|Local ablative therapy of oligoprogressive disease prolongs disease control by tyrosine kinase inhibitors in oncogene-addicted non-small-cell lung cancer.|
|PMID: 23154552 Owner: NLM Status: MEDLINE|
|INTRODUCTION: Many patients with oncogene-driven non-small-cell lung cancer (NSCLC) treated with tyrosine kinase inhibitors experience limited sites of disease progression. This study investigated retrospectively the benefits of local ablative therapy (LAT) to central nervous system (CNS) and/or limited systemic disease progression and continuation of crizotinib or erlotinib in patients with metastatic ALK gene rearrangement (ALK+) or EGFR-mutant (EGFR-MT) NSCLC, respectively.
METHODS: Patients with metastatic ALK+ NSCLC treated with crizotinib (n = 38) and EGFR-MT NSCLC treated with erlotinib (n = 27) were identified at a single institution. Initial response to the respective kinase inhibitors, median progression-free survival (PFS1), and site of first progression were recorded. A subset of patients with either nonleptomeningeal CNS and/or four sites or fewer of extra-CNS progression (oligoprogressive disease) suitable for LAT received either radiation or surgery to these sites and continued on the same tyrosine kinase inhibitors. The subsequent median progression-free survival from the time of first progression (PFS2) and pattern of progression were recorded.
RESULTS: Median progression-free survival in ALK+ patients on crizotinib was 9.0 months, and 13.8 months for EGFR-MT patients on erlotinib. Twenty-five of 51 patients (49%) who progressed were deemed suitable for local therapy (15 ALK+, 10 EGFR-MT; 24 with radiotherapy, one with surgery) and continuation of the same targeted therapy. Post-LAT, 19 of 25 patients progressed again, with median PFS2 of 6.2 months.
DISCUSSION: Oncogene-addicted NSCLC with CNS and/or limited systemic disease progression (oligoprogressive disease) on relevant targeted therapies is often suitable for LAT and continuation of the targeted agent, and is associated with more than 6 months of additional disease control.
|Andrew J Weickhardt; Benjamin Scheier; Joseph Malachy Burke; Gregory Gan; Xian Lu; Paul A Bunn; Dara L Aisner; Laurie E Gaspar; Brian D Kavanagh; Robert C Doebele; D Ross Camidge|
|Type: Journal Article|
|Title: Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer Volume: 7 ISSN: 1556-1380 ISO Abbreviation: J Thorac Oncol Publication Date: 2012 Dec|
|Created Date: 2012-11-16 Completed Date: 2013-05-07 Revised Date: 2014-08-21|
Medline Journal Info:
|Nlm Unique ID: 101274235 Medline TA: J Thorac Oncol Country: United States|
|Languages: eng Pagination: 1807-14 Citation Subset: IM|
|APA/MLA Format Download EndNote Download BibTex|
Aged, 80 and over
Brain Neoplasms / mortality, secondary, therapy*
Carcinoma, Non-Small-Cell Lung / mortality, pathology, therapy*
Combined Modality Therapy
Lung Neoplasms / mortality, pathology, therapy*
Mutation / genetics
Protein Kinase Inhibitors / therapeutic use*
Pyrazoles / therapeutic use
Pyridines / therapeutic use
Quinazolines / therapeutic use
Receptor Protein-Tyrosine Kinases / genetics*
Receptor, Epidermal Growth Factor / genetics*
|K12 CA086913/CA/NCI NIH HHS; P50 CA058187/CA/NCI NIH HHS|
|0/Protein Kinase Inhibitors; 0/Pyrazoles; 0/Pyridines; 0/Quinazolines; 53AH36668S/crizotinib; EC 184.108.40.206/EGFR protein, human; EC 220.127.116.11/Receptor Protein-Tyrosine Kinases; EC 18.104.22.168/Receptor, Epidermal Growth Factor; EC 22.214.171.124/anaplastic lymphoma kinase; J4T82NDH7E/erlotinib|
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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