Anaplastic lymphoma kinase inhibitor related pneumonitis in patients with non-small cell lung cancer

Anaplastic lymphoma kinase (ALK) inhibitor-related pneumonitis (ALK-IIP) is relatively rare but sometimes fatal, so the timely diagnosis of ALK-IIP is important for enabling prompt management. However, the detailed radiologic characteristics and clinical course of ALK-IIP are still unclear. This study was performed to investigate the clinical and radiologic characteristics and risk factors of ALK-IIP in patients with non-small cell lung cancer (NSCLC).

A total of 250 NSCLC patients who had been treated with ALK inhibitors were retrospectively enrolled. Chest computed tomography (CT) was classified into 4 CT patterns using the 2013 guideline for idiopathic interstitial pneumonia: cryptogenic organizing pneumonia (COP), hypersensitivity pneumonitis (HP), acute interstitial pneumonia (AIP), and nonspecific interstitial pneumonia. Clinical characteristics including toxicity grading and treatment course were analyzed in regarding to CT patterns. Clinical characteristics were compared betwe..... READ ARTICLE

Medicine DOI:10.1097/MD.0000000000018131

Authors: Hwang Hye Jeon, Kim Mi Young, Choi Chang-Min, Lee Jae Cheol

Targeted next-generation sequencing revealed distinct clinicopathologic and molecular features of VCL-ALK RCC

Anaplastic lymphoma kinase (ALK)-rearranged renal cell carcinoma (RCC) is a novel entity of rare tumors with only 10 cases reported in the literature. Three RCC cases bearing VCL-ALK gene fusion were all young African American patients and associated with sickle cell trait notably. In contrast to the 3 reported cases, this neoplasm occurred in a middle-age woman (57 years old) without any evidence of sickle cell trait and demonstrated an infiltrating growth pattern with tubular, tubulopapillary, and tubulocystic structures, overlapping with collecting duct carcinoma and renal medullary carcinoma. Abundant intraluminal mucin was also noted significantly in the histologic sections. Immunostaining showed strong membranous labeling for ALK protein. We applied a large panel-targeted next-generation sequencing to explore the molecular alterations in the current case, revealing a driver oncogene VCL-ALK gene fusion co-occurring with pathogenic mutations in EP300 and TRRAP genes. Thereafter, f..... READ ARTICLE

Pathology - Research and Practice DOI:10.1016/j.prp.2019.152651

Authors: Xiao-tong Wang, Ru Fang, Sheng-bing Ye, Ru-song Zhang, Rui Li, Xuan Wang, Rong-hao Ji, Zhen-feng Lu, Heng-hui Ma, Xiao-jun Zhou, Qiu-yuan Xia, Qiu Rao

Assessment of a Radiomic Signature Developed in a General NSCLC Cohort for Predicting Overall Survival of ALK-Positive Patients With Different Treatment Types

Background: The purpose of the study was to investigate the potential of a radiomic signature developed in a general non–small-cell lung cancer (NSCLC) cohort for predicting the overall survival of anaplastic lymphoma kinase (ALK)-positive (ALK+) patients with different treatment types. Conclusion: This preliminary study suggests that the applicability of a general signature to ALK+ patients is limited. The general radiomic signature seems to be only applicable to ALK+ patients who had received nontargeted therapy, which indicates that developing special radiomics signatures for patients treated with tyrosine kinase inhibitors might be necessary. READ ARTICLE

Clinical Lung Cancer DOI:10.1016/j.cllc.2019.05.005

Authors: Lyu Huang, Jiayan Chen, Weigang Hu, Xinyan Xu, Di Liu, Junmiao Wen, Jiayu Lu, Jianzhao Cao, Junhua Zhang, Yu Gu, Jiazhou Wang, Min Fan

Early Onset Pulmonary Toxicity With Lorlatinib in a Patient With Previous Pulmonary Toxicity From Brigatinib

"A 53-year-old female ex-smoker (10 pack-years) presented with progressive dyspnea in February 2014. Her performance status was 1. She was diagnosed with stage IV lung adenocarcinoma with lung, lymph node, and bone involvement. Molecular testing revealed an ALK receptor tyrosine kinase (ALK) translocation with no other concomitant alterations. Our case describes a patient with ALK-rearranged NSCLC who developed pulmonary toxicity on brigatinib that recurred after exposure to lorlatinib at early onset. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.06.013

Authors: Xavier Monzonís, Edurne Arriola"

EditorialKirk SmithNovember 1, 2019Pulmonary Toxicity, Lorlatinib, Brigatinib

P2.14-18 Upregulation of AURKA Leads to Acquired Resistance in EML4-ALK NSCLC Cell Line

Background: Molecular targeted therapies in NSCLC often results in profound initial patient responses, these responses are short-term due to the development of acquired resistance. In an EML4-ALK NSCLC background, acquired resistance can be developed in two ways ALK dependent (ALK secondary mutations) and ALK independent (alternative oncogenic pathways). In our study, we have shown that increased expression of Aurora kinase A (AURKA) leads to acquired resistance upon treatment with ALK TKI crizotinib. Conclusion: Our results indicate a new mechanism to acquire resistance upon treatment with ALK TKI crizotinib. Inhibition of both ALK and AURKA activity might be beneficial for ALK TKI resistant tumors with increased AURKA gene expression/activity. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1803

Authors: G. Umapathy, R. Palmer, B. Hallberg

Conference PaperKirk SmithOctober 21, 2019EML4-ALK, AURKA, Resistance

Targeting YAP to overcome acquired resistance to ALK inhibitors in ALK-rearranged lung cancer

Clinical benefit of ALK tyrosine kinase inhibitors (ALK-TKIs) in ALK-rearranged lung cancer has been limited by the inevitable development of acquired resistance, and bypass-molecular resistance mechanisms remain poorly understood. We investigated a novel therapeutic target through screening FDA-approved drugs in ALK-TKI-resistant models. Cerivastatin, the rate-limiting enzyme inhibitor of the mevalonate pathway, showed anti-cancer activity against ALK-TKI resistance in vitro/in vivo, accompanied by cytoplasmic retention and subsequent inactivation of transcriptional co-regulator YAP. The marked induction of YAP-targeted oncogenes (EGFR, AXL, CYR61, and TGFβR2) in resistant cells was abolished by cerivastatin. YAP silencing suppressed tumor growth in resistant cells, patient-derived xenografts, and EML4-ALK transgenic mice, whereas YAP overexpression decreased the responsiveness of parental cells to ALK inhibitor. In matched patient samples before/after ALK inhibitor treatment, nuclear..... READ ARTICLE

EMBO Molecular Medicine DOI:10.15252/emmm.201910581

Authors: Mi Ran Yun, Hun Mi Choi, You Won Lee, Hyeong Seok Joo, Chae Won Park, Jae Woo Choi, Dong Hwi Kim, Han Na Kang, Kyoung-Ho Pyo, Eun Joo Shin, Hyo Sup Shim, Ross A Soo, James Chih-Hsin Yang, Sung Sook Lee, Hyun Chang, Min Hwan Kim, Min Hee Hong, Hye Ryun Kim, Byoung Chul Cho

Pre-ClinicalKirk SmithOctober 21, 2019YAP, acquired resistance, ALK inhibitors, ALK-rearranged lung cancer

Sequential EGFR mutation and ALK rearrangement in adenocarcinoma lung, with rare metastasis to bilateral breast, ovary and endometrium

With the advent of targeted therapies there was a paradigm shift in the treatment of metastatic adenocarcinoma of lung. Immuno-histopathology and molecular subtyping in metastatic adenocarcinoma lung have enabled personalized treatment for each patient. Oncogenic driver mutations in non-small cell lung cancer are commonly EGFR (Epidermal Growth Factor Receptor) gene mutation and ALK (Anaplastic Lymphoma Kinase) gene rearrangement, which are mutually exclusive. Almost 60–64% patients have oncogenic mutation, which are mutually exclusive. Here, we present a case with EGFR mutation and ALK gene rearrangement which was expressed sequentially and with metastasis to rarest sites bilateral breast, ovaries and endometrium. Even though presented with upfront metastatic disease, patient was treated with multiple lines of targeted agents, by which patient survived for 5 years with good quality of life. READ ARTICLE

Respiratory Medicine Case Reports DOI:10.1016/j.rmcr.2019.100954

Authors: V. R. Anjali, Rambha Pandey, Astha Srivastava, Madhu Rajeshwari, Durgatosh Pandey, M. C. Sharma

Ceritinib plus Nivolumab in Patients with Advanced ALK-Rearranged Non–Small Cell Lung Cancer: Results of an Open-Label, Multicenter, Phase 1B Study

Induction of programmed death ligand 1 (PD-L1) expression due to constitutive oncogenic signaling has been reported in NSCLC models harboring echinoderm microtubule associated protein like 4 gene (EML4)–ALK receptor tyrosine kinase gene (ALK) rearrangements. We assessed the safety and activity of ceritinib plus nivolumab in these patients.In this open-label, phase 1B, multicenter, dose escalation and expansion study, previously treated (with ALK receptor tyrosine kinase [ALK] inhibitor [ALKI]/chemotherapy) or treatment-naive patients with stage IIIB or IV ALK-rearranged NSCLC received nivolumab, 3 mg/kg intravenously every 2 weeks, plus ceritinib, 450 mg/300 mg daily, with a low-fat meal. Ceritinib plus nivolumab has activity; ORR appears to correlate with PD-L1 at baseline. Toxicity, especially rash, is more common than with either single agent. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.10.006

Authors: Enriqueta Felip, Filippo G. de Braud, Michela Maur, Herbert H. Loong, Alice Tsang Shaw, Johan F. Vansteenkiste, Thomas John, PGeoffrey Liu, Martijn P. Lolkema, Giovanni Selvaggi, Vanessa Giannone, Pilar Cazorla, Jason Baum, O. Alejandro Balbin, Luojun (Victor) Wang, Yvonne Y. Lau, Jeffrey W. Scott, Daniel Shao-Weng Tan

Clinical TrialsKirk SmithOctober 18, 2019Ceritinib, Nivolumab, ALK, PD-1, NSCLC

Efficacy, safety, and biomarker analysis of ensartinib in crizotinib-resistant, ALK-positive non-small-cell lung cancer: a multicentre, phase 2 trial

Background: Ensartinib is a potent new-generation ALK inhibitor with high activity against a broad range of known crizotinib-resistant ALK mutations and CNS metastases. We aimed to assess the efficacy and safety of ensartinib in ALK-positive patients with non-small-cell lung cancer (NSCLC), in whom crizotinib therapy was unsuccessful. The associations between ensartinib efficacy and crizotinib-resistant mutations were also explored. Interpretation: Ensartinib has activity and is well tolerated in patients with crizotinib-refractory, ALK-positive NSCLC, including those with brain metastases. The role of ensartinib in patients in whom other second-generation ALK inhibitors have been unsuccessful warrants further studies. READ ARTICLE

The Lancet Respiratory Medicine DOI:10.1016/S2213-2600(19)30252-8

Authors: Yunpeng Yang, Jianya Zhou, Jianying Zhou, Jifeng Feng, Wu Zhuang, Prof Jianhua Chen, Jun Zhao, Wei Zhong, Yanqiu Zhao, Yiping Zhang, Yong Song, Yi Hu, Prof Zhuang Yu, Youling Gong, Yuan Chen, Feng Ye, Shucai Zhang, Lejie Cao, Yun Fan, Prof Gang Wu, Yubiao Guo, Chengzhi Zhou, Kewei Ma, Jian Fang, Weineng Feng, Prof Yunpeng Liu, Zhendong Zheng, Prof Gaofeng Li, Prof Ning Wu, Prof Wei Song, Xiaoqing Liu, Shijun Zhao, Lieming Ding, Prof Li Mao, Giovanni Selvaggi, Xiaobin Yuan, Yuanqing Fu, Tao Wang, Shanshan Xiao, Li Zhang

Pooled overall survival and safety data from the pivotal phase II studies (NP28673 and NP28761) of alectinib in ALK-positive non-small-cell lung cancer

Objectives: A pooled analysis of two open-label phase II studies of alectinib (NP28673 [NCT01801111] and NP28761 [NCT01871805]) demonstrated clinical activity in patients with advanced, anaplastic lymphoma kinase-positive (ALK+) non-small-cell lung cancer (NSCLC) previously treated with crizotinib. Longer-term and final pooled analyses of overall survival (OS) and safety data from the two studies are presented here. Conclusion: Updated results from this pooled analysis further demonstrate that alectinib has robust clinical activity and a manageable safety profile in patients with advanced, ALK+ NSCLC pretreated with crizotinib. READ ARTICLE

Lung Cancer DOI:10.1016/j.lungcan.2019.10.015

Authors: Sai-Hong Ignatius Ou, Shirish M. Gadgeel, Fabrice Barlesi, James Chih-Hsin Yang, Luigi De Petris, Dong-Wan Kim, Ramaswamy Govindan, Anne-Marie Dingemans, Lucio Crino, Hervé Léna, Sanjay Popat, Jin Seok Ahn, Eric Dansin, Emmanuel Mitry, Barbara Müller, Walter Bordogna, Bogdana Balas, Peter N. Morcos, Alice T. Shaw

Clinical TrialsKirk SmithOctober 14, 2019Alectinib, ALK+, NSCLC, Overall survival, Pooled analysis, Safety

Complete Pathological Response to Crizotinib in a Patient with ALK-rearranged Lung Adenocarcinoma

Gene fusions of anaplastic lymphoma kinase (ALK) are common drivers in non–small-cell lung cancer that can be effectively treated with crizotinib. READ ARTICLE

Clinical Lung Cancer DOI:10.1016/j.cllc.2019.10.002

Authors: Marissa S. Mattar, Jason Chang, Ryma Benayed, Darragh Halpenny, Astin Powers, David E. Kleiner, Alexander Drilon, Mark G. Kris

$Efficacy of Platinum/Pemetrexed Combination Chemotherapy in ALK-Positive NSCLC Refractory to Second-Generation ALK Inhibitors$

Efficacy of Platinum/Pemetrexed Combination Chemotherapy in ALK-Positive NSCLC Refractory to Second-Generation ALK Inhibitors

This was a retrospective study performed at three institutions. Patients were eligible if they had advanced ALK-positive NSCLC refractory to one or more second-generation ALK TKI(s) and had received platinum/pemetrexed-based chemotherapy. Among 58 patients eligible for this study, 37 had scans evaluable for response with measurable disease at baseline. The confirmed objective response rate to platinum/pemetrexed-based chemotherapy was 29.7% (11 of 37 patients; 95% confidence interval [CI]: 15.9% – 47.0%), with median duration of response of 6.4 months (95% CI: 1.6 months – not reached). The median progression-free survival for the entire cohort was 4.3 months (95% CI: 2.9 – 5.8 months). Progression-free survival was longer in patients who received platinum/pemetrexed in combination with an ALK TKI compared to those who received platinum/pemetrexed alone (6.8 months vs. 3.2 months, respectively; hazard ratio ¼ 0.33; p ¼ 0.025). Platinum/pemetrexed-based chemotherapy shows modest efficacy in ALK-positive NSCLC after failure of second-generation ALK TKIs. The activity may be higher if administered with an ALK TKI, suggesting a potential role for continued ALK inhibition. READ ARTICLE

Journal of Thoracic Oncology DOI: 10.1016/j.jtho.2019.10.014

Authors: Jessica J. Lin, Adam J. Schoenfeld, Viola W. Zhu, Beow Y. Yeap, ScD, Emily Chin, BA, Marguerite Rooney, BA, Andrew J. Plodkowski, Subba R. Digumarthy, Ibiayi Dagogo-Jack, Justin F. Gainor, Sai-Hong Ignatius Ou, Gregory J. Riely, Alice T. Shaw

Real-World OutcomesKirk SmithOctober 12, 2019Chemotherapy, Efficacy, ALK, non-small cell lung cancer (NSCLC)

Patient-reported outcomes from the randomized phase III ALEX study of alectinib versus crizotinib in patients with ALK-positive non-small-cell lung cancer

Objectives: Alectinib demonstrated superior efficacy and a safety profile that compared favorably with crizotinib in treatment-naïve ALK+ non-small-cell lung cancer (NSCLC) in the phase III ALEX study. We present patient-reported outcomes (PROs) from ALEX to assess disease burden, treatment-related symptom tolerability, and health-related quality of life (HRQoL) with alectinib versus crizotinib. Conclusion: PRO data support the superior efficacy and tolerability of alectinib relative to crizotinib demonstrated in the ALEX study.

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Lung Cancer DOI: 10.1016/j.lungcan.2019.10.002

AUTHORS: Maurice Pérol, Nick Pavlakis, Evgeny Levchenko, Marco Platania, Julio Oliveira, Silvia Novello, Rita Chiari, Teresa Moran, Emmanuel Mitry, Eveline Nüesch, Ting Liu, Bogdana Balas, Krzysztof Konopa, Solange Peters

Clinical TrialsKirk SmithOctober 11, 2019Alectinib, ALK-positive, Crizotinib, NSCLC, Patient-reported outcomes, ALEX

ALK immunohistochemistry positive, FISH negative NSCLC is infrequent, but associated with impaired survival following treatment with crizotinib

Objective: Metastasized non-small cell lung cancer (NSCLC) with an anaplastic lymphoma kinase (ALK) rearrangement is usually sensitive to a range of ALK-tyrosine kinase inhibitors. ALK-positive NSCLC have been identified in pivotal phase III trials with fluorescence in situ hybridization (ALK FISH+). These tumors are also expressing the fusion product (ALK immunohistochemistry (IHC)+). However, discrepant cases occur, including ALK IHC + FISH-. The aim of this study was to collect ALK IHC + cases and compare within this group response to crizotinib treatment of ALK FISH + cases with ALK FISH- cases. Conclusion: ALK IHC + FISH- NSCLC is infrequent and associated with a worse outcome on personalized treatment. A suitable predictive testing strategy may be to screen first with IHC and then confirm with FISH instead of considering ALK IHC equivalent to ALK FISH according to the current guidelines. READ ARTICLE

Lung Cancer DOI:10.1016/j.lungcan.2019.09.023

Authors: E. Thunnissen, B.I. Lissenberg-Witte, M.M. van den Heuvel, K. Monkhorst, B.G. Skov, J.B. Sørensen, A. Mellemgaard, A.M.C. Dingemans, E.J.M. Speel, A.J. de Langen, S.M.S. Hashemi, I. Bahce, M.A. van der Drift, M.G. Looijen-Salamon, J. Gosney, P.E. Postmus, S.M.S. Samii, F Duplaquet, B. Weynand, X. Durando, F. Penault-Llorca, S. Finn, A.O Grady, B. Oz, N. Akyurek, R. Buettner, J. Wolf, L. Bubendorf, S. Duin, I. Marondel, L.C. Heukamp, W. Timens, E.M.D. Schuuring, P. Pauwels, E.F. Smit

Design, synthesis and biological evaluations of 2-amino-4-(1-piperidine) pyridine derivatives as novel anti crizotinib-resistant ALK/ROS1 dual inhibitors

ALK and ROS1 kinases have become promising therapeutic targets since Crizotinib was used to treat non-small-cell lung cancer clinically. Aiming to explore new potent inhibitors, a series of 2-amino-4-(1-piperidine) pyridine derivatives that stabilized a novel DFG-shifted conformation in the kinase domain of ALK were designed and synthesized on the base of lead compound A. Biological evaluation highlighted that most of these new compounds could also potently inhibit ROS1 kinase, leading to the promising inhibitors against both ROS1 and ALK. Among them, the representative compound 2e stood out potent anti-proliferative activity against ALK-addicted H3122 and ROS1-addicted HCC78 cell lines (IC50 = 6.27 μM and 10.71 μM, respectively), which were comparable to that of Crizotinib. Moreover, 2e showed impressive enzyme activity against clinically Crizotinib-resistant ALKL1196M with an IC50 value of 41.3 nM, which was about 2-fold more potent than that of Crizotinib. 2e also showed potent inhi..... READ ARTICLE

European Journal of Medicinal Chemistry DOI:10.1016/j.ejmech.2019.06.043

Authors: Siming Liu, Ying Jiang, Ruohong Yan, Zhonghuang Li, Shanhe Wan, Tingting Zhang, Xiaoyun Wu, Ju Hou, Zhengguang Zhu, Yuanxin Tian, Jiajie Zhang

Ensartinib (X-396): what does it add for patients with ALK-rearranged NSCLC

Ensartinib is a unique, potent ALK inhibitor that has promising clinical activity and low toxicity in patients with ALK-rearranged NSCLC, most of whom had CNS metastases and had previous ALK-TKI treatment. Further study is needed to determine its role as either an initial or post-resistance therapy in ALK-rearranged NSCLC or other types of cancers. READ ARTICLE

Chinese Clinical Oncology DOI: 10.21037/cco.2018.10.12

Author: Tianhong Li, Weijie Ma, Eddie C. Tian

EditorialKirk SmithOctober 1, 2019ensartinib (X396)

P114-01 Are Pretreatment Inflammation-Based Prognostic Scores Useful in Predicting the Outcomes of Patients with ALK-Positive NSCLC?

To date, upfront treatment with ALK-tyrosine-kinase inhibitors (ALK-TKIs) has replaced chemotherapy in the first line setting for this subset of patients with excellent results, but reliable prognostic markers are lacking. An increased systemic inflammatory response has been shown to be associated with a poor prognosis, and some of the parameters used to characterize this response can easily be measured in clinical practice in several tumor types, but have not been analyzed extensively in ALK+ lung cancer in the era of crizotinib.We reviewed the medical records of all patients with previously treated advanced ALK-positive NSCLC who received crizotinib between January 2013 and March 2018 outside of a clinical trial. The study found that, in a cohort of patients with ALK positive NSCLC treated with crizotinib in routine practice, elevated pre-treatment SII was associated with shorter OS and PFS in univariate analysis and PNI was associated with shorter OS in multivariate analyses. Moreov..... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1152

Authors: O.F. Olmez, A. Bilici, P. Gursoy, E. Çubukçu, O. Yildiz, A. Sakin, T. Korkmaz, I. Cil, B. Cakar, S. Menekse, T. Demir, O. Acikgoz, J. Hamdard

P103-15 Non-Invasive Detection of Secondary Resistance Mutations in ALK-Positive NSCLC Patients by Next-Generation Sequencing

Remarkably different mutations can confer different sensitivities to different ALK inhibitors. However, 2nd and 3rd line treatment is often prescribe empirically without knowing the molecular mechanism underlying treatment failure.21 samples from ALK-positive NSCLC patients were collected at disease progression. Circulating Nucleic Acids were isolated from platelets, exosomes and plasma. Libraries were prepared using 20ng of template and Oncomine™ Pan-Cancer Cell-Free Assay. Samples were sequenced on an Ion GeneStudio S5 Plus System. Sequencing data was first analyzed using Torrent Suite software. Subsequently variant calling, annotation and filtering was performed on the Ion Reporter (v5.10) platform using the Oncomine TagSeq Pan-Cancer Liquid Biopsy w2.1 workflow. The results show that secondary ALK-TKI resistance mutations could be detected using liquid biopsies in a high proportion of patients. Non-invasive molecular profiling of samples collected at disease progression is feasible being useful for further treatment selection in ALK-positive NSCLC patients.
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Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.867

Authors: E. Sánchez Herrero, M. Barquin, V. Calvo De Juan, M. Auglyte, R. Garcia Campelo, J.M. Sánchez, M. Domine, B. Massuti, E. Jantus, C. Camps, N. Reguart, M. Provencio, A. Romero

Conference PaperKirk SmithOctober 1, 2019ctDNA, liquid biopsy, ALK

P101-129 Preclinical Genetic Evaluation of Alternating ALK TKI Therapy Versus Continuous Dosing in ALK NSCLC to Inform the ALKternate Clinical Trial

In a many patients the underlying cause of drug resistance is unexplained. ALKternate is a clinical trial recruiting pre-treated patients, testing the hypothesis that with fixed alternating TKI therapy, the emergence of ALK resistant clones can be suppressed through applying variable selection pressure compared to continuous treatment with a TKI. This has been tested pre-clinically with a human cell line to complement the clinical trial in progress, ALKternate.In keeping with the hypothesis, the genetic profiles identified demonstrate the emergence of different clones over time and between treatment strategies. This supports further investigation into the novel strategy of alternating therapy as planned in the ALKternate trial.
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Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.844

Authors: M. Itchins, A. Hudson, S. Hayes, R. Harvie, G.H. Wei, M. Buckland, S. Clarke, V. Howell, N. Pavlakis

Conference PaperKirk SmithOctober 1, 2019NSCLC, ALK, genetic, ALKernate

P101-93 Metastases Sites as a Prognostic Factor in a Real-World Multicenter Cohort Study of Spanish ALK-Positive NSCLC Patients (p)

To date, published real-world data on the prognostic factors of patients with ALK-positive advanced NSCLC in Spain are limited. We aim to evaluate the effect of number of metastases (M1) organs on overall survival (OS) in a multicenter cohort of Spanish ALK-positive NSCLC p diagnosed between 2008 and 2017. We included p with stage IV at diagnosis since 2011 to April 2018. OS was worse with increased metastatic sites involved at diagnosis in p with ALK positive NSCLC, being liver M1 associated with the highest risk of mortality. Brain metastases at diagnosis were not a prognostic factor for OS in our series. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.808

Authors: L. Angelats, R. Garcia Campelo, R. Bernabe, E. Arriola, P. Rocha, V. Calvo De Juan, E. Sais, A. Barba, N. Viñolas, M. Gil Moreno, L. Vilà, O. Juan, N. Vilariño, M. Cobo, M. Domine, S. Vazquez, J. Coves, R. Marse-Fabregat, A.M. Esteve Gomez, E. Carcereny

Conference PaperKirk SmithOctober 1, 2019Metastases sites, Prognostic factor, ALK-positive NSCLC