tbuckley/cabot-search huggingface dataset:
A phase Ib study of abemaciclib with therapies for metastatic breast cancer.
Authors: Sara M. Tolaney, Muralidhar Beeram, J. Thaddeus Beck, Alison Katherine Conlin, Elizabeth Claire Dees, Maura N. Dickler, Teresa L. Helsten, Paul R. Conkling, William Jeffery Edenfield, Donald A. Richards, P. Kellie Turner, Na Cai, Edward Michael Chan, Shubham Pant, Carlos Becerra, Kevin Kalinsky, Shannon Puhalla, Brent Neil Rexer, Howard A. Burris, Matthew P. Goetz
Journal: Journal of Clinical Oncology (2015)

522 Background: Abemaciclib, an inhibitor of cyclin dependent kinases CDK4 and CDK6, demonstrated safety and clinical activity as a single agent for hormone receptor positive (HR+) metastatic breast cancer (MBC) irrespective of HER2 amplification (Tolaney, SABCS 2014). This study (NCT02057133) evaluates safety, pharmacokinetics (PK), and antitumor activity of abemaciclib combined with endocrine or HER2-targeted therapies for MBC. Methods: Patients (pts) in 6 cohorts received abemaciclib 150-200 mg every 12 hours (Q12H) with letrozole 2.5 mg/d (Part A), anastrozole 1 mg/d (Part B), tamoxifen 20 mg/d (Part C), exemestane 25 mg/d (Part D), exemestane 25 mg/d + everolimus 5 mg/d (Part E), or trastuzumab 6-8 mg/kg every 21 days (Part F). Pts in Parts A-E had HR+, HER2- MBC and in Part F had HER2+ MBC. Eligibility included measurable disease or nonmeasurable bone disease by RECIST v1.1, ECOG performance status ≤ 1, no prior chemotherapy for metastatic disease (Parts A-E), and ≥ 1 chemotherapy regimen for metastatic disease (Part F). Abemaciclib was given continuously until progression. Patients were assessed every 28 days in Parts A-E and every 21 days in Part F. Dose escalation cohorts of ≥ 3 pts receiving abemaciclib at 150 mg and 200 mg Q12H were included in Parts E and F. Results: A total of 65 pts started treatment with abemaciclib (200mg Q12H) by 16-Dec-2014 in Parts A-D. Pts had a median age of 57 years (range: 28-77) and a median of 3 prior systemic therapies (range: 1-8) for breast cancer. The most common ( ≥ 20% overall in Parts A-D) possibly related treatment-emergent adverse events (TEAEs) (all grades %, G3 %) were diarrhea (95, 31), fatigue (71, 14), nausea (62, 6), neutropenia (31, 17), abdominal pain (31, 3), decreased appetite (29, 0), vomiting (28, 3), and anemia (25, 0). Diarrhea was manageable with antidiarrheal agents or dose reduction. No G4/5 TEAEs occurred. The disease control rate (CR + PR + SD) was 67% for Parts A+B [nonsteroidal aromatase inhibitors (36 pts)] with 2 confirmed PRs and 75% for Part C [tamoxifen (16 pts)]. Safety, PK, and efficacy results will be updated at presentation. Conclusions: Combinations of abemaciclib with endocrine therapies demonstrate manageable safety and early clinical evidence of antitumor activity. Clinical trial information: NCT02057133.
miRNA21 as a specific marker for the detection of circulating tumor cell.
Authors: Jose Manuel Ordonez, M. Jose Serrano, José Luis García-Puche, Francisco Gabriel Ortega, Juan JosÃÂ© Diaz-Monchon, jose Antonio Lorente, Diego de Miguel Perez
Journal: Journal of Clinical Oncology (2015)

e22025 Background: To develop clinical applications of Circulating Tumor Cells (CTC), their phenotypic and genetic characterization is required. Here, we present the first protocol to detect miRNAs in CTCs by in situ hybridization (ISH) combined with both immunomagnetic selection based on cytokeratin (CK) expression and immunocytochemistry. Methods: LNA probes associated with an enzyme-labeled fluorescence (ELF) signal amplification approach were used to detect miRNA in CTCs. This protocol was optimized using both tumor and non-tumor epithelial cell lines, MDA-MB468 and MCF-10, respectively , and miRNA-21 was chosen as the target miRNA due to its known role as an onco-miRNA. Results: Hematopoietic cells did not express miRNA-21, making it a perfect marker for detecting CTCs. The peripheral blood of 25 cancer patients was analyzed, with 11 of the 25 patients presenting CTCs. In every case, isolated CTCs expressed both cytokeratin (CK) and miRNA-21. Finally, the protocol was applied to monitor miRNA-21 expression in epithelial to mesenchymal transition (EMT)-induced MCF-7 cells, a tumor epithelial cell line. While CK was lost in those cells, miRNA-21 was still expressed. Conclusions: Our results suggest that miRNA-21 might be a good marker for detection of different subpopulations of CTCs including CTCs with EMT phenotype.
Abstract P367: Association of Risk Factor Exposure Patterns Through Young Adulthood With Left Ventricular Structure/Function in Middle Age: The Coronary Artery Risk Development in Young Adults (CARDIA) Study
Authors: Donald M Lloyd-Jones, Laura Colangelo, Beth Lewis, Pamela Schreiner, Stephen Sidney, Samuel S Gidding, Amanda M Perak, Myron Gross, David C Goff, Jared Reis, Kiang Liu, Joao Lima
Journal: Circulation (2017)

Background: Data are sparse regarding associations of risk factors (RF) across young adulthood with development of adverse left ventricular (LV) structure and function by middle age, and it is unclear whether baseline, cumulative, or longitudinal RF exposure patterns best represent that risk. Methods: We included up to 2335 CARDIA participants (ppts) who had echocardiographic data from exam year (Y)5, Y25, and Y30, and RF data from at least 3 exams including Y0 and Y25. Echo outcomes included Y30 indexed LV end-systolic (ESD/ht) and -diastolic (EDD/ht) dimensions, and LV mass (M/ht 2.7 ), septal and posterior wall thickness, ejection fraction (EF), and incident adverse geometry (defined as LV concentric remodeling [CR], concentric hypertrophy [cLVH], or eccentric hypertrophy [eLVH]). We used multivariable linear, logistic or polytomous regression (as appropriate to endpoint) to examine associations of RF exposures measured as: 1) baseline (Y0); 2) change from Y0 to Y25; 3) cumulative exposure from Y0 to Y25 (e.g., pack-yrs, mmHg-yrs); or 4) latent class trajectories (using PROC TRAJ) from Y0 to Y25, with adjustment for demographics and relevant Y5 echo measures. Results: At Y30, ppts were 55±4 yrs, 56% women and 44% black; 12% smoked, mean BMI was 30.4±7, 37% had hypertension, and 17% diabetes; 20.5% had incident LVH; 4.5% EF&lt;50%; and 37.2% adverse LV geometry. Models representing cumulative RF exposures tended to have the highest adjusted R 2 and lowest AIC for continuous and categorical Y30 LV outcomes. The table shows associations of cumulative RFs from Y0 to Y25 with incident LVH, EF&lt;50%, and adverse LV geometry at Y30. Few RFs were consistently associated with Y25-Y30 change in echo measures, but they included education and SBP. Conclusions: Among initially healthy young adults, cumulative risk factor exposures (often within clinically normative ranges) over 25 years are significantly associated with continuous LV echo measures and adverse LV outcomes by middle age, suggesting the importance of primordial prevention.
Phase 1 trial of p28 (NSC745104), a non-HDM2 mediated peptide inhibitor of p53 ubiquitination in children with recurrent or progressive CNS tumors: A final report from the Pediatric Brain Tumor Consortium.
Authors: Rishi Ramesh Lulla, Stewart Goldman, Craig Beattie, Tohru Yamada, Ian Pollack, Paul Graham Fisher, Shengjie Wu, James M. Boyett, Maryam Fouladi
Journal: Journal of Clinical Oncology (2015)

10059 Background: Wild type and mutated TP53 are common in pediatric CNS tumors. p28 is a cell penetrating peptide that preferentially enters cancer cells and binds to wild type and mutant p53 protein inhibiting COP1 mediated ubiquitination and proteasomal degradation. This results in an increase in levels of p53, which induces cell cycle arrest at G2/M. A Phase I trial in 15 TP53 positive, adult patients with stage IV tumors reported no AEs and 1CR and 3PR with 4 patients alive greater than 40 weeks. Regression analysis suggested that p28 has activity in patients whose tumors express both wild type and mutated TP53. Methods: Intravenous p28 was administered 3 times weekly for 4 consecutive weeks of a 6-week cycle at 4.16 mg/kg/dose (the adult MTD) using a rolling 6 study design. TP53 expression status was characterized by immunohistochemistry and serum pharmacokinetics were established on the second dose. Results: Of the 18 patients registered on the study, 12 patients (8 males, median age 11 years (range 3-19)) completed the DLT period and are evaluable for toxicity with malignant glioma (n = 4), choroid plexus carcinoma (n- = 2), medulloblastoma (n = 2), pineoblastoma (n = 2), DIPG (n = 1) and AT/RT (n = 1). p28 was well tolerated; 7 patients received 2 or more courses and the most common adverse event attributed to drug was transient Grade I infusional reaction. One patient with metastatic pineoblastoma with bone marrow involvement had 2 DLTs of Grade 4 neutropenia and thrombocytopenia. Pharmacokinetic analysis of 16 patients revealed an overall t½ and t½α similar to adults. An increased AUC was observed in pediatric patients, as a result of a higher Cmax and longer t½αβ. p53 expression in tumor cell nuclei was high in 7 of 12 available tissue samples; correlation with response to p28 will be presented. Conclusions: This phase I study demonstrates that p28 is well tolerated in children with recurrent CNS malignancies at the adult MTD. Future combination studies are being explored. Clinical trial information: NCT01975116.
Smoking status to predict sensitivity to PARP inhibitor, veliparib, in patients with advanced NSCLC.
Authors: Suresh S. Ramalingam, Normand Blais, Julien Mazières, Martin Reck, C. Michael Jones, Erzsebet Juhasz, Laszlo Urban, Sergey Orlov, Fabrice Barlesi, Ebenezer A. Kio, Ulrich Keilholz, Jane Qian, Qin Qin, Martin Dunbar, Hao Xiong, Rajendar K. Mittapalli, Peter Ansell, Mark D. McKee, Vincent L. Giranda, Vera Gorbunova
Journal: Journal of Clinical Oncology (2015)

8038 Background: Tobacco-related non-small cell lung cancer (NSCLC) is associated with reduced survival and greater genomic instability. Veliparib (V) is a PARP inhibitor that augments platinum-induced DNA damage in preclinical studies, and a recent Ph 2 trial of advanced NSCLC trended to improved survival (HR 0.80; CI 0.54–1.18) when V was added to carboplatin (C) and paclitaxel (P). Here we report outcomes based on smoking status from a randomized Ph 2 study of CP with either V or placebo in advanced NSCLC. Methods: Patients (pts) with previously untreated advanced/metastatic NSCLC were randomized 2:1 to CP with either V at 120 mg BID or placebo (pre-specified stratification by histology and smoking history). Cotinine (COT) was measured in pt plasma samples as an index of recent tobacco use. Results: Of 158 pts, 68% were male, and 49% had squamous NSCLC. At study entry, 60% of pts were self-reported current smokers (CS), 27% former smokers, and 13% never smoked. There were no significant differences in V PK parameters between the COT-high and low pts.Most common AE in CS were neutropenia (41% VCP; 27% CP), alopecia (36%; 33%), and anemia (31%; 40%). G3/4 AEs were elevated in CS treated with VCP vs CP (66% vs. 40%, p=0.026); all-grade AEs and SAEs were similar between the two groups. In a COT sensitivity analysis of OS, HR VCP/CP for COT-high was 0.52 (0.29–0.92) and COT-low was 1.07 (0.63–1.81). Conclusions: Smoking status was a strong predictor of efficacy for veliparib-chemotherapy combination in advanced NSCLC. No differences in PK of V were seen based on plasma COT; toxicity of VCP was acceptable regardless of smoking history. A Ph 3 study has been initiated in pts with smoking history. Clinical trial information: NCT01560104. Median months (95% CI) CP CS, n=31 Former, 14 Never, 8 VCP CS, n=64 Former, 28 Never, 13 HR VCP/CP HRadj VCP/CP (Adjusted for gender and ECOG PS) PFS CS Former Never 3.3 (1.4–4.2) NA (3.3–NA) 5.6 (1.4–8.2) 5.6 (4.1–7.0) 6.0 (2.4–NA) 6.4 (1.0–NA) 0.38 (0.21–0.67) 2.10 (0.66–6.65) 1.03 (0.27–3.85) 0.37 (0.21–0.68) 0.77 (0.20–3.06) 0.96 (0.21, 4.46) OS CS Former Never 5.4 (3.8–8.8) 14.6 (9.2–NA) NA (3.6–NA) 12.5 (9.9–16.6) 8.6 (5.9–17.5) 13.2 (5.0–NA) 0.43 (0.26–0.70) 1.62 (0.73–3.6) 1.34 (0.40–4.44) 0.45 (0.27–0.76) 0.72 (0.27–1.92) 0.71 (0.18–2.74)
A phase I, dose-escalation trial of continuous and pulsed-dose afatinib (A) combined with pemetrexed (P) in patients (pts) with advanced solid tumors: Final analysis.
Authors: Quincy S. Chu, Randeep S. Sangha, Sebastien J Hotte, Gwen Sergenson, Vikram K. Chand, Roxana Sufan, Yu Gu, David Schnell, Hal W. Hirte
Journal: Journal of Clinical Oncology (2013)

2523 Background: A is an irreversible ErbB Family Blocker that has shown additive effects when combined with P in EGFR-mutant NSCLC cell lines. This Ph I trial assessed the MTD, safety and PK of continuous and pulsed-dose A + P in pts with advanced solid tumors. Methods: In a3+3 dose-escalation design, IV P (500 mg/m 2 ) was administered on day (d) 1 of each 21-d cycle combined with either continuous oral A qd (Schedule A; SA) on d1–21 (d2–21 in Cycle 1) or pulsed-dose oral A qd (Schedule B; SB) on d1–6 of each 21-d cycle. In SA, A starting dose was 30 mg, escalated to maximum of 50 mg. Once the MTD was reached in SA, A was administered at a starting dose of 50 mg in SB. Pts received up to 6 cycles of P with the option for A monotherapy thereafter. P and steady state A PK were analyzed by intra-individual comparison in SA only for possible drug–drug interaction. Results: 53 pts were treated (SA: n=23, median age 58 yrs; ECOG 0/1/2 [30%/65%/4%]; SB: n=30, median age 62 yrs, ECOG 0/1/2 [27%/70%/3%]). MTD of A in SA was 30 mg; 8 pts had dose-limiting toxicities (DLTs) in Cycle 1 (40 mg: 2/3 pts; 30 mg; 6/19 pts). 30-mg cohort included 19 evaluable pts; 1 pt was replaced during expansion (incomplete PK collection) and had a DLT. MTD of A in SB was 50 mg; 11 pts had DLTs in Cycle 1 (70 mg: 4/5 pts; 60 mg: 6/17 pts; 50 mg: 1/6 pts). Most frequent drug-related AEs in SA were diarrhea (91%), stomatitis (65%) and rash (61%) and in SB were diarrhea (83%), rash (83%) and fatigue (80%); most were Grade 1/2. 6 pts in SA and 8 pts in SB completed 6 treatment cycles; 1 pt in each schedule remain on treatment. Best response in SA was 1 confirmed partial response (CPR; NSCLC, prior sequential chemotherapies and erlotinib) and 6 pts with stable disease (SD). In SB, best response was 1 CPR (bladder cancer, prior sequential chemotherapies) and 10 pts with SD. No clinically relevant PK interactions between A and P were observed. Conclusions: Continuous or pulsed-dose A combined with P exhibited a manageable safety profile. No clinically relevant PK interactions were seen in SA. Continuous dose A 30 mg/d with P 500 mg/m 2 (d1 of each 21d cycle) is the recommended dose for further Ph II studies. No apparent safety or dose advantage was observed in SB. Clinical trial information: NCT01169675.
Multicenter Phase I Studies To Evaluate the Safety, Tolerability, and Clinical Response to Intensive Dosing with the Proteasome Inhibitor PR-171 in Patients with Relapsed or Refractory Hematological Malignancies.
Authors: Owen A. O’Connor, Robert Z. Orlowski, Melissa Alsina, Keith Stewart, Suzanne Trudel, Marcy K. Vallone, Tina M. Woo, Pedro R. Urquilla, Christopher J. Molineaux, Andre Goy
Journal: Blood (2006)
A phase I study of the safety and activation of a cathepsin-activatable fluorescent cancer-specific probe LUM015.
Authors: Melodi Javid Whitley, Diana M. Cardona, Dan G. Blazer, Shelley E. Hwang, Paul J. Mosca, Joan Cahill, Jorge M. Ferrer, David B. Strasfeld, Jeffrey K. Mito, Kyle C. Cuneo, Nicole Larrier, Nerissa Williams, Ivan Spasojevic, Richard F. Riedel, William Eward, W. David Lee, Linda G. Griffith, Moungi Bawendi, David G. Kirsch, Brian E. Brigman
Journal: Journal of Clinical Oncology (2014)

TPS11135 Background: Local recurrence is a common mode of failure for patients with cancer. Intra-operative detection of microscopic residual disease in the tumor bed could be used to decrease the risk of a positive surgical margin, reduce the rate of re-excision, and tailor adjuvant therapy. Previously, we utilized a primary mouse model of soft tissue sarcoma (STS) to develop a novel imaging system to detect cancer (Cancer. 2012). Because cathepsin proteases are preferentially expressed in tumors compared to normal tissue, we used cathepsin-activatable fluorescent imaging agents with a novel imaging device for intra-operative assessment of residual cancer within tumor beds of mice. We demonstrated that residual fluorescence detected in the tumor bed by the imaging system correlates with local recurrence and that image guided surgery improves outcomes for mice with positive residual fluorescence. LUM015 is a pegylated cathepsin-activated imaging agent containing a Cy5 fluorophore attached to a quencher by a polypeptide linker. Upon cleavage of the linker by cathepsin proteases, the quencher is released, allowing fluorescence to be detected. A phase I clinical trial is open at Duke to test the safety of LUM015 (NCT01626066). Methods: This open-label nonrandomized trial compares up to four dose cohorts of LUM015 (cohorts -1 to 3: 0.25, 0.5, 1 and 1.5 mg/kg) in order to determine a safe and recommended phase II dose of LUM015 that labels tumors in human patients. Subjects with STS or breast cancer receive LUM015 by peripheral intravenous injection 2-72 hours prior to scheduled surgical resection. Safety evaluations prior to and during the 24-hour period after injection consist of vital signs, ECG, PFTs, blood and urine studies and documentation of any adverse pharmacological activity (APA). This evaluation is repeated at 2, 7 and 14 days after study agent delivery and an end of study APA assessment occurs 30-35 days after surgery. Pharmacokinetic parameters are also determined. Correlative studies include quantitative imaging as well as histological and biochemical analyses of the resected tissues. To date, cohorts 1 and 2 (n=9 patients) have been enrolled without APA. Enrollment in cohort 3 began in January 2014. Clinical trial information: NCT01626066.
Ocular toxicity with MEK inhibitors in phase I trials: A single centre experience across six clinical trials.
Authors: Vasiliki Michalarea, Maria Jose de Miguel Luken, Nikolaos Diamantis, Anurag Garg, Laura Maubon, Timothy Anthony Yap, L Rhoda Molife, Johann Sebastian De Bono, Paul Ursell, Udai Banerji
Journal: Journal of Clinical Oncology (2015)

11090 Background: MEK is a crucial signalling protein downstream of multiple receptor and non-receptor protein kinases that drive cancer. A range of allosteric MEK inhibitors have been developed and one has been licensed for use in malignant melanoma. We have assessed ocular toxicity in detail across a range of MEK inhibitors. Methods: Patients enrolled in phase I trials of MEK inhibitors between February 2009 and November 2014 were considered eligible for this study. Patients underwent testing of visual acuity by Snellen's chart, ocular pressure assessment and ocular tomography (OCT) at baseline and at various points in each trial. Results: 94 (M:F, 42:52) patients were assessed in 6 trials. The most common tumour types included colorectal, lung, ovarian cancer and melanoma. Significant retinal changes on OCT were detected in 30/94 (31%) patients. 15 (50%) of these patients were symptomatic due to peripheral epithelial detachment (PED), central serous detachment (CSR) and a combination (PED+CSR) in 9/15, 3/15 and 3/15 cases. In 15 asymptomatic patients, significant retinal changes on OCT included PED in 13/15 and PED+CSR in 2/15. National Cancer Institute Common Toxicity Criteria (NCI-CTC) Grade 0, 1, 2 and 3 numbered 60, 30, 4 and 2 events respectively. In patients where OCT was performed, there was a statistically significant difference in average thickness and central thickness of the macula (p = 0.0009 and p = < 0.0001, respectively), but not in total macular volume (p = 0.67), between patients who reported any Grade 0-3 ocular toxicities on ANOVA. There were no episodes of toxicity related drug discontinuations or irreversible ocular toxicity. Conclusions: Reversible retinal changes occur across a diverse number of MEK inhibitors indicating this to be a class effect. Approximately half of patients were symptomatic; however, with careful monitoring by OCT, appropriate dose delays and dose reductions, it is possible to continue treatment in most instances.
Clonal Hematopoiesis Is Associated with Therapy-Related Myeloid Malignancies in the Elderly
Authors: Nancy K Gillis, Markus Ball, Qing Zhang, YuLong Zhao, Sean Yoder, Maria E. Balasis, Tania E. Mesa, David Sallman, Jeffrey E. Lancet, Rami S. Komrokji, Alan F List, Howard L McLeod, Dana E Rollison, Eric Padron
Journal: Blood (2016)
BATLLE-2: <i>KRAS</i> mutation and outcome in a biomarker-integrated study in previously treated patients (pts) with advanced non-small cell lung cancer (NSCLC).
Authors: Vassiliki Papadimitrakopoulou, J. Jack Lee, Ignacio Ivan Wistuba, Anne S. Tsao, Frank V. Fossella, John Heymach, Neda Kalhor, Sanjay Gupta, Scott N. Gettinger, Lauren Averett Byers, Julie Izzo, Vincent A. Miller, Lixia Diao, Jing Wang, Caimiao Wei, Kevin R. Coombes, David J. Mauro, Eric H. Rubin, Waun Ki Hong, Roy S. Herbst
Journal: Journal of Clinical Oncology (2014)

8042 Background: BATTLE-2 is building on the personalized medicine approach pioneered in the Biomarker-integrated Approaches of Targeted Therapy for Lung Cancer Elimination (BATTLE-1) trial, and is designed to address mutant KRAS and identify predictive biomarkers for targeted therapies in chemo-refractory pts. Methods: Pts refractory to at least 1 prior therapy, were adaptively randomized (AR), in this phase II, multi-center study, after tumor biopsy and exclusion of sensitizing EGFR mutations (mut+) or ALK fusions to 4 arms: erlotinib (E) 150 mg qd, E plus the AKT inhibitor MK-2206 (M) 135 mg q week, M 100 mg q week plus the MEK inhibitor AZD6244 (A) 100 mg qd, and sorafenib (S) 400 mg bid. The primary objective is 8-week disease control rate (DCR). In Stage 1, 200 pts are randomized and in Stage 2, AR of 200 pts will incorporate the best predictive biomarkers from Stage 1, to be derived from protein expression, gene expression profiling, 16-gene Sequenom mutation analysis and next generation sequencing (NGS) of 182 genes by Foundation Medicine. Results: From 6/2011 to 11/2013, 198 pts randomized to E (22 pts), EM (42 pts), MA (73 pts), S (61 pts). Demographics: Median age 62 (range 22-82); male 48%; ECOG PS 0-1 83%, PS 2 17%; Caucasian 89%, Asian 3%, other 8%; never/former/current smokers 33%/60%/7%; adenocarcinoma 73%, squamous 19%, other NSCLC 8%; prior E 37%, KRAS mut+ 23%, median prior therapies for metastatic NSCLC: 2 (range 1-9). Treatment was well tolerated. With 167 pts evaluable, overall 8-week DCR was 47%, worse with E (20%) than with EM (51%), MA (53%) and S (43%) (Fisher’s exact test p= 0.06, 0.02, and 0.14). For KRAS wild type pts, DCR was worse for E (25%) than all other 3 arms (53%, 50%, and 44%, for EM, MA and S). For KRAS mut+ pts, DCR was highest for MA (61%) (0%, 40%, and 43% for E, EM, and S).Partial responses to MA were seen in 2 pts (KRAS mut+/ ARAF mut+, and CDKN2A/FBXW7/TP53mut+). Conclusions: Improved DCR was observed with EM and MA compared with E. The MA combination is active in KRAS mut+ NSCLC and merits further study. Biomarker analysis is ongoing to define better predictive markers and Stage 2 of BATTLE-2 is being redesigned. (Supported by NCI R01CA155196-01A1). Clinical trial information: NCT01248247.