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

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498s Lung Cancer—Non-small Cell Metastatic 7575 General Poster Session (Board #49A), Sat, 1:15 PM-5:15 PM Prospective randomized phase II trial of oral vinorelbine (NVBo) and cisplatin (P) or pemetrexed (Pem) and P in first-line metastatic or locally advanced non-small cell lung cancer (M or LA NSCLC) patients (pts) with nonsquamous (non SCC) histologic type: NAVoTRIAL01—Preliminary results. Presenting Author: Jaafar Bennouna, Institut de Cancerologie de l’Ouest/Site René Gauducheau, Nantes, France Background: NVBo�P is considered as a standard treatment (trt) in M or LA NSCLC. The recent approval of Pem�P as front line chemotherapy (CT) for non-SCC demonstrates that today, histology could become a “new guidance” to treat patients (pts). Phase III trial (Scagliotti. JCO 2008) showed efficacy of Pem�P in patients with non-SCC pts. Moreover, the higher chemosensitivity of non-SCC is recognised and reported with other chemotherapies (Ardizzoni.JNCI 2007). In GLOB 3 study, NVBo�P also showed better survival in adenocarcinoma (11.7m) than in SCC (8.9m) (Tan.Ann of Oncol 2009). This trial was set up to assess the efficacy of NVBo�P compared to Pem�P for pts with non-SCC histological type. The primary end-point was disease control rate (DCR) including overall response rate (ORR) and stable disease (SD). Methods: Pts were randomised to receive NVBo 80 mg/m² D1D8 (60 at Cycle 1) � P 80 mg/m² D1 q3w or Pem 500 mg/m² � P 75 mg/m² D1 q3w. After 4 cycles of trt, for pts showing a disease control, single agent as continuation maintenance (CM) was proposed until progression or toxicity. Given that Pem�P is now considered as a reference trt in non-SCC, pts were randomised on a 2/1 basis and stratified according to stage (IIIB - IV - relapse), non-SCC confirmed by histology or cytology, gender, smoking status and centre. Results: From 10/09 to 02/11, 153 pts were randomised to receive NVBo�P (102 pts) or Pem�P (51 pts). The efficacy between the 2 arms is similar: The ORR/DCR (Recist 1.1) after 4 cycles of trt are 26%/75% in the NVBo arm (100 eval pts in ITT population) and 24%/78% in the Pem arm (50 eval pts in ITT population). At the end of December 2011, 7 patients are still treated in CM: 5 pts in the NVBo arm and 2 pts in the Pem arm. Conclusions: The2CT regimen, NVBo�P orPem�P have a similar efficacy in terms of ORR/DCR for pts with advanced non-SCC NSCLC. These results appear to be in line with the published data. As the analysis is currently in progress, final results including safety data, PFS and OS will be presented during the meeting. 7577 General Poster Session (Board #49C), Sat, 1:15 PM-5:15 PM The relevance of stable disease (SD) as a surrogate end-point in advanced non-small cell lung cancer (NSCLC) patients treated with erlotinib (E) as the second/third line. Presenting Author: Francesco Grossi, Lung Cancer Unit, National Institute for Cancer Research, Genova, Italy Background: SD has often been viewed as a result with an uncertain clinical value.With the advent of E in advanced NSCLC, increasing numbers of patients (pts) achieve SD as a best response. A common observation in clinical practice is that a high proportion of patients receiving E have durable SD.The aim of this analysis was to compare the progression-free survival (PFS) and overall survival (OS) in pts with advanced NSCLC who achieved confirmed SD or complete/partial response (CR�PR) after second/ third line treatment with E. Methods: Data from 684 Italian pts from the TRUST trial (Tiseo M et al. Lung Cancer 2008) were analyzed. E was administered orally at 150 mg per day and was continued until disease progression, development of unacceptable toxicity or patient’s refusal. We define confirmed SD (cSD) if the patients’ PFS was �5 months (response to E was evaluated per protocol every two months) and reconfirmed SD (rSD) if the patients’ PFS was �8 months. Results: Pts’ characteristics included the following: median age, 67 years (31-89); females/males� 219/465 pts (32%/68%); never/former smokers� 191/493 pts (28%/72%); squamous/ adeno/BAC/large cell/NOS� 163/361/26/21/113 pts (24%/53%/4%/3%/ 16%); ECOG PS 0-1/2-3� 557/127 pts (81%/19%). In 83 pts (12%), E was administered as the first-line therapy in pts who were unable to receive chemotherapy; 305 pts (45%) had received 1 prior line of chemotherapy, and 296 pts (43%) had received 2 prior lines of chemotherapy. A total of 428 pts were evaluable for a response: 44 pts (10%) exhibited CR�PR, 226 pts (53%) attained SD, which consisted of 139 pts (32%) with cSD and 83 pts (19%) with rSD. The median PFS estimates (with 95% CI) were 13.1 months (9.8-16.4) for CR�PR pts, 9.9 months (8.2-11.4) for cSD pts and 14 months (12-16) for rSD. The median OS estimates (with 95% CI) were 24.0 months (17-31) for CR�PR pts, 17.9 months (14.4-21.5) for cSD pts and 24.9 months (18.1-31.7) for rSD. Conclusions: Our findings are the first to demonstrate the relevance of achieving stable disease with E treatment. Pts obtaining cSD or rSD had durable PFS and OS comparable, particularly for rSD, with PFS and OS of those having CR�PR. 7576 General Poster Session (Board #49B), Sat, 1:15 PM-5:15 PM Difference in incidence and pattern of salvage treatment after failure to first-line epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR- TKI) monotherapy and standard cytotoxic chemotherapy in pts with advanced non-small cell lung cancer (NSCLC) harboring EGFR mutations: Okayama Lung Cancer Study Group experience. Presenting Author: Yuka Kato, Okayama University Hospital, Okayama, Japan Background: EGFR-TKI (E) therapy yielded a better PFS than standard cytotoxic chemotherapy (C) therapy and a comparable OS in untreated pts with EGFR-mt tumors, suggesting each of the treatments is now crucial for such subpopulation. But, it has not been fully evaluated yet which of each should be initiated first, and to what degree both of two are actually administered in early line setting in the treatment course. We here investigated a potential difference in incidence and pattern of delivery of subsequent crossover therapy after failure to each of the treatments in pts with EGFR-mt tumors. Methods: Consecutive 79 pts with advanced EGFR-mt NSCLC were retrospectively assessed who underwent E therapy (n � 39) or standard C therapy (n � 40) in the 1st-line setting between 2007 and 2011. Results: In E group 16 (41%) of 39 pts were still on 1st-line E therapy. Nine (39%) of the remaining 23 could not receive standard C therapy after failure to E therapy due to symptomatic CNS metastasis(mets) in 6, skeletal events in 2, and patient refusal in 1, whilst in C group only one (3%) of 40 failed to receive subsequent E therapy because of relapse (carcinomatous lymphangitis) (�2-test; p � .001). Also, at the time of relapse to the 1-st line therapy, PS deteriorated more frequently in E group (8/23 vs. 7/40; p � .042) and, relapse with symptomatic CNS mets seemed frequently observed in E group (6/23 vs. 4/40; p � .093). Multivariate analysis revealed type of regimens undergone in the 1st-line setting (E vs. C) correlated with failure of administration of subsequent crossover therapy (odd ratio: 3.224, 95%CI: .1.032 – 5,417, p � .004). Conclusions: It seems that pts with EGFR-mt tumors who were treated with 1st-line C had better opportunity to receive post-progression E therapy than those treated with 1st-line E had chance to receive subsequent C therapy, possibly due to difference in PS deterioration rate and relapse pattern. 7578 General Poster Session (Board #49D), Sat, 1:15 PM-5:15 PM KIF5B-RET: Discovery of a novel fusion oncogene in lung adenocarcinomas by a systematic screen for tyrosine kinase fusions and identification of patients for a RET targeted therapy trial. Presenting Author: Yoshiyuki Suehara, Memorial Sloan-Kettering Cancer Center, New York, NY Background: The mutually exclusive pattern of major targetable driver oncogenes in lung adenocarcinomas (ADC) suggests that other similar driver oncogenes may exist. We therefore performed a systematic screen for tyrosine kinase (TK) fusions in cases without known driver oncogenes by measuring aberrantly high RNA expression of kinase domain (KD) exons relative to more 5’ exons. Methods: We studied 74 patients whose lung ADC lacked mutations in KRAS, EGFR, BRAF, HER2, and ALK fusions. A NanoString-based assay was designed to query the transcripts of 90 TKs at two points: 5’ to the KD and within or 3’ to the KD. Tumor RNAs were hybridized to the NanoString probes and analyzed for outlier 3’ to 5’ expression ratios. The assay was validated on samples with known ALK and ROS fusions. Presumed novel fusion events were followed up by rapid amplification of cDNA ends (RACE) and confirmatory RT-PCR. Results: The NanoString assay identified aberrant 5’ to 3’ ratios in ROS and RET in 2 cases, respectively, out of 74. RACE analysis isolated a novel GOPC-ROS fusion in the former and a novel KIF5B-RET fusion in the latter, both confirmed by RT-PCR. Further screening by RT-PCR for KIF5B-RET identified one more positive sample in the study set that had not been detected by NanoString. At the RNA level, both fusions joined exon 15 of KIF5B to exon 12 of RET, thus retaining a portion of the dimerization domain of KIF5B and the entire KD of RET, analogous to RET fusions in papillary thyroid carcinoma (TC). One KIF5B-RET patient was a 60 y.o. female never smoker, the other, a 73 y.o. male former smoker. Conclusions: The novel KIF5B-RET fusion described here and also recently reported by Ju YS et al. (Genome Res, Dec 22, 2011) defines a new subset of lung ADC with a potentially targetable driver oncogene. Based on these genetic data and the preclinical activity of the RET inhibitor XL184 (Exelixis) in papillary TC and its known activity in medullary TC with RET mutations, we have initiated prospective testing for KIF5B-RET as part of our lung ADC screening panel in anticipation of a planned phase 2 trial with XL184 in patients with KIF5B-RET or related variant RET fusions. Visit abstract.asco.org and search by abstract for the full list of abstract authors and their disclosure information.
7579 General Poster Session (Board #49E), Sat, 1:15 PM-5:15 PM Family history of lung cancer in never smokers with non-small cell lung cancer (NSCLC) and its association with tumors harboring epidermal growth factor receptor (EGFR) mutations. Presenting Author: Elizabeth Mary Gaughan, Beth Israel Deaconess Medical Center/Harvard Medical School, Boston, MA Background: Inherited susceptibility to lung cancer is an understudied subject, however it has been described among never smokers (�100 cigarettes/lifetime). Never smokers with NSCLC comprise an important subgroup of patients enriched for tumors harboring oncogene aberrations in the EGFR and ALK genes. We aimed to better characterize the incidence of family history of lung cancer in the setting of routine tumor genotyping among never smokers with NSCLC. Methods: Clinicopathologic data plus tumor genotype (EGFR, KRAS, ALK) from 230 consecutive never smokers seen at Beth Israel Deaconess Medical Center and Dana-Farber Cancer Institute was compiled. We retrospectively analyzed the incidence of a family history of any cancer and lung cancer in these patients. Results: In our cohort, the average age was 56 years, 67% of the patients were women, 75% were white, 41% had advanced NSCLC and 87% had adenocarcinoma histology. In these tumors, 98/230 (43%) had an EGFR mutation, 16/155 (10%) had KRAS mutations and 27/127 (17%) had an ALK translocation. Family history of any cancer was common (57%) and specific family history of lung cancer was present in 42/230 cases (18%). Out of thecases with a family history of any cancer, 22/53 (41.5%) EGFRmutated, 1/6 (17%) KRAS-mutated and 3/20 (15%) ALK-translocated cohorts had a family history of lung cancer. The rate of family history of lung cancer to family history of cancer was significantly higher in the EGFRmutated cohort when compared to the ALK translocated plus KRASmutated cohorts (p�0.023). Conclusions: Family history of lung cancer is common in never smokers with NSCLC, and there seems to be a particular link in families in which the proband has an EGFR-mutated tumor. Further study of families with EGFR-mutated NSCLC may yield insights into the pathogenesis of this tumor type. 7581 General Poster Session (Board #49G), Sat, 1:15 PM-5:15 PM NGR-hTNF plus chemotherapy as first-line therapy of non-small cell lung cancer (NSCLC). Presenting Author: Vanesa Gregorc, Department of Oncology, Istituto Scientifico San Raffaele, Milan, Italy Background: NGR-hTNF (asparagine-glycine-arginine human tumor necrosis factor) is a selective vascular targeting agent able to improve intratumoral chemotherapy uptake. Methods: Chemo-naive, stage IIIb-IV NSCLC patients (pts), stratified by histology (nonsquamous or squamous) and PS (0 or 1), were randomized to cisplatin 80 mg/m2 /day(d)1 plus either pemetrexed 500 mg/m2 /d1 (nonsquamous) or gemcitabine 1,250 mg/m2 / d1�8 (squamous) every 3 weeks (q3w) up to 6 cycles with (arm A) or without (arm B) NGR-hTNF 0.8 �g/m2 /d1 q3w until progression. Progression free survival (PFS) was primary end point of this phase 2 trial (��20%, ��20%, HR�0.62, and n�102). Secondary end points included adverse events (AEs), response rate (RR) and overall survival (OS). Results: 59 pts were assigned to arm A and 57 to arm B. Baseline characteristics in arm A/B were: median age 62/63; male 34/37; PS 1 21/21; squamous 15/15; nonsmokers 14/12; EGFR mutations 5/5. For the nonsquamous group, 281 cycles (mean 6.5; range 1-18) were given in arm A and 190 (mean 4.7; range 1-6) in arm B, while for the squamous group, 88 (mean 6.3; range 1-19) in arm A and 48 (mean 3.7; range 1-6) in arm B. Most common grade 3/4 AEs were neutropenia 14% vs 17% and fatigue 7% vs 11% in arm A and B, respectively. No grade 3/4 AEs related to NGR-hTNF or bleeding in pts with squamous histology were noted. Median follow-up was 12.4 months. In the whole study population, median (m)PFS was 5.8 vs 5.7 months (HR�0.95), RR was 23% vs 19%, and 1-year OS was 62% vs 62% in arm A and B, respectively. In the nonsquamous subset, a trend toward longer mPFS in arm A compared to arm B was noted in pts with a PS of 1 (6.7 vs 4.6 months, respectively), nonsmoking history (6.2 vs 3.4), younger age (6.5 vs 3.4), and EGFR mutations (7.2 vs 3.3). In the squamous subset, mPFS was 5.1 vs 3.9 months (HR�0.71) and mOS was 14.2 vs 10.8 months (HR�0.73) in arm A and B, respectively. In these pts, ORR was 36% in arm A and 23% in arm B, while median changes from baseline in target tumor size after 2, 4, and 6 cycles were -29%, -45%, and -41%, respectively in arm A, and -18%, -22%, and -14%, respectively in arm B. Conclusions: Regardless of histology, NGR-hTNF can be safely given with standard chemotherapy, showing tolerability and hint of activity in squamous NSCLC. Lung Cancer—Non-small Cell Metastatic 499s 7580 General Poster Session (Board #49F), Sat, 1:15 PM-5:15 PM Comparison of the KRAS/EGFR mutation profile and survival of “collegiate smokers” and never smokers with advanced lung cancers. Presenting Author: Anna M. Varghese, Memorial Sloan-Kettering Cancer Center, New York, NY Background: In practice, we encounter patients (pts) with lung cancers who state they smoked only while in college. The impact of this degree of tobacco use on cancer biology is unknown. We have shown that EGFR mutations are less common in pts who smoked � 15 pack years (PY). We hypothesize that among pts with lung cancer the KRAS / EGFR mutation profile and overall survival (OS) of “collegiate smokers” (former smokers who smoked between 101 lifetime cigarettes and 5 PY) will be distinct from never smokers and former smokers with � 15 PY. Methods: We collected age, sex, stage, and survival for pts evaluated from 2004 - 2009 with stage IIIB/IV lung cancer with known KRAS and EGFR status. ALK testing was not available routinely during this time. Smoking history was obtained using a patient completed survey. The Fisher exact test was used to compare mutation profiles. The log rank test was used to compare OS. Results: Smoking history and clinical data were available for 852 pts with Stage IIIB/IV lung cancer with known KRAS and EGFR status: 307 never smokers, 178 current smokers, and 367 former smokers. Of the former smokers, 55 were “collegiate smokers”, 61 had smoked 5-15 PY, and 251 had smoked � 15 PY. The KRAS / EGFR mutation profiles by smoking history are shown below (Table). The KRAS / EGFR mutation profile of “collegiate smokers” is distinct from those of pts who were never smokers (p � .001) and former smokers with � 15 PY (p � .001) but similar to that of pts who were former smokers with 5-15 PY (p � 0.9). Median OS after diagnosis of stage IIIB/IV lung cancer for “collegiate smokers” was 25 months (mos), compared to 32 mos for never smokers (p � 0.4) and 21 mos for former smokers with � 15 PY (p � 0.63). Conclusions: “Collegiate smokers” are a distinct group of pts with a higher incidence of KRAS mutations and lower incidence of EGFR mutations compared to never smokers. These data suggest that even a small amount of cigarette smoking influences the biology of lung cancer. These findings reinforce the importance of doing mutation testing routinely for all pts with lung cancer to guide clinical care. Total EGFR KRAS N N % N % Never smokers 307 149 49 13 4 �Collegiate smokers� 55 15 27 8 15 Former smokers with > 15 pack years 251 27 11 100 40 7582 General Poster Session (Board #49H), Sat, 1:15 PM-5:15 PM Thymidylate synthase (TS) gene expression in patients with ALK positive (�) non-small cell lung cancer (NSCLC): Implications for therapy. Presenting Author: David R. Gandara, University of California Davis Cancer Center, Sacramento, CA Background: ALK� NSCLC represents a molecular target-defined patient population highly responsive to the ALK inhibitor crizotinib. Previous reports have also suggested increased sensitivity of ALK� NSCLC to the chemotherapeutic agent pemetrexed. Thymidylate synthase (TS) is a candidate predictive biomarker for pemetrexed activity. Here we report analysis of the Response Genetics Inc. (RGI) database for this association and implications for therapy. Methods: ALK fusion was identified by a novel RT-PCR assay (Danenberg et al: ASCO 2010). For TS, RNA from microdissected formalin-fixed paraffin-embedded tumors was analyzed as previously described, reported as the ratio of gene expression to �-actin. For reference, a TS level �2.33 is the cutpoint for sensitivity. Results: TS levels were available from 63 ALK� patients and 1,698 ALK- control lung adenocarcinoma patients. All ALK� patients had adenocarcinomas without EGFR or KRAS mutations. Median age: 59.0 (range 33-88), gender (male/female) 32/31 (51%/49%). Median TS RNA level in ALK� patients was 2.02, range (0.55-19.44), and in ALK- patients was 3.32 (0.36- 53.51), p�0.0001 (Mann-Whitney test). The majority of ALK� patients (N�43, 68%) had a TS level �2.33 cutpoint, compared to only 32% of ALK- patients (N�551, p�0.0001). Conclusions: This analysis demonstrates relatively low TS gene expression in ALK� patient tumors as determined by RT-PCR. These data provide a mechanism of action supportive of pemetrexed sensitivity for ALK� NSCLC. TS expression N Median 95% CI Range Mean 95% CI p value ALK� patients 63 2.02 1.60-2.11 0.55-19.44 2.53 1.89-3.16 �0.0001 ALK- patients 1698 3.32 3.15-3.45 0.36-53.51 7.87 1.68-14.05 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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Letter from the Editor The 2012 ASC
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2012 ASCO Annual Meeting Proceeding
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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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Ben-Aharon, Irit 548, 2556, e13080
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Dahlheimer, Tambra 2546 Dahmane, El
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DeLacure, Mark D. e16052 Delage, Ju
Page 730 and 731:
Domingo, Gelenis 6568, 6575, 6588 D
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El Sherbeiny, Esam e15129 El-Deiry,
Page 734 and 735:
Fayad, Luis 6501, 8067 Fayette, Jer
Page 736 and 737:
Foroni, Chiara e11546 Foroni, Letiz
Page 738 and 739:
Gang, Wu 7091, e14511 Gangaram, Anj
Page 740 and 741:
Gimenez Capitan, Ana 4068, 10596, e
Page 742 and 743:
Granowetter, Linda 9537 Grant, Barb
Page 744 and 745:
Hainsworth, John D. 618, 1018, 1086
Page 746 and 747:
Heerschap, Arend e13111 Heersink, M
Page 748 and 749:
Hong, Seung-Mo 3568 Hong, Sook Hee
Page 750 and 751:
Im, Young-Hyuck 598^, 644, TPS649,
Page 752 and 753:
Ji, Yongling e17527 Jia, Jingquan e
Page 754 and 755:
Kaparelou, Maria 583 Kapaun, Christ
Page 756 and 757:
Kim, Chan Kyu e14688 Kim, Chang Won
Page 758 and 759:
Komatsu, Yoshihiro e14689 Komatsu,
Page 760 and 761:
Laack, Nadia N. 2032, e14507 Laadem
Page 762 and 763:
Lee, Ji-Hyun TPS3114, 6100 Lee, Jih
Page 764 and 765:
Lim, Kian-Huat e14584 Lim, Kiat Hon
Page 766 and 767:
Loupakis, Fotios 3518, 3540, 3546,
Page 768 and 769:
Man, Shan e11061, e15177^ Manaloor,
Page 770 and 771:
Mathieu-Nicot, Florence e19623 Math
Page 772 and 773:
Mergenthaler, Hans-Guenther e15026
Page 774 and 775:
Molero, Xavier e21035 Moles-Moreau,
Page 776 and 777:
Munoz-Sanchez, MM e19590 Munsell, M
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Ng, Daniel e15050 Ng, Dawn Marie e1
Page 780 and 781:
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
Page 804 and 805:
Su, Xinying 4124 Su, Yu-Chieh e1600
Page 806 and 807:
Tan, Chee Seng 1064, e19523 Tan, Ch
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Tillmanns, Todd D. 5014, e15514 Til
Page 810 and 811:
Uchiyama, Tomotaka e21108 Udovitsa,
Page 812 and 813:
Videtic, Gregory M.M. e14611, e1466
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Wang, Yuan e15124 Wang, Yunfei 547
Page 816 and 817:
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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