor,
Epidermal Growth Factor Receptor-Related Tumor Markers and Clinical Outcomes with Erlotinib in Non-small Cell Lung Cancer: An Analysis of Patients from.

Epidermal Growth Factor Receptor-Related Tumor Markers and Clinical Outcomes with Erlotinib in Non-small Cell Lung Cancer: An Analysis of Patients from.
Implementation of Amplicon Parallel Sequencing Leads to Improvement of Diagnosis and Therapy of Lung Cancer Patients  Katharina König, PhD, Martin Peifer,

Implementation of Amplicon Parallel Sequencing Leads to Improvement of Diagnosis and Therapy of Lung Cancer Patients  Katharina König, PhD, Martin Peifer,
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.
Hironori Yoshida, MD, Young Hak Kim, MD  Journal of Thoracic Oncology 

Hironori Yoshida, MD, Young Hak Kim, MD  Journal of Thoracic Oncology 
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.
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.
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.
Rapid Acquisition of T790M Mutation after Treatment with Afatinib in an NSCLC Patient Harboring EGFR Exon 20 S768I Mutation  Alessandro Russo, MD, Tindara.

Rapid Acquisition of T790M Mutation after Treatment with Afatinib in an NSCLC Patient Harboring EGFR Exon 20 S768I Mutation  Alessandro Russo, MD, Tindara.
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,
Efficacy of the Irreversible ErbB Family Blocker Afatinib in Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitor (TKI)–Pretreated Non–Small-Cell.

Efficacy of the Irreversible ErbB Family Blocker Afatinib in Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitor (TKI)–Pretreated Non–Small-Cell.
Dramatic Response to Combination Erlotinib and Crizotinib in a Patient with Advanced, EGFR-Mutant Lung Cancer Harboring De Novo MET Amplification  Justin.

Dramatic Response to Combination Erlotinib and Crizotinib in a Patient with Advanced, EGFR-Mutant Lung Cancer Harboring De Novo MET Amplification  Justin.
Next-Generation Sequencing Reveals a Novel NSCLC ALK F1174V Mutation and Confirms ALK G1202R Mutation Confers High-Level Resistance to Alectinib (CH5424802/RO5424802)

Next-Generation Sequencing Reveals a Novel NSCLC ALK F1174V Mutation and Confirms ALK G1202R Mutation Confers High-Level Resistance to Alectinib (CH /RO )
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,
Durable Response to Tyrosine Kinase Inhibitor Therapy in a Lung Cancer Patient Harboring Epidermal Growth Factor Receptor Tandem Kinase Domain Duplication 

Durable Response to Tyrosine Kinase Inhibitor Therapy in a Lung Cancer Patient Harboring Epidermal Growth Factor Receptor Tandem Kinase Domain Duplication 
Erlotinib Response in an NSCLC Patient with a Novel Compound G719D+L861R Mutation in EGFR  Eamon M. Berge, MD, Dara L. Aisner, MD, PhD, Robert C. Doebele,

Erlotinib Response in an NSCLC Patient with a Novel Compound G719D+L861R Mutation in EGFR  Eamon M. Berge, MD, Dara L. Aisner, MD, PhD, Robert C. Doebele,
Acquired BRAF V600E Mutation as Resistant Mechanism after Treatment with Third- Generation EGFR Tyrosine Kinase Inhibitor  Alessandra Bearz, MD, Elisa.

Acquired BRAF V600E Mutation as Resistant Mechanism after Treatment with Third- Generation EGFR Tyrosine Kinase Inhibitor  Alessandra Bearz, MD, Elisa.
MET-Mutated NSCLC with Major Response to Crizotinib

MET-Mutated NSCLC with Major Response to Crizotinib

Similar presentations

Ads by Google