Annual Meeting Proceedings Part 1 - American Society of Clinical ...

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486s Lung Cancer—Non-small Cell Metastatic 7524 Poster Discussion Session (Board #14), Tue, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Chemotherapy with erlotinib or chemotherapy alone in advanced NSCLC with acquired resistance to EGFR tyrosine kinase inhibitors (TKI). Presenting Author: Sarah B. Goldberg, Massachusetts General Hospital Cancer Center, Boston, MA Background: EGFR-mutant NSCLC has an oncogene-addicted phenotype that confers sensitivity to EGFR TKIs. Prior data suggests EGFR addiction persists after development of TKI resistance, leading many clinicians to continue TKI along with chemotherapy (chemo); however, this strategy has not been formally evaluated. Methods: An institutional database was reviewed to identify patients (pts) with advanced NSCLC and acquired resistance to EGFR TKIs by Jackman criteria. Pts were included if they subsequently received chemo. Objective response rate (RR) to chemo/ erlotinib or chemo alone was assessed by blinded radiographic review and compared by Fisher’s exact test and multivariable logistic regression. Progression-free survival (PFS) and overall survival (OS) from TKI failure (defined as chemo initiation date) were compared by log-rank test and multivariable Cox analysis. Results: 78 pts were eligible (34 chemo/ erlotinib, 44 chemo alone). 70 pts (90%) had a documented EGFR mutation and were on TKI for a median of 15 months (range 4-51); in the 8 pts with unknown genotype the median duration on TKI was 11 months (range 5-16). Baseline characteristics were well balanced except more pts received erlotinib as initial TKI in the chemo/erlotinib group. RR was evaluable in 57 pts and was higher with chemo/erlotinib compared to chemo alone (41% vs 18%; OR 0.31, 95% CI 0.09, 1.04; p�0.08). RR adjusted for chemo regimen and time to TKI failure yielded OR 0.20 (95% CI 0.05, 0.78; p�0.02), favoring chemo/erlotinib. Median PFS was 4.4 months in the chemo/erlotinib group and 4.2 months in the chemo alone group (crude HR�0.84, 95% CI 0.52, 1.38; p�0.50; adjusted HR 0.79, 95% CI 0.48, 1.29; p�0.34). There was no significant difference in OS in the crude or adjusted analyses. Conclusions: This is the first study, to our knowledge, to show that continuation of an EGFR TKI with chemo compared to chemo alone significantly increases the RR in pts with advanced NSCLC and acquired TKI resistance, though we did not observe an impact on PFS or OS. Continued concurrent TKI may be a valuable strategy, particularly for pts with symptomatic progression, when a higher response rate may be beneficial. Further study is warranted. 7526 Poster Discussion Session (Board #16), Tue, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Continuation of EGFR/ALK inhibition after local therapy of oligoprogressive disease in EGFR mutant (Mt) and ALK� non-small cell lung cancer (NSCLC). Presenting Author: Andrew James Weickhardt, University of Colorado Cancer Center, Denver, CO Background: This study aimed to investigate the benefits of local treatment of limited disease progression and continuation of crizotinib (C) or EGFR-TKI in patients with ALK� or EGFR-Mt metastatic NSCLC, respectively. Methods: Patients with advanced ALK� NSCLC treated with C (n�38) and EGFR-Mt NSCLC treated with EGFR TKIs (erlotinib or gefitinib) (n�27) were identified. Patients were evaluated for initial response, site of first progression (CNS or extra CNS (eCNS)) and median progression free survival (PFS1). A subset of patients with limited sites of progression (oligoprogressive disease) suitable for local therapy received either radiation or surgery to these sites and continued on the same TKI. The subsequent pattern of progression and median progression free survival from the time of first progression (PFS2) were recorded. Results: In 38 ALK� patients, PFS1�9.0 months on C. In 27 EGFR-Mt patients, PFS1�13.8 months on EGFR-TKI. CNS was the first site of progression in 13/28 (46%) of ALK� patients and 5/23 (22%) EGFR-Mt patients. 25 of 51 patients who progressed (49%) were deemed suitable for local therapy (15 ALK�, 10 EGFR-Mt; 24 with radiotherapy (Body: 3 XRT, 9 SBRT; CNS: 7 WBRT, 5 SRS), 1 with surgery (adrenalectomy)) and continuation of the same targeted therapy. 19/25 patients progressed post local therapy, median PFS2 � 6.2 months. In patients who progressed at PFS1 only in the CNS, there was a trend to longer PFS2 than patients who progressed at PFS1 in eCNS (7.1 months vs 4.0 months, p�0.26). 60% who progressed only in the CNS at PFS1, progressed eCNS at PFS2 (n�10). Conclusions: Progression of oncogene addicted NSCLC on relevant targeted therapies is often suitable for local therapy (oligoprogressive disease). Continuation of the targeted therapy following local therapy is associated with �6 months of additional disease control. Sites of first progression and median PFS1 and PFS2 in patients continuing TKI after local therapy of oligoprogressive disease. Site of progression Number of patients PFS1 (months) PFS2 (months) CNS 1st site of prog. 10 10.9 7.1 eCNS 1st site of prog. 15 9.6 4.0 All patients 25 10.0 6.2 * Includes 3 patients who prog. eCNS and CNS at PFS1. 7525 Poster Discussion Session (Board #15), Tue, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Response to EGFR tyrosine kinase inhibitor (TKI) retreatment after a drug-free interval in EGFR-mutant advanced non-small cell lung cancer (NSCLC) with acquired resistance. Presenting Author: Stephanie Heon, Dana-Farber Cancer Institute, Boston, MA Background: Patients (pts) with advanced NSCLC and sensitizing EGFR mutations who initially respond to gefitinib or erlotinib eventually develop acquired resistance to the TKIs. Anecdotal and retrospective reports suggest that EGFR-TKI resistant cancers can respond again to gefitinib or erlotinib after an interval off the TKI. This retrospective study was undertaken to investigate the impact of EGFR-TKI retreatment after a drug-free interval in EGFR mutant NSCLC with acquired resistance to gefitinib or erlotinib. Methods: Pts with stage IV or relapsed NSCLC with sensitizing EGFR mutations and acquired resistance to EGFR-TKI seen at the DFCI/MGH between 8/00 and 8/11 who were retreated with single agent gefitinib or erlotinib after an EGFR-TKI-free interval were identified from a prospective trial. The objective tumor response (CR, PR, SD, PD) was determined using RECIST 1.1. Results: 19 pts were eligible and had adequate scans for radiographic assessments after the reinstitution of an EGFR-TKI. The response rate and median PFS to the initial course of gefitinib (n�4) or erlotinib (n�15) were 16/19 (84%) and 9.8 months (95% CI, 7.8-11.3) respectively. All pts were retreated with erlotinib after 1 to 4 intervening systemic regimens. The median interval from EGFR-TKI discontinuation to erlotinib retreatment was 11 months (range, 2-46). 4 of the 19 pts (21%) had PD as the best response to erlotinib retreatment, 14 (74%) had SD for at least 1 month, and 1 (5%) had a PR. The median PFS was 4.4 months (95% CI, 3.0-6.7). 3 pts remained on erlotinib without progression for 6 months. 3 pts had their tumors rebiopsied before (n�2) or during (n�1) erlotinib retreatment; 1 of the 3 had EGFR T790M in association with the initial sensitizing EGFR mutation, and another had a secondary PIK3CA mutation. Conclusions: Our findings suggest that erlotinib retreatment is an option for EGFR mutated NSCLC with acquired resistance to EGFR-TKI after a drug-free interval and progression on intervening therapy. Additional advanced NSCLC pts without a documented EGFR mutation who fulfill the clinical definition of acquired resistance are undergoing review to expand our cohort. 7527 Poster Discussion Session (Board #17), Tue, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Local therapy as a treatment strategy in EGFR-mutant advanced lung cancers that have developed acquired resistance to EGFR tyrosine kinase inhibitors. Presenting Author: Helena Alexandra Yu, Memorial Sloan- Kettering Cancer Center, New York, NY Background: The utility of EGFR directed therapy for the treatment of EGFR mutant lung cancer is limited by the development of acquired resistance (AR) to EGFR tyrosine kinase inhibitor (TKI) therapy, which occurs after a median of 16 months (mos). There are no approved targeted therapies after disease progression on EGFR TKI therapy. Local therapy for oligometastatic disease is used with regularity in other solid tumors, and can lead to long term survival in selected individuals. EGFR mutant lung cancers with AR to TKI therapy can follow an indolent course that is amenable to local therapy to treat progression of disease when used in conjunction with continued EGFR inhibition. Outcomes following local therapy in this setting have not been assessed. Methods: Patients (pts) with AR to EGFR TKI’s who received local therapy excluding treatment of CNS metastases or local therapy prior to AR were identified in an IRB-approved prospective registry of 184 pts with AR enrolled from August 2004- November 2011. We collected treatments as well as progression free survival (PFS) and overall survival (OS) after local therapy. Results: 18 pts received local therapy. Treatments included surgical resection and radiation to lung, lymph nodes, adrenal gland or bone. Median age was 57, 56% were women, and 61% were never smokers. 14 had EGFR Exon 19 deletions, and 4 L858R. The median time to development of AR on TKI was 19 mo (range 5-33). Known mechanisms of AR included T790M (11 pts), MET amplification (1 pt) and small cell transformation (1 pt). The median PFS after local therapy was 10 mo (95% CI: 4-NA), median time from local therapy until change in systemic therapy was 22 mo (95%CI: 6 - 30), and median OS from local therapy was 41 mo (95% CI: 26-NA). Local therapy was tolerated well, with 85% of pts restarting TKI therapy within one month of completing local therapy. Conclusions: Local therapy is well tolerated and in combination with continued EGFR TKI therapy prolongs time until change in systemic therapy is required and may lead to outcomes that are superior to currently available treatment options in selected individuals. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
7528 Poster Discussion Session (Board #18), Tue, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Rebiopsy of non-small cell lung cancer patients with acquired resistance to EGFR-TKI: Comparison between T790M mutation-positive and -negative populations. Presenting Author: Akito Hata, Division of Integrated Oncology, Institute of Biomedical Research and Innovation, Kobe, Japan Background: The secondary epidermal growth factor receptor (EGFR) mutation T790M accounts for approximately half of acquired resistances to EGFR-tyrosine kinase inhibitors (TKI). A recent report has demonstrated the presence of T790M predicts a favorable prognosis and indolent progression, compared to the absence of T790M after TKI failure. However, rebiopsy to confirm T790M status can be challenging due to limited tissue availability and procedural feasibility, and little is known regarding the differences among patients with or without T790M. Methods: We investigated 73 patients harboring EGFR sensitive mutations who had undergone rebiopsy to confirm the emergence of T790M after TKI failure. The peptide nucleic acid-locked nucleic acid PCR clamp method was used in EGFR mutational analyses. Patient characteristics (age, gender, smoking history, performance status, EGFR mutation site, initial TKI, response to initial TKI, line of initial TKI, progression-free survival with initial TKI, and biopsy site) and postprogression survivals (PPS) after initial TKI failure, were retrospectively compared in patients with and without T790M. Results: We identified T790M in 2 (10%) of 21 central nervous system (CNS) (19 cerebrospinal fluid and 2 brain tissue) specimens, and in 20 (38%) of 52 other lesions (25 lung tissue, 24 pleural effusion, and 3 lymph node) (p � 0.0225). Other characteristics had no statistical association with the detection of T790M. Median PPS in patients with T790M was 34.0 months, and in those without T790M, 14.5 months (p � 0.0038). Although none of our patients received TKIs continuously after initial failure, 56 (77%) patients were re-administered TKIs. Regardless of T790M status, PPS in patients with TKI re-administration (23.4 months) was significantly longer than without re-administration (10.4 months) (p � 0.0085). Conclusions: The emergence of T790M in CNS is rare compared with other lesions. Patients with T790M after TKI failure have significantly better prognosis than those without T790M. The effectiveness of TKI re-administration or continuous administration beyond progression is suggested after initial TKI failure. 7530 Poster Discussion Session (Board #20), Tue, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM First-line dacomitinib (PF-00299804), an irreversible pan-HER tyrosine kinase inhibitor, for patients with EGFR-mutant lung cancers. Presenting Author: Mark G. Kris, Memorial Sloan-Kettering Cancer Center, New York, NY Background: Dacomitinib irreversibly inhibits EGFR, HER2 and HER4, and showed superior activity vs. reversible EGFR tyrosine kinase inhibitors in EGFR-mutant lung cancer models, including resistant forms. This openlabel Phase II study evaluates dacomitinib as 1st-line treatment (tx) for patients (pts) with lung cancers. Pts with sensitizing EGFR deletions/ mutations in exons 19 or 21 are reported here. Methods: Pts had stage IIIB/IV adenocarcinoma, no prior systemic tx, had smoked �10 pack years (none within 15 years of enrollment) or had known EGFR mutation. Pts received dacomitinib orally once daily continuously at 45 mg, or 30 mg with the option to escalate to 45 mg; evaluation was every 28 days. Endpoints included progression-free survival rate at 4 months (PFS at 4M, primary); PFS, and partial response (PR) rate. Results: 92 pts enrolled; 47 had EGFR mutation in exons 19 (n�25) or 21 (n�22), 33 were female and 27 Asian. 34/46 evaluable pts with EGFR exon 19 or 21 mutations had a PR (PR rate � 74%; 95% CI: 59–86; exon 19 � 72%; exon 21 � 76%). PR rates and preliminary PFS were not significantly different for exons 19 and 21. Preliminary PFS at 4M was 96% (95% CI: 84–99), preliminary PFS rate at 1 year was 77% (95% CI: 61–87) and preliminary median PFS was 17 months (95% CI: 13–24). Median tx duration was 13.1 months. For pts with EGFR wild-type lung cancers, PR and PFS at 4M rates were 7% (n�14; 95% CI: 0–34) and 33% (n�14; 95% CI: 11–58), respectively, and for pts with EGFR unknown lung cancers, 46% (n�22; 95% CI: 24–68) and 68% (n�24; 95% CI: 45– 83), respectively. 7 pts had lung cancers with non-sensitizing EGFR mutations; 2 had a PR and 3 SD. For all 92 pts, common side effects included dermatitis acneiform (grade 3/4 � 17%/0) and diarrhea (14%/0). 3/46 pts with EGFR exon 19 or 21 mutations discontinued tx due to drug-related toxicity. Conclusions: 74% of pts in this cohort with EGFR exon 19 or 21 mutant lung cancers experienced PRs with 1st-line dacomitinib; preliminary PFS rate was 77% at 1 year; preliminary median PFS was 17 months; further research is planned in this pt population. As dacomitinib is well tolerated, with preclinical activity against HER2, a cohort of pts with HER2 mutant lung cancers is recruiting. Lung Cancer—Non-small Cell Metastatic 487s 7529 Poster Discussion Session (Board #19), Tue, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM Concordance of driver mutations in primary and matched metastasis from patients with non-small cell lung cancer (NSCLC) using next-generation sequencing (NGS). Presenting Author: Stéphane Vignot, Institut Gustave Roussy, INSERM U981, Villejuif, France Background: Progress in treating NSCLC continues to be limited by high recurrence rates after definitive treatment of localized disease and frequent presentation with metastatic disease. In these pts, diagnostic samples are often limited in size and may be inadequate for genotyping necessary in this disease. In applying genomic profiling to aid treatment planning for patients with metastatic NSCLC, it is critical to determine whether archived primary tumor adequately reflects the genomic spectrum of the patient’s metastatic disease or whether biopsy of a metastatic site is required. We undertook this study using NGS technology to characterize paired primarymetastatic biopsy genomic profiles. Methods: Primary and matched metastatic tumor pairs plus adjacent normal tissue from 15 pts with NSCLC (adenocarcinoma 9/squamous 4/large cell 2) and heavy smoking history were analyzed using a targeted NGS assay in a CLIA laboratory (Foundation Medicine). Genomic libraries were captured for 3230 exons in 182 cancer-related genes plus 37 introns from 14 genes often rearranged in cancer and sequenced to average median depth of 778X with 99% of bases covered �100X. Results: Among the 30 tumors, 373 somatic alterations were identified; 96 were known NSCLC drivers including: TP53 (14 pts), KRAS (4 pts), SOX2 (4 pts), STK11 (2 pts), CDKN2A (2 pts) and SMARCA4 (2 pts) in full agreement with their respective histological type. In all cases (15/15), primary and metastatic tumors from the same patient demonstrated 90% driver mutation concordance (74/82, 95 % CI, 82- 95%). For other mutations, the majority of which are likely passengers, the 69% (201/291) concordance rate was significantly lower (p� .001).The total number of alterations between primaries (190) and metastases (183) was remarkably similar. Conclusions: These results suggest that genomic profiles of primary tumor can identify the key somatic alterations present in matched NSCLC metastases and therefore is a suitable specimen for clinical decision making in the majority of cases. Our data does not support the routine need for a new biopsy upon recurrence since variability in mutational status is low. 7531 Poster Discussion Session (Board #21), Tue, 8:00 AM-12:00 PM and 11:30 AM-12:30 PM A randomized discontinuation phase II trial of ridaforolimus in non-small cell lung cancer (NSCLC) patients with KRAS mutations. Presenting Author: Gregory J. Riely, Memorial Sloan-Kettering Cancer Center, New York, NY Background: Mutations in KRAS are present in ~25% of patients with advanced NSCLC. Preclinical data support the role of mammalian target of rapamycin (mTOR) in KRAS mediated oncogenesis. Ridaforolimus is an inhibitor of mTOR which has been shown to have efficacy in advanced endometrial cancer and soft tissue sarcoma. Everolimus, another mTOR inhibitor was previously evaluated in unselected patients with advanced NSCLC and found to have a response rate �5%. We hypothesized that by enrichment for patients with NSCLC and KRAS mutations, treatment with ridaforolimus would be associated with prolonged stable disease relative to available standard treatments for NSCLC. Methods: Patients with stage IIIB/IV non-small cell lung cancer with KRAS mutation who had received prior chemotherapy for NSCLC began treatment with oral ridaforolimus 40 mg once daily on a 5 day/week schedule. After 8 weeks, patients with �30% tumor shrinkage remained on ridaforolimus and patients with �20% tumor growth discontinued treatment. Patients with stable disease were randomized 1:1 to placebo or ridaforolimus. The primary endpoint of the study was progression-free survival (PFS) after randomization. Results: 79 patients were enrolled (40 women, median age 58 [range 28-85]). The overall response rate (CR�PR) at 8 weeks was 1/79 (1%, 95% CI 0-7%). 28 patients with stable disease at 8 weeks were randomized to ridaforolimus or placebo. Median PFS based on investigator assessment from randomization was significantly longer with ridaforolimus (4 months) than placebo (2 months, p�0.013, HR 0.36). Median OS from randomization was 18 months in the ridaforolimus treated arm and 5 months in the placebo treated group, (HR 0.46, p�0.09). The most common grade �3 adverse events were fatigue (10%), mucositis/stomatitis (10%), pneumonia (10%), dyspnea (9%), diarrhea (6%), and hyperglycemia (6%). Conclusions: In patients with KRAS mutant NSCLC who had stable disease after 8 weeks of ridaforolimus, ridaforolimus was associated with prolonged progression-free survival. Further evaluation of ridaforolimus in this patient population is warranted. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
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Volume 30, Issue 15S, Part I of II
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Editor: Michael A. Carducci, MD Man
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Volume 30, Issue 15S Supplement to
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Author Index Note: Numerals refer t
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Alexanian, Raymond 8093 Alexeev, Bo
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Arkenau, Hendrik-Tobias 2540, 3000,
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Ballen, Karen K. 6606, 6617, 6618,
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Blancas, Isabel e11535, e11545, e21
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Brandes, Johann Christoph 7048, 106
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Cakir, Betul 9567 Calabek, Bernadet
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Ceraulo, Domenica 4017 Cerbone, Lin
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Chinen, Ludmilla T.D. e16046 Chinen
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Come, Steven E. 9071, 9100 Comis, S
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Dahlheimer, Tambra 2546 Dahmane, El
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DeLacure, Mark D. e16052 Delage, Ju
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Domingo, Gelenis 6568, 6575, 6588 D
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El Sherbeiny, Esam e15129 El-Deiry,
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Fayad, Luis 6501, 8067 Fayette, Jer
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Gang, Wu 7091, e14511 Gangaram, Anj
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Granowetter, Linda 9537 Grant, Barb
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Hainsworth, John D. 618, 1018, 1086
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Heerschap, Arend e13111 Heersink, M
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Hong, Seung-Mo 3568 Hong, Sook Hee
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Ji, Yongling e17527 Jia, Jingquan e
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Kaparelou, Maria 583 Kapaun, Christ
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Kim, Chan Kyu e14688 Kim, Chang Won
Page 758 and 759:
Komatsu, Yoshihiro e14689 Komatsu,
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Laack, Nadia N. 2032, e14507 Laadem
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Lee, Ji-Hyun TPS3114, 6100 Lee, Jih
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Lim, Kian-Huat e14584 Lim, Kiat Hon
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Loupakis, Fotios 3518, 3540, 3546,
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Man, Shan e11061, e15177^ Manaloor,
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Mathieu-Nicot, Florence e19623 Math
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Mergenthaler, Hans-Guenther e15026
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Molero, Xavier e21035 Moles-Moreau,
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Munoz-Sanchez, MM e19590 Munsell, M
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Ng, Daniel e15050 Ng, Dawn Marie e1
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Oguri, Senri 5556 Oh, Do Youn 1003
Page 782 and 783:
Palassini, Elena 10026, 10053, 1006
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Peisker, Uwe 10600 Peker, Deniz e18
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Piwnica-Worms, Helen 3047 Pizzo, Fa
Page 788 and 789:
Rabinowits, Guilherme 5501, 5582, 9
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Reyes-Rivera, Irmarie CRA3503 Reyna
Page 792 and 793:
Rose, Steven C. 3590 Rosell, Rafael
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Sakata, Shinya e18059 Sakata, Yuh 3
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Schenkein, David P. 6606 Schepp, Wo
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Sha, Dan 3564 Sha, Huifang e13528 S
Page 800 and 801:
Silva, Jose D. 5567 Silva, Milton J
Page 802 and 803:
Sousa, Carlos Eduardo Pires 643 Sou
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Su, Xinying 4124 Su, Yu-Chieh e1600
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Tan, Chee Seng 1064, e19523 Tan, Ch
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Tillmanns, Todd D. 5014, e15514 Til
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Uchiyama, Tomotaka e21108 Udovitsa,
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Videtic, Gregory M.M. e14611, e1466
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Wang, Yuan e15124 Wang, Yunfei 547
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Wischnewsky, Manfred 1078 Wischnik,
Page 818 and 819:
Yasuda, Hiromi e14029 Yasuda, Hiroy
Page 820:
Zhang, Xinmin e16022 Zhang, Xu Dong
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