Response and resistance to savolitinib and osimertinib in a patient with EGFR-mutant NSCLC harboring MET amplification. Response and resistance to savolitinib.

Slides:



Advertisements
Similar presentations
James R. Rigas Comprehensive Thoracic Oncology Program
Advertisements

Shyamala Maherswaran, Ph.D. et al. Sarah Gomez and Rachael Holmes Detection of Mutations in EGFR in Circulating Lung-Cancer Cells.
Detection of Mutations in EGFR in Circulating Lung-Cancer Cells Colin Reisterer and Nick Swenson S. Maheswaran et al. The New England Journal of Medicine.
Mechanisms of Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors (EGFR-TKI) in Non-Small Cell Lung Cancer (NSCLC) Victor.
Activity and Tolerability of Afatinib (BIBW 2992) and Cetuximab in NSCLC Patients with Acquired Resistance to Erlotinib or Gefitinib Janjigian YY et al.
The highlight of resistance mechanism of targeted therapy on clinical therapy Zuhua Chen Dep. of GI oncology.
Anna Buder Institute of Cancer Research Department of Medicine I Medical University of Vienna Liquid Biopsies Analysis of circulating cell-free tumor-DNA.
Samsung Genome Institute Samsung Medical Center
Application of a Highly Sensitive Detection System for Epidermal Growth Factor Receptor Mutations in Plasma DNA  Tomomi Nakamura, MD, Naoko Sueoka-Aragane,
Dose-escalation patient response.
Patient Case 1 Patient Case 1: PET/CT Scan.
Clinical Considerations in the Management of EGFR-Mutated Advanced NSCLC.
The New Taxonomy of Metastatic NSCLC and Physician Treatment Based on Pathologic and Molecular Characteristics The New Taxonomy of Metastatic Non-Small.
Clonal evolution of resistance to sequential ALK inhibitor therapy.
Receptor Tyrosine Kinase Fusions and BRAF Kinase Fusions are Rare but Actionable Resistance Mechanisms to EGFR Tyrosine Kinase Inhibitors  Alexa B. Schrock,
Assessing the Impact: New Data in T790+ NSCLC
New Patient Journeys in Non-small cell lung cancer
Application of a Highly Sensitive Detection System for Epidermal Growth Factor Receptor Mutations in Plasma DNA  Tomomi Nakamura, MD, Naoko Sueoka-Aragane,
Proof-of-concept clinical studies validating AZD9291 as a mutant-selective EGFR kinase T790M inhibitor. Proof-of-concept clinical studies validating AZD9291.
Updates and Perspectives on Third-Generation EFGR TKIs in Advanced NSCLC.
Meta-analysis of randomised phase III clinical trials comparing EGFR tyrosine kinase inhibitor (TKI) shows that male patients with non-small cell lung.
Monitoring EGFR mutation status in Non-small cell lung cancer (NSCLC) patients using circulating Tumour DNA (ctDNA). Matthew Smith Molecular Pathology.
Osimertinib and Cabozantinib Combinatorial Therapy in an EGFR-Mutant Lung Adenocarcinoma Patient with Multiple MET Secondary-Site Mutations after Resistance.
T790M Mutation-Positive NSCLC: A Multidisciplinary Case Conference
Volume 9, Issue 6, Pages (June 2006)
High-throughput drug screen and validation to nominate patient-specific therapeutic options. High-throughput drug screen and validation to nominate patient-specific.
A, baseline and 4-week PET scan from patient 2 (MET c
Rapid Acquisition of T790M Mutation after Treatment with Afatinib in an NSCLC Patient Harboring EGFR Exon 20 S768I Mutation  Alessandro Russo, MD, Tindara.
Acquired BRAF V600E Mutation as Resistant Mechanism after Treatment with Osimertinib  Chao-Chi Ho, MD, PhD, Wei-Yu Liao, MD, PhD, Chih-An Lin, Jin-Yuan.
Moving Care Forward in Advanced NSCLC
Acquired BRAF V600E Mutation as Resistant Mechanism after Treatment with Third- Generation EGFR Tyrosine Kinase Inhibitor  Alessandra Bearz, MD, Elisa.
Serum vs FNA:.
Volume 9, Issue 6, Pages (June 2006)
Beyond Erlotinib: Better EGFR Inhibitors?
Progress of the NSCLC Revolution
Defining Patient-Centered Care: Spotlight on Advanced Non-Small Cell Lung Cancer.
Effects of Pharmacokinetic Processes and Varied Dosing Schedules on the Dynamics of Acquired Resistance to Erlotinib in EGFR-Mutant Lung Cancer  Jasmine.
Representative CT and PET/CT images of three patients with NSCLCs
Fig. 5 EGFR mutation status of patients with NSCLC, detected by histological examination and ARMS PCR. EGFR mutation status of patients with NSCLC, detected.
This program will include a discussion of off-label treatment and investigational agents not approved by the FDA for use in the United States, and data.
Multidisciplinary Management in Non-Small Cell Lung Cancer (NSCLC)
Optimizing Characterization of NSCLC Through Specialty Collaboration
Detection rate of EGFR mutations in cfDNA by characteristics
EGFR Mutations Detected in Plasma Are Associated with Patient Outcomes in Erlotinib Plus Docetaxel-Treated Non-small Cell Lung Cancer  Philip C. Mack,
Compound Uncommon EGFR Mutations in a Patient with Advanced NSCLC and Durable Response to Sequential EGFR Targeted Therapies  Mary Linton B Peters, MD,
Concomitant Epidermal Growth Factor Receptor Mutation and EML4-ALK Fusion in a Patient with Multifocal Lung Adenocarcinomas  Jun Fan, MD  Journal of Thoracic.
Presentation and progression of glioblastoma with PNET features in an adult patient. Presentation and progression of glioblastoma with PNET features in.
Finding the Right Sequence in Patients With EGFR-Mutated NSCLC
Computed tomographic images from a patient with BRAFL597S-mutant metastatic melanoma responding to therapy with the MEK inhibitor TAK-733. Computed tomographic.
What's on the Horizon in the Management of EGFR-Mutated Lung Cancer?
Detection of somatic mutations in plasma allows for non-invasive real time therapy response monitoring of lung cancer patients José Carlos Machado.
ALK resistance mutations predict for sensitivity to lorlatinib in patient-derived cell line models of acquired resistance to ceritinib. ALK resistance.
Representative examples of estrogen receptor α and β immunohistochemical expression (top figures) and EGFR mutations (bottom figures) in lung adenocarcinomas.
Saturation analysis and the discovery of actionability of mutational hotspots. Saturation analysis and the discovery of actionability of mutational hotspots.
Representative CT and PET/CT images of three patients with NSCLCs
Location of common clinically relevant mutations in EGFR
Serial chest CT scans of 33-year-old male with lung adenocarcinoma harboring EGFR-KDD documenting response to afatinib and subsequent acquired resistance.
Noninvasive detection of acquired MET amplification as a mechanism of afatinib/trastuzumab resistance using cfDNA. Noninvasive detection of acquired MET.
Molecular heterogeneity drives secondary resistance to anti-EGFR therapies in mCRC. Molecular heterogeneity drives secondary resistance to anti-EGFR therapies.
Molecular heterogeneity can drive mixed response and treatment failure in EGC. A, PET images from Patient #4 obtained before treatment and upon disease.
Prevalence of germline T790M.
Combined inhibition of coamplified RTKs is required for response.
Frequent coamplification of RTKs in MET-amplified EGC
Genetic analysis suggests the presence of four clinically relevant groups of histologically defined anaplastic oligodendrogliomas. Genetic analysis suggests.
Tracking resistance to TRKA inhibition in ctDNA of a patient with colorectal cancer. Tracking resistance to TRKA inhibition in ctDNA of a patient with.
Response to crizotinib in an 8-year-old boy with refractory IMT harboring a TFG–ROS1 fusion. Response to crizotinib in an 8-year-old boy with refractory.
Concordance between liquid versus tissue biopsies.
Updates in Best Practices in Non-Small Cell Lung Cancer
BIM expression predicts the response of patients with EGFR-mutant lung cancers. BIM expression predicts the response of patients with EGFR-mutant lung.
Patterns of clinical relapse and algorithm for the therapeutic strategy when AR to EGFR TKI occurs in patients with EGFR-mutant NSCLC. *After discussion.
Presentation transcript:

Response and resistance to savolitinib and osimertinib in a patient with EGFR-mutant NSCLC harboring MET amplification. Response and resistance to savolitinib and osimertinib in a patient with EGFR-mutant NSCLC harboring MET amplification. A, Treatment timeline. B, Despite being refractory to prior EGFR inhibitors, a dramatic response to the combination was seen after 4 weeks. C, After 36 weeks on therapy, an isolated lung nodule appeared and was resected; however, further progression was seen. D, Serial plasma genotyping demonstrates response of the known EGFR exon 19 deletion followed by progression with development of an acquired D1228V mutation, in the absence of EGFRT790M. Magda Bahcall et al. Cancer Discov 2016;6:1334-1341 ©2016 by American Association for Cancer Research