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Pralsetinib for RET fusion-positive non-small-cell lung cancer (ARROW): a multi-cohort, open-label, phase 1/2 study

The lancet oncology, 2021-07, Vol.22 (7), p.959-969

2021

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Impact of EML4-ALK Variant on Resistance Mechanisms and Clinical Outcomes in ALK-Positive Lung Cancer

Journal of clinical oncology, 2018-04, Vol.36 (12), p.1199-1206

2018

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Spectrum of Mechanisms of Resistance to Crizotinib and Lorlatinib in ROS1 Fusion-Positive Lung Cancer

Clinical cancer research, 2021-05, Vol.27 (10), p.2899-2909

2021

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Receptor Tyrosine Kinase Fusions and BRAF Kinase Fusions are Rare but Actionable Resistance Mechanisms to EGFR Tyrosine Kinase Inhibitors

Journal of thoracic oncology, 2018-09, Vol.13 (9), p.1312-1323

2018

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Catalog of 5' Fusion Partners in ALK -positive NSCLC Circa 2020

JTO clinical and research reports, 2020-03, Vol.1 (1), p.100015-100015, Article 100015

2020

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Thromboembolism in ALK+ and ROS1+ NSCLC patients: A systematic review and meta-analysis

Lung cancer (Amsterdam, Netherlands), 2021-07, Vol.157, p.147-155

2021

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Liquid Biopsy to Identify Actionable Genomic Alterations

American Society of Clinical Oncology educational book, 2018-05, Vol.38 (38), p.978-997

2018

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Dual occurrence of ALK G1202R solvent front mutation and small cell lung cancer transformation as resistance mechanisms to second generation ALK inhibitors without prior exposure to crizotinib. Pitfall of solely relying on liquid re-biopsy?

Lung cancer (Amsterdam, Netherlands), 2017-04, Vol.106, p.110-114

2017

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Receptor Tyrosine Kinase Fusions as an Actionable Resistance Mechanism to EGFR TKIs in EGFR-Mutant Non-Small-Cell Lung Cancer

Trends in cancer, 2019-11, Vol.5 (11), p.677-692

2019

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Will the clinical development of 4th-generation “double mutant active” ALK TKIs (TPX-0131 and NVL-655) change the future treatment paradigm of ALK+ NSCLC?

Translational oncology, 2021-11, Vol.14 (11), p.101191-101191, Article 101191

2021

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Beyond Osimertinib: The Development of Third-Generation EGFR Tyrosine Kinase Inhibitors For Advanced EGFR+ NSCLC

Journal of thoracic oncology, 2021-05, Vol.16 (5), p.740-763

2021

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Catalog of 5′ fusion partners in RET+ NSCLC Circa 2020

JTO clinical and research reports, 2020-06, Vol.1 (2), p.100037-100037, Article 100037

2020

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A Novel Sequentially Evolved EML4-ALK Variant 3 G1202R/S1206Y Double Mutation In Cis Confers Resistance to Lorlatinib: A Brief Report and Literature Review

JTO clinical and research reports, 2021-01, Vol.2 (1), p.100116-100116, Article 100116

2021

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Going beneath the tip of the iceberg. Identifying and understanding EML4-ALK variants and TP53 mutations to optimize treatment of ALK fusion positive (ALK+) NSCLC

Lung cancer (Amsterdam, Netherlands), 2021-08, Vol.158, p.126-136

2021

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The Role of Chemotherapy Plus Immune Checkpoint Inhibitors in Oncogenic-Driven NSCLC: A University of California Lung Cancer Consortium Retrospective Study

JTO clinical and research reports, 2022-12, Vol.3 (12), p.100427-100427, Article 100427

2022

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CNS metastasis in ROS1+ NSCLC: An urgent call to action, to understand, and to overcome

Lung cancer (Amsterdam, Netherlands), 2019-04, Vol.130, p.201-207

2019

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Activity and Safety of Mobocertinib (TAK-788) in Previously Treated Non-Small Cell Lung Cancer with EGFR Exon 20 Insertion Mutations from a Phase I/II Trial

Cancer discovery, 2021-07, Vol.11 (7), p.1688-1699

2021

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Response to Immune Checkpoint Inhibition as Monotherapy or in Combination With Chemotherapy in Metastatic ROS1-Rearranged Lung Cancers

JTO clinical and research reports, 2021-07, Vol.2 (7), p.100187-100187, Article 100187

2021

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Repotrectinib (TPX-0005) Is a Next-Generation ROS1/TRK/ALK Inhibitor That Potently Inhibits ROS1/TRK/ALK Solvent- Front Mutations

Cancer discovery, 2018-10, Vol.8 (10), p.1227-1236

2018

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Pralsetinib for patients with advanced or metastatic RET-altered thyroid cancer (ARROW): a multi-cohort, open-label, registrational, phase 1/2 study

The lancet. Diabetes & endocrinology, 2021-08, Vol.9 (8), p.491-501

2021

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EGFR exon 20 insertion mutations in Chinese advanced non-small cell lung cancer patients: Molecular heterogeneity and treatment outcome from nationwide real-world study

Lung cancer (Amsterdam, Netherlands), 2020-07, Vol.145, p.186-194

2020

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Identification of Novel CDH1-NRG2α and F11R-NRG2α Fusions in NSCLC Plus Additional Novel NRG2α Fusions in Other Solid Tumors by Whole Transcriptome Sequencing

JTO clinical and research reports, 2021-02, Vol.2 (2), p.100132-100132, Article 100132

2021

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U.S. Phase I First-in-human Study of Taletrectinib (DS-6051b/AB-106), a ROS1/TRK Inhibitor, in Patients with Advanced Solid Tumors

Clinical cancer research, 2020-09, Vol.26 (18), p.4785-4794

2020

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Emergence of novel and dominant acquired EGFR solvent-front mutations at Gly796 (G796S/R) together with C797S/R and L792F/H mutations in one EGFR (L858R/T790M) NSCLC patient who progressed on osimertinib

Lung cancer (Amsterdam, Netherlands), 2017-06, Vol.108, p.228

2017

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Pralsetinib for RET fusion-positive non-small-cell lung cancer (ARROW): a multi-cohort, open-label, phase 1/2 study

Impact of EML4-ALK Variant on Resistance Mechanisms and Clinical Outcomes in ALK-Positive Lung Cancer

Spectrum of Mechanisms of Resistance to Crizotinib and Lorlatinib in ROS1 Fusion-Positive Lung Cancer

Receptor Tyrosine Kinase Fusions and BRAF Kinase Fusions are Rare but Actionable Resistance Mechanisms to EGFR Tyrosine Kinase Inhibitors

Catalog of 5' Fusion Partners in ALK -positive NSCLC Circa 2020

Thromboembolism in ALK+ and ROS1+ NSCLC patients: A systematic review and meta-analysis

Liquid Biopsy to Identify Actionable Genomic Alterations

Dual occurrence of ALK G1202R solvent front mutation and small cell lung cancer transformation as resistance mechanisms to second generation ALK inhibitors without prior exposure to crizotinib. Pitfall of solely relying on liquid re-biopsy?

Receptor Tyrosine Kinase Fusions as an Actionable Resistance Mechanism to EGFR TKIs in EGFR-Mutant Non-Small-Cell Lung Cancer

Will the clinical development of 4th-generation “double mutant active” ALK TKIs (TPX-0131 and NVL-655) change the future treatment paradigm of ALK+ NSCLC?

Beyond Osimertinib: The Development of Third-Generation EGFR Tyrosine Kinase Inhibitors For Advanced EGFR+ NSCLC

Catalog of 5′ fusion partners in RET+ NSCLC Circa 2020

A Novel Sequentially Evolved EML4-ALK Variant 3 G1202R/S1206Y Double Mutation In Cis Confers Resistance to Lorlatinib: A Brief Report and Literature Review

Going beneath the tip of the iceberg. Identifying and understanding EML4-ALK variants and TP53 mutations to optimize treatment of ALK fusion positive (ALK+) NSCLC

The Role of Chemotherapy Plus Immune Checkpoint Inhibitors in Oncogenic-Driven NSCLC: A University of California Lung Cancer Consortium Retrospective Study

CNS metastasis in ROS1+ NSCLC: An urgent call to action, to understand, and to overcome

Activity and Safety of Mobocertinib (TAK-788) in Previously Treated Non-Small Cell Lung Cancer with EGFR Exon 20 Insertion Mutations from a Phase I/II Trial

Response to Immune Checkpoint Inhibition as Monotherapy or in Combination With Chemotherapy in Metastatic ROS1-Rearranged Lung Cancers

Repotrectinib (TPX-0005) Is a Next-Generation ROS1/TRK/ALK Inhibitor That Potently Inhibits ROS1/TRK/ALK Solvent- Front Mutations

Pralsetinib for patients with advanced or metastatic RET-altered thyroid cancer (ARROW): a multi-cohort, open-label, registrational, phase 1/2 study

Landscape of Acquired Resistance to Osimertinib in EGFR -Mutant NSCLC and Clinical Validation of Combined EGFR and RET Inhibition with Osimertinib and BLU-667 for Acquired RET Fusion

EGFR exon 20 insertion mutations in Chinese advanced non-small cell lung cancer patients: Molecular heterogeneity and treatment outcome from nationwide real-world study

Identification of Novel CDH1-NRG2α and F11R-NRG2α Fusions in NSCLC Plus Additional Novel NRG2α Fusions in Other Solid Tumors by Whole Transcriptome Sequencing

U.S. Phase I First-in-human Study of Taletrectinib (DS-6051b/AB-106), a ROS1/TRK Inhibitor, in Patients with Advanced Solid Tumors

Emergence of novel and dominant acquired EGFR solvent-front mutations at Gly796 (G796S/R) together with C797S/R and L792F/H mutations in one EGFR (L858R/T790M) NSCLC patient who progressed on osimertinib

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