Posts in Conference Paper
The Humanistic Burden of ALK+ NSCLC: Findings from the ALKConnect Patient Insight Network and Research Platform
The Humanistic Burden of ALK+ NSCLC: Findings from the ALKConnect Patient Insight Network and Research Platform

The ALKConnect Patient Insight Network (www.alkconnect.com) is a patient-centered online registry that provides support to and collects information from patients living with Anaplastic Lymphoma Kinase-Positive (ALK+) Non-Small Cell Lung Cancer (NSCLC). The objectives of this study were to: (1) describe the characteristics of patients in ALKConnect; (2) quantify patients’ preferences, ALK+ NSCLC symptom burden, and health-related quality of life (HRQoL); and (3) determine whether disease treatment and employment status were associated with HRQoL.ALKConnect gathered humanistic burden data directly from patients with ALK+ NSCLC. Participants reported that the most burdensome symptoms were fatigue, sleep disturbance, and drowsiness, and that symptoms interfered most with work and general activity. A 3-month delay in cancer progression and HRQoL were important treatment attributes. Patients’ HRQoL was positively associated with ALK TKI treatment and the ability to maintain employment status, suggesting that these aspects may be important for ALK+ NSCLC patients’ well-being. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1254

Authors: H. Lin, X. Pan, A. Biller, K. Covey, H. Huang, V. Rangel Miller, M. Smith, H. West

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Conference PaperKirk Smithhumanistic burden, Health-related quality of life, Anaplastic Lymphoma Kinase-Positive Non-Small Cell Lung Cancer
P114-57 Post-Ensartinib Outcomes in Refractory Anaplastic Lymphoma Kinase (ALK)-Rearranged Non-Small Cell Lung Cancer (NSCLC)
P114-57 Post-Ensartinib Outcomes in Refractory Anaplastic Lymphoma Kinase (ALK)-Rearranged Non-Small Cell Lung Cancer (NSCLC)

With the advent of novel ALK inhibitors utilized in sequence, the survival of patients with ALK-rearranged tumors has improved dramatically. This case series serves to compare tumor response rates and long-term survival outcomes among four patients treated with ensartinib over the course of four years at our institution.We found that ensartinib is well tolerated and has clinical activity in advanced ALK-rearranged NSCLC patients with brain metastases, despite previously progressing on crizotinib, with durable post-ensartinib survival on subsequent next-generation ALK inhibitors such as brigatinib and lorlatinib. READ ARTICLE

Journal of Thoracic Oncology DOI:10.5455/jpma.3142. PMID: 32296229.

Authors: H. Kim, P. Vu, K. Harrow, C. Liang, G. Selvaggi, E. Weihe, W. Mitchell, L. Bazhenova, S. Patel

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Conference PaperKirk SmithNSCLC, ALK, ensartinib
Safety and efficacy of WX-0593 in ALK-positive or ROS1-positive non-small cell lung cancer
Safety and efficacy of WX-0593 in ALK-positive or ROS1-positive non-small cell lung cancer

WX-0593 is a potent ALK inhibitor against ALK and ROS1 rearrangement and a series of crizotinib (CRZ)-resistant mutants. We explored the safety and efficacy of WX-0593 in patients (pts) diagnosed with ALK+ or ROS-1+ malignancies, including non-small cell lung cancer (NSCLC). READ ARTICLE

Annals of Oncology DOI:https://doi.org/10.1093/annonc/mdz260.007

Authors: Y-K Shi, J. Fang, S. Zhang, Y. Liu, L. Wang, M. Si, M. Ge and H Geng

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Conference PaperKirk SmithWX-0593, ALK+, ROS1, clinical trial
P114-53 Co-Occurring CDKN2A/2B Alteration Is Associated with Poorer Survival in ALK-Positive Lung Cancer
P114-53 Co-Occurring CDKN2A/2B Alteration Is Associated with Poorer Survival in ALK-Positive Lung Cancer

We analyzed whether variants or co-occurring mutations influence the outcome of AKL TKI treatment in ALK+ non-small-cell lung cancer (NSCLC). Between March 2017 and October 2018, 489 NSCLC tumor specimens were examined with OncoPanel AMC version3 which is a NGS based assay for the detection of single-nucleotide variants, insertions, deletions, copy number alterations and structural variants across 382 genes. 43 patients were identified as having ALK rearrangement. And 37 patients received ALK TKI treatment. Progression free survival (PFS) and overall survival (OS) were analyzed respectively according to ALK variants and other co-occuring mutations. We found that in ALK+ NSCLC, having co-occurring CDKN2A/2B alteration was associated with a poorer OS when treated with an anti-ALK agent. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1204

Authors: J.Y. Ha, S. Yoon, D.H. Lee, J. Choi, S. Kim

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Conference PaperKirk SmithALK, CDKN2A/2B, TKI
P114-39 Acquired ALK Rearrangement in EGFR-Mutant Lung Adenocarcinoma Treated with EGFR TKIs
P114-39 Acquired ALK Rearrangement in EGFR-Mutant Lung Adenocarcinoma Treated with EGFR TKIs

Few studies have been reported on acquired anaplastic lymphoma kinase (ALK) rearrangement in epidermal growth factor receptor (EGFR)-mutant lung adenocarcinoma patients with EGFR tyrosine kinase inhibitors (TKIs).EGFR-mutant lung adenocarcinoma patients were screened after resistance to EGFR TKIs from September 2017 to December 2018 at the Guangdong Lung Cancer Institute. Both EGFR mutation and ALK rearrangement were tested by next-generation sequencing (NGS). Acquired ALK rearrangement was defined as positive ALK rearrangement after resistance to EGFR TKIs, but negative result detected by NGS at the baseline of EGFR TKI treatments.The frequency of acquired ALK rearrangement is similar in EGFR-mutant lung adenocarcinomas after resistance to the first-, second-, or third-generation EGFR TKIs. The majority of acquired ALK-fusion partners are non-EML4. Combination of EGFR TKIs and ALK inhibitors might be a strategy to overcome such resistance. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1190

Authors: Q. Wang, R. Chen, J. Kang, H. Chen, B. Wang, Z. Wang, Q. Zhou, Y. Wu, J. Yang

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Conference PaperKirk Smithlung adenocarcinoma, ALK rearrangement, EGFR
P114-35 Epithelial-To-Mesenchymal Transition Is a Mechanism of ALK Inhibitor Resistance in Lung Cancer Independent of ALK Mutation Status
P114-35 Epithelial-To-Mesenchymal Transition Is a Mechanism of ALK Inhibitor Resistance in Lung Cancer Independent of ALK Mutation Status

ALK rearrangement, most commonly EML4-ALK, is detected in approximately 3%–5% of NSCLC. ALK tyrosine kinase inhibitor (TKI), shows dramatic clinical efficacy, however, almost all patients acquire resistance over time. The most defined mechanism of crizotinib resistance is secondary ALK mutations. A recent study reported that epithelial-to-mesenchymal transition (EMT) and ALK resistance mutation were simultaneously detected in a single tumor lesion in patients with ALK-rearranged lung cancer who were resistant to ALK-TKIs. However, it is still unknown whether ALK-TKI resistant tumor cells combine mesenchymal phenotype with ALK resistance mutation, or each of the mesenchymal type tumor cells and ALK resistance mutation–positive cells coexist in a single lesion. In any of these cases, no therapy for EMT-associated targeted drug resistance has yet been established. Specimens from a patient with ALK-rearranged lung adenocarcinoma who acquired resistance to crizotinib were stained with IHC, ..... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1186

Authors: K. Fukuda, S. Takeuchi, S. Arai, S. Nanjo, R. Katayama, K. Takeuchi, M. Nishio, S. Yano

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Conference PaperKirk SmithEpithelial-mesenchymal-transition (EMT), Anaplastic lymphoma kinase(ALK), resistance
P114-32 Rash and Efficacy in Anaplastic Lymphoma Kinase Positive (ALK+) Non-Small Cell Lung Cancer Patients Treated with Ensartinib
P114-32 Rash and Efficacy in Anaplastic Lymphoma Kinase Positive (ALK+) Non-Small Cell Lung Cancer Patients Treated with Ensartinib

In a phase 1/2 study, ensartinib was generally well tolerated and demonstrated good clinical activity in pts with ALK+ non-small cell lung cancer (NSCLC). This post hoc analysis sought to determine the relationship between ensartinib-related rash and clinical benefit. The study found that ensartinib was associated with mild to moderate rash that was easily managed. Preliminary findings suggest that rash is potentially associated with better clinical benefit with ensartinib. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1183

Authors: H. Wakelee, K. Reckamp, T. Leal, A. Chiappori, S. Waqar, K. Zeman, J. Neal, C. Liang, K. Harrow, A. Holzhausen, J. Zhou, G. Selvaggi, L. Horn

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Conference PaperKirk SmithALK, rash, clinical benefit, ensartinib
Is there any prognostic significance in pleural involvement and/or effusion (Ple-I/E) in patients with ALK-positive NSCLC?
Is there any prognostic significance in pleural involvement and/or effusion (Ple-I/E) in patients with ALK-positive NSCLC?

Conclusions: Brain, liver and bone metastases are lower in ALKþpatients with Ple-I/E. Presentation with Ple-I/E in patients with ALKþ NSCLC is associated with longer overall and progression-free survival. Background: ALK mutation occurs in approximately 3-5% of patients with NSCLC. At the baseline, Ple-I/E are more frequent in ALKþ patients with NSCLC. In the study, we aimed to evaluate characteristics of ALKþpatients who have Ple-I/E. Methods: In this multicenter study, patients with ALKþ NSCLC who have Ple-I/E were retrospectively analyzed. Clinical and demographic characteristics of the disease, response rates, median PFS and OS were evaluated in 362 ALKþpatients with NSCLC. Results: Of the patients, 198 (54.7%) were male. The median age at the time of diagnosis was 54 (21-85) years. The median age was higher in male (57 vs 52 years; p¼0.011). The most common histology was adenocarcinoma (100%). At the baseline, 57 (15.7%) patients had Ple-I/E. The median age of patients with Ple-I/..... READ ARTICLE

Annals of Oncology DOI:10.1093/annonc/mdz260

Authors: Kılıçkap, Saadettin; Buğdaycı Basal, Fatma; Demirkazık, Ahmet; Gürsoy, Pınar; Demirci, Ufuk; Erman, Mustafa; Yumuk, Fulden; Çay Şenler, Filiz; Çakar, Burcu; Çiçin, İrfan; Öztürk, Akın; Coşkun, Hasan Şenol; Çubukçu, Erdem; Işıkdoğan, Abdurrahman; Ölmez, Ömer Fatih; Tatlı, Ali Murat; Karaağaç, Mehmet Onur; Sakalar, Teoman; Eralp, Yeşim; Korkmaz, Taner

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Conference PaperKirk SmithPleural involvement, effusion (Ple-I/E), ALK-positive NSCLC
P114-26 ALK Fusion Variant Detection by Targeted RNA-Seq in TKIs Treated ALK-Positive Lung Adenocarcinoma
P114-26 ALK Fusion Variant Detection by Targeted RNA-Seq in TKIs Treated ALK-Positive Lung Adenocarcinoma

We retrospectively characterized fusion variant distribution in a cohort of ALK+ lung adenocarcinomas (ADC) with paired clinical data about treatments and outcomes.Diagnostic tumor tissue from advanced ALK+ (by FISH and/or IHC) ADC diagnosed from 2010 to 2018 and treated with single or multiple ALKis were collected (expanded cohort from Gobbini et al. Lung Cancer, 2017). The OncomineTM Solid Tumor Fusion Transcript Kit on an Ion PGM™ system and the Ion Reporter™ software were used to identify targeted ALK fusion gene products (ThermoFisher).Our analysis suggests that different ALK fusion variant might affect ALKi treatment duration in ALK+ lung ADC READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1177

Authors: F. Tabbò, E. Gobbini, L. Muscarella, A. Rigutto, D. Trombetta, A. Bonfitto, D. Galetta, E. Maiello, O. Martelli, M. Tiseo, P. Bordi, V. Scotti, L. Ghilardi, V. Gregorc, C. Sergi, S. Pilotto, A. Del, Conte, F. Cappuzzo, D. Cortinovis, G. Osman, C. Bareggi, M. Di Maio, A. Rossi, G. Rossi, E. Bria, M. Volante, G. Scagliotti, P. Graziano, S. Novello, L. Righi

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Conference PaperKirk SmithALK, ALK inhibitor, Fusion variant
P114-18 ALK Inhibitor Sequencing and Outcomes Among ALK-Positive (ALK+) NSCLC Patients in the US Community Oncology Setting
P114-18 ALK Inhibitor Sequencing and Outcomes Among ALK-Positive (ALK+) NSCLC Patients in the US Community Oncology Setting

A retrospective observational cohort study of patients with ALK+ NSCLC treated with 1st generation (crizotinib) and 2nd generation (alectinib, brigatinib, ceritinib) ALK inhibitors from 1 September 2011 to 31 December 2017. Structured data were obtained via programmatic extraction from the iKnowMed EHR database of the US Oncology Network. Patient demographics and treatment sequences were characterized. Index was the start date of the first ALK. Duration of therapy (DOT) from index to end of the last ALK, and overall survival (OS) were assessed using the Kaplan-Meier method. Patients received a range of 1 to 4 ALK inhibitors. Crizotinib-led sequences were most common, likely reflecting the approval history of ALK inhibitors during the study period. Longer DOT and OS were observed in patients receiving multiple ALK inhibitors. This study provides an initial view of treatment patterns following the emergence of new ALK inhibitors and suggests feasibility of sequential ALK therapies. Follo..... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1169

Authors: D. Waterhouse, J. Espirito, M. Chioda, B. Baidoo, J. Mardekian, N. Robert, E. Masters

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Conference PaperKirk SmithALK-inhibitor, treatment-sequence, NSCLC
P114-15 Lorlatinib in ALK- or ROS1-Positive Non-Small Cell Lung Cancer Patients: Experience from an Early Access Program in Turkey
P114-15 Lorlatinib in ALK- or ROS1-Positive Non-Small Cell Lung Cancer Patients: Experience from an Early Access Program in Turkey

The aim of this study is to evaluate the efficacy and safety of lorlatinib in an Expanded Access Program (EAP) in Turkey.The EAP was open-label, multicenter, and single-arm. Patients were eligible to receive lorlatinib (100 mg p.o/day) if they had advanced stage ALK- or ROS1-positive NSCLC and had progressed on crizotinib and/or second generation ALK inhibitors such as ceritinib or alectinib. The primary endpoint was PFS with lorlatinib. Secondary endpoints were objective response rate, overall survival, and safety. In this EAP, lorlatinib showed systemic activity in patients with advanced ALK+ or ROS1+ NSCLC, regardless of CNS metastases and previous TKI treatment. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1166

Authors: S. Kilickap, U. Demirci, F. Bugdayci, D. Tural, T. Korkmaz, S. Paydas, C. Yilmaz, H. Turna, A. Sezer, H. Yesil Cinkir, K. Okutur, M. Erman, Y. Eralp, D. Cabuk, A. Isikdogan, A. Demirkazik, A. Karaoglu, D. Yazilitas, F. Cay Senler, P.F. Yumuk, H. Coskun, I. Yildiz, I. Oztop, I. Beypinar, K. Aydin, M. Kaplan, N. Meydan, O.F. Olmez, O. Ozyilkan, S. Seber, C. Arslan, M.A. Sendur, I. Cicin

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Conference PaperKirk SmithALK positive, ROS1 positive, Lorlatinib, Turkey, Advanced stage lung cancer
P114-09 Unveiling Hidden MET-Mediated Primary Alectinib Resistance in ALK-Positive Non-Small Cell Lung Cancer
P114-09 Unveiling Hidden MET-Mediated Primary Alectinib Resistance in ALK-Positive Non-Small Cell Lung Cancer

More recently, alectinib has superseded crizotinib, an ALK/ROS1/MET inhibitor, as a first-line therapy due to its superiority in phase III trials. Although patients enjoy durable responses to alectinib, they eventually develop resistance. Here we describe four cases of primary resistance to alectinib in which the patients show little to no response to alectinib when administered as first or second-line therapy. In order to investigate primary resistance to alectinib, tissue was obtained during re-biopsy and subjected to routine clinical genetic analyses including gene fusion detection and genetic mutation analysis using the Archer FusionPlex and VariantPlex assays, respectively. Concurrently, at the time of biopsy, additional fresh tissue was procured for cell line derivation. The primary cell line was then used to assess ALK and other inhibitors’ potency by cell viability assays. Targeted analysis of signaling pathways was performed in the cell lines via western blot analysis and prox..... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1160

Authors: A. Le, L. Tyler, K. Davies, K. Kondo, J. Pacheco, D. Merrick, D. Aisner, D.R. Camidge, R. Doebele

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Conference PaperKirk SmithALK, MET, alectinib
2-Deoxy-D-Glucose Sensitizes Non-Small Cell Lung Cancer with EML4-ALK Fusion to Crizotinib via Suppression of HK2 Through AKT/mTOR Passway
2-Deoxy-D-Glucose Sensitizes Non-Small Cell Lung Cancer with EML4-ALK Fusion to Crizotinib via Suppression of HK2 Through AKT/mTOR Passway

Background: ALK-positive NSCLC cells (ALK+ NSCLC) present high glycolysis. Targeting cancer cell metabolism with the glycolysis inhibitor, 2-deoxyglucose (2DG), is a viable strategy that sensitizes the fist-line ALK-TKI crizotinib; but the effects of combination of 2DG and Crizotinib on ALK+ NSCLC cells and the mechanism of action are unknown. Conclusion: This study demonstrated that 2DG would be a promising drugs to sensitize crizotinib via suppressing HK2 expression to inhibit the activity of AKT/mTOR signaling pathway induced by ALK phosphorylation. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1820

Authors: EML4-ALK, crizotinib, high glycolysis

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Conference PaperKirk SmithEML4-ALK, crizotinib, high glycolysis
Osimertinib Overcomes Alectinib Resistance Caused by Amphiregulin in a Leptomeningeal Carcinomatosis Model of EML4-ALK Lung Cancer
Osimertinib Overcomes Alectinib Resistance Caused by Amphiregulin in a Leptomeningeal Carcinomatosis Model of EML4-ALK Lung Cancer

Background: Central nervous system (CNS) metastasis, such as brain metastasis and leptomeningeal carcinomatosis (LMC), occurs in 20–40% of all patients with cancer. Anaplastic lymphoma kinase (ALK) is a clinically validated drug target and ALK rearrangements are found in approximately 3-5% of non-small cell lung cancer (NSCLC). ALK tyrosine kinase inhibitor (TKI) shows dramatic clinical efficacy in ALK-rearranged NSCLC patients, and the second-generation ALK-TKI alectinib is effective against CNS metastasis of ALK-rearranged NSCLC. However, the patients with ALK-rearrangement acquire resistance to alectinib over time and develop recurrent LMC metastasis. This study aimed to clarify the mechanism of resistance to alectinib in LMC and seek a novel therapeutic strategy. Conclusion: We demonstrated that EML4-ALK lung cancer cells acquired moderate resistance to alectinib in the leptomeningeal space due to amphiregulin-triggered EGFR activation. Moreover, combined use of alectinib and EGFR..... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1841

Authors: S. Arai, S. Takeuchi, K. Fukuda, A. Nishiyama, A. Tanimoto, H. Taniguchi, M. Satouchi, S. Nanjo, R. Katayama, M. Nishio, M. Zheng, Y. Wu, S. Yano

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Conference PaperKirk SmithLeptomeningeal carcinomatosis, alectinib resistance, Osimertinib
P114-07 Genomic Profiling of Liquid Biopsies During 2nd/3rd Generation ALK Inhibitor Therapy to Identify Novel Mechanisms of Resistance
P114-07 Genomic Profiling of Liquid Biopsies During 2nd/3rd Generation ALK Inhibitor Therapy to Identify Novel Mechanisms of Resistance

Second- and third-generation ALK inhibitors each have diverse mechanisms of resistance. Only a fraction of resistance is due to secondary mutations of the ALK gene. Altered bypass tracts are likely the case in some other instances. Genomic alterations of other genes and pathways may be a third mechanism of resistance. Repeat liquid biopsies during the course of patients’ treatments can provide a minimally invasive method for sampling cancer-specific genomic information that leads to improved treatment selection. In the Lung Cancer Clinic of the Princess Margaret Cancer Centre, serial plasma samples were collected from six lung cancer patients with ALK rearrangement at multiple serial clinic visits pre- and post- progression on next-generation ALK inhibitors. We focused on next generation agents, as there has been previous focus on crizotinib resistance mechanisms already.The study found that broad panel-based NGS of plasma cfDNA enabled noninvasive detection of systemic (but not CNS-pr..... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1158

Authors: E. Stewart, A. Wang, J. Huang, H. Bao, X. Wu, D. Patel, Z. Chen, J. Law, P. Bradbury, F. Shepherd, A. Sacher, M. Tsao, S. Bratman, N. Leighl, T. Pugh, G. Liu

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Conference PaperKirk SmithNGS, plasma, cfDNA, ALK, resistance, Genomic alterations, liquid biopsy
EML4-ALK Fusion Subtype Is Associated with Therapeutic Efficacy in Advanced Non-Small Cell Lung Cancer
EML4-ALK Fusion Subtype Is Associated with Therapeutic Efficacy in Advanced Non-Small Cell Lung Cancer

Background: The aim of this study was to investigate the molecular characteristics of each subtype of the EML4-ALK fusion gene and to evaluate the efficacy of first-line crizotinib or pemetrexed in combination with platinum in the treatment of patients with advanced NSL4-ALK fusion subtypes of advanced NSCLC. Conclusion: Among all ALK fusion subtypes, E13:A20 subtype (V1 variants) is the most common. Smoking history was a factor affecting crizotinib PFS. Compared with chemotherapy, patients with E20:A20 subtype (V2 variant) showed significant benefit with crizotinib. The median PFS of the pemetrexed combined with platinum regimen was lower than that of the E13:A20 subtype. READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1830

Authors: H. Wang, H. Li, J. Ma, X. Yan, P. Li, M. Zhang, X. Zhang, G. Zhang, Z. Ma

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Conference PaperKirk SmithEML4-ALK fusion gene, Non-Small Cell Lung Cancer, Variant
Exosomal Analysis of ALK Rearrangements by Spin Column with Porous Glass Filter
Exosomal Analysis of ALK Rearrangements by Spin Column with Porous Glass Filter

Background: ALK rearrangements account for about 3-5% of non-small cell lung cancer (NSCLC). ALK-tyrosin kinase inhibitors (TKI) demonstrated robust efficacy compared with cytotoxic chemotherapy in patients with ALK alterations detected in the tumor tissues. Identifying ALK rearrangement was performed using tissue samples, which are not always available. The spin column with porous glass filter has been developed by Nagoya university and AGC Inc, resulting in highly efficient and easy to use exosome isolation. The exosomes contain various molecules of their cell of origin, including proteins and RNA. The purpose of this study was to explore the spin column to capture exosome and detect ALK alterations in exosomal RNA from blood. Conclusion: Exosome remains relatively stable in the blood, making it an attractive target for liquid biopsy. Our preliminary results showed potential capability in the detection of ALK alteration in exosomes from blood. These findings require confirmation in ..... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.1434

Authors: T. Hatta, T. Hase, N. Ozawa, N. Yogo, H. Yukawa, H. Tanaka, D. Onoshima, M. Sato, M. Hori, Y. Baba, Y. Hasegawa

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Conference PaperKirk SmithExosome, ALK, Non-Small Cell Lung Cancer, technique
EP103-32 Prevalence of EGFR and ALK Mutations in Non Small Cell Lung Cancer in Viet Nam National Cancer Hospital
EP103-32 Prevalence of EGFR and ALK Mutations in Non Small Cell Lung Cancer in Viet Nam National Cancer Hospital

The prospective study of formalin fixed paraffin embedded (FFPE) tissues from patients diagnosed with NSCLC was performed to assess the prevalence of EGFR and ALK mutations in NSCLC in Viet Nam National Cancer Hospital. Patients with NSCLC in Viet Nam National Cancer Hospital were prospectively enrolled. FFPE tissue samples were tested for EGFR mutation by PCR and for EML4-ALK translocation by fluorescence in situ hybridization (FISH). In this sudy investigating the prevalence of EGFR and ALK mutations in non small cell lung cancer in Vietnam National Cancer Hospital, 26.2% had EGFR mutation and 10.7% had ALK translocation mutations, as compared to 35% and 6.1%, respectively, in Asian READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.2113

Authors: V. Dang

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Conference PaperKirk SmithThe prospective study of formalin fixed paraffin embedded (FFPE) tissues from patients diagnosed with NSCLC was performed to assess the prevalence of EGFR and ALK mutations in NSCLC in Viet Nam National Cancer Hospital. Patients with NSCLC in Viet Nam National Cancer Hospital were prospectively enrolled. FFPE tissue samples were tested for EGFR mutation by PCR and for EML4-ALK translocation by fluorescence in situ hybridization (FISH). In this sudy investigating the prevalence of EGFR and ALK mutations in non small cell lung cancer in Vietnam National Cancer Hospital, 26.2% had EGFR mutation and 10.7% had ALK translocation mutations, as compared to 35% and 6.1%, respectively, in Asian READ ARTICLEJournal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.2113Authors: V. Dang
EP101-62 The Safety Profile and Preliminary Efficacy of Ceritinib 450mg with Food in Chinese ALK/ROS-1 Positive NSCLC Patients
EP101-62 The Safety Profile and Preliminary Efficacy of Ceritinib 450mg with Food in Chinese ALK/ROS-1 Positive NSCLC Patients

Ceritinib have shown potent efficacy in both ALK and ROS-1 rearranged NSCLC. However, high rate of treatment interruption was suffered due to gastrointestinal or liver toxicity using Ceritinib 750mg fasting in previous study. Recently, ASCEND-8 study reported an improved tolerance and a trend to better efficacy with 450mg with food, but little data is available in Chinese patients. This first-time real-world study aims to assess the safety profile and preliminary efficacy of Ceritinib 450mg with food in Chinese patients. From Oct 2018 to March 2019, 51 ALK or ROS1 positive NSCLC patients received ceritinib were enrolled from 8 centers in Sichuan province. Safety profile and preliminary efficacy were retrospectively analyzed. The follow-up was to 31st March 2019. The study found Ceritinib 450mg with food demonstrated a good safety profile and efficacy with lower AE incidence rate and better compliance rate compare to ASCEND-8 data for Chinese patients in real-world setting...... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.2035

Authors: Y. Tian, P. Yu, X. Yin, K. Wang, M. Huang, Y. Wang, Y. Gong, J. Li

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Conference PaperKirk SmithCeritinib, non-small-cell lung cancer, Safety
EP101-56 Co-Presentation of Adenocarcinoma and Squamous Cell Lung Carcinoma Harbouring ALK Rearrangement in Different Sites
EP101-56 Co-Presentation of Adenocarcinoma and Squamous Cell Lung Carcinoma Harbouring ALK Rearrangement in Different Sites

We describe an unique case of co-presentation of ADC and SCC in two different disease sites, both harbouring ALK rearrangement. A 57-year-old male never smoker presented with a left adrenal mass. CT Scan showed a right superior lobe mass, bilateral pulmonary nodules (Fig. 1 A), and bone metastases. The lung biopsy documented ADC with moderate differentiation and ALK rearrangement by fluorescence in situ hybridization (FISH) and immunohistochemistry (IHC). The patient was treated with Crizotinib but, after 4 months, the CT showed a near complete response of the pulmonary disease (Fig. 1 B), while a progression of the left adrenal metastasis was observed. (Fig. 2 A, Fig. 2B). A left adrenal biopsy showed a SCC histology, with ALK rearrangement confirmed both by IHC and FISH. The treatment was switched to alectinib without respoinse so the patient received chemotherapy. The absence of an initial biopsy of the adrenal mass doesn't allow to distinguish between a lung ADC to SCC transdiffere..... READ ARTICLE

Journal of Thoracic Oncology DOI:10.1016/j.jtho.2019.08.2028

Authors: V. Longo, A. Catino, D. Galetta, G. Del Bene, R. Lacalamita, M. Montrone, F. Pesola, D. Petriella, P. Pizzutilo, S. Tommasi

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Conference PaperKirk SmithADC, SCC, ALK rearrangement