bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low skeletal muscle area and association with toxicity and hospitalization with chemotherapy in advanced non–small cell lung cancer.
Authors: Saraf Anurag , He John , Shin Kee-Young , Weiss Jakob , Chen Yu-Hui , Catalano Paul J. , Awad Mark M. , Christiani David C. , Aerts Hugo , Mak Raymond H. 
Published: June 2022

8532 Background: Significant toxicity is common in the treatment of advanced non-small cell lung cancer (NSCLC) and can be associated with adverse events, such as unplanned hospitalization, and worse clinical outcomes. Baseline low skeletal muscle (SM) area is a marker of sarcopenia and has been associated with worse survival in other malignancies, but the association of SM area and toxicity in NSCLC is less studied. Methods: Patients with locally advanced or oligo-metastatic NSCLC treated with combined chemotherapy and radiotherapy with or without surgery from 2002-2013 at a single institution were reviewed. A deep-learning pipeline utilized existing pre-treatment computed tomography scans to calculate SM area at the 3rd lumbar vertebral level. Gold standard SM index (SMI) was calculated, adjusting for height, sex, and dichotomized per previously validated cutoff values. Grade 3 or higher hematologic (G3+ heme) toxicity, was assessed per NCI CTCAE v5.0, within 21-days of first chemotherapy cycle. Hospital use was defined as unplanned ED visit or inpatient hospitalization during chemotherapy. Multivariate analysis (MVA) of toxicity endpoints with SMI and baseline characteristics were analyzed by logistic regression analysis, and with overall survival (OS) using Cox regression analysis. Results: A total of 369 patients met inclusion criteria with median follow-up of 23.0mo (range 1-193mo), median age of 64y (range 29-88y), and were mostly male (51%). Most were clinical stage (AJCC 7th edition) IIIA (44%), IIIB (31%), or IV (10%), while 10% had upfront surgery and adjuvant chemotherapy. Most common regimen was cisplatin-based (48%). Median OS was 25.5mo and PFS was 14.0mo. Patients with low SMI were more likely to be younger (median age 70y vs 62y), ECOG performance status (PS) > 0 (74% vs 59%), lower BMI (median BMI 23.3 vs 27.7), and not receive cisplatin-based regimen (35% vs 53%). There was no difference in histology, stage, surgery, or every 3-week (q3w) chemotherapy dosing. On MVA, low SMI was associated with increased risk of G3+ heme toxicity (OR 1.74, p = 0.04) and increased hospital use (OR 1.79, p = 0.04). G3+ heme toxicity was also associated with surgery and q3w dosing, but not age, PS, BMI, or regimen. Hospital use was also associated with BMI, surgery, and cisplatin-based regimen, but not age, PS, or q3w dosing. G3+ heme toxicity (HR 1.48, p < 0.01), older age (HR 1.02, p = 0.02), and stage 4 (HR 3.32, p < 0.01) were associated with worse survival on MVA, but not low SMI (HR 1.25, p = 0.11), PS, BMI, surgery, or regimen. Conclusions: Low SMI predicted higher risk of G3+ toxicity during first cycle of chemotherapy. High-risk patients with low SMI experienced significant adverse events and should be considered for more aggressive symptom management or alternative treatment strategies.
Lung cancer risk in persons enrolled in low-dose CT screening (LDCT) versus incidental lung nodule programs (ILNP).
Authors: Liao Wei , Faris Nicholas , Fehnel Carrie , Goss Jordan , Pacheco Alicia , Pinsky Paul F , Smeltzer Matthew , Osarogiagbon Raymond U. 
Published: June 2022

8553 Background: LDCT screening saves lives, but <10% of eligible persons participate; eligibility criteria are imperfect; geographic, racial and socio-economic disparities have emerged. ILNP may expand access to early detection. We compared rates of lung cancer diagnosis in LDCT and ILNP population subsets. Methods: Prospective observational cohort study of enrollees in LDCT and ILNP in a community healthcare system in AR, MS and TN. We compared LDCT vs 4 ILNP cohorts (C) based on USPSTF 2021 LDCT eligibility criteria: <50 years (C1, too young); >80 years (C2, too old); 50 – 80 years (C3, ineligible smoking history); 50 – 80 years (C4, eligible). For certain analyses, we stratified the LDCT cohort by baseline (T0) Lung-RADS score (0-2 v 3-4). We used a Cox model to calculate crude and adjusted hazard ratios (aHR) for lung cancer diagnosis within 24 months of enrollment. Results: From 2015-2021, 7050 persons were in LDCT- 6073 (86%) Lung-RADS 0-2 (no/benign lesions), 977 (14%) Lung-RADS 3 or 4 (possibly malignant lesion) on T0 scan; 17,579 were in ILNP, 16%, 10%, 57% and 16% respectively in C1-4. Demographics and tobacco use history of the ILNP cohorts differed strikingly; C4 was very similar to LDCT (Table). Black persons were significantly more in C1 (too young) and C3 (insufficient tobacco use). Diagnosis of lung cancer at 36 months ranged from 1% in C1 to 15% in C4, compared to 3% in LDCT; aHR for lung cancer diagnosis within 2 years ranged from 0.23 to 5.12 (all LDCT ref), but ranged from 0.04 to 1.02 with reference to LDCT Lung-RADS 3-4. Most patients in LDCT and ILNP C2-4 had early stage. There were proportionately more Black lung cancer patients in C1-4, and 3 times more Black patients in C3 and 4 than in LDCT. Conclusions: ILNP provides early-detection access to a larger, more diverse population than LDCT, potentially alleviating race and socio-economics-based outcomes disparities. [Table: see text]
Impact of trilaciclib on multilineage chemotherapy-induced myelosuppression events in patients with extensive-stage small cell lung cancer: Post-hoc analyses of data from randomized clinical trials.
Authors: Goldschmidt Jerome H. , Weiss Jared , Zhou Jenny , Wang Jessie , Young Joshua A. , Lemus Wirtz Esteban , Ruiz Julio , Huang Huan , Hart Lowell L. 
Published: June 2022

8568 Background: Trilaciclib is a short-acting CDK4/6 inhibitor administered prior to chemotherapy for multilineage myeloprotection. Reduced occurrence of chemotherapy-induced myelosuppression (CIM) events across neutrophil, red blood cell, and platelet lineages was reported in 3 Phase 2 clinical trials of trilaciclib versus placebo in patients with extensive-stage small cell lung cancer (ES-SCLC). In this post-hoc trial analysis, we further assessed the impact of trilaciclib on the occurrence of single and concurrent multilineage CIM events. Methods: Analyses were conducted separately by line of chemotherapy. In the first-line (1L) setting, pooled data from the G1T28-05 and G1T28-02 trials, in which trilaciclib or placebo was administered prior to etoposide, carboplatin, and atezolizumab [E/P/A] and E/P, respectively, were used. In the 2/3L setting, analyses were based on data from the G1T28-03 trial where patients received trilaciclib or placebo prior to topotecan. The proportion of patients with single and concurrent multilineage CIM events and incidence rate were estimated per cycle and during the first 4 cycles of chemotherapy. Severe (grade ≥ 3 per CTCAE definition) CIM events of neutropenia (SN), anemia (SA), and thrombocytopenia (ST) were assessed. Concurrent CIM events were defined as having 2 or 3 lineage-specific CIM events overlap for ≥ 1 day. As sensitivity analyses, the occurrence of CIM events in patients with ES-SCLC receiving 1L treatment in the G1T28-05 and G1T28-02 studies was analyzed separately. Results: Compared with placebo, fewer patients receiving trilaciclib had single-lineage CIM events and concurrent events in 2 or 3 lineages during cycles 1–4 of 1L chemotherapy using pooled data from G1T28-05 and G1T28-02 (Table). A similar trend was observed in the 2/3L setting. Generally, SN occurred more frequently in earlier cycles, whereas SA and ST tended to occur later. The sensitivity analysis in each individual 1L trial yielded consistent results with the pooled analysis. Conclusions: Patients with ES-SCLC receiving trilaciclib prior to chemotherapy had fewer single and concurrent multilineage CIM events than patients receiving placebo. Clinical trial information: NCT03041311, NCT02499770, NCT02514447. [Table: see text]
Checkpoint inhibitor accessibility in 15,000+ Indian patients.
Authors: Ravikrishna Madala , Abraham George , Patil Vijay Maruti , Bhattacharjee Atanu , Noronha Vanita , Menon Nandini Sharrel , Joshi Amit , Prabhash Kumar 
Published: June 2022

9012 Background: Access to newer therapies is an issue in low and low middle income countries. Hence we decided to audit our practice in the head and neck and thoracic medical oncology unit from 2015 to 2019 to study the accessibility of checkpoint inhibitors and factors influencing them. Methods: All patients who were registered in the head and neck and thoracic medical oncology unit between 2015-2019 were included in the study. The number of patients who received immunotherapy among them was identified from the prospective database of immunotherapy maintained in the department. We made a list of patients who were eligible for immunotherapy per year and identified how many of them received recommended immunotherapy. The indication for eligibility of immunotherapy was based on published pivotal data and its date of publication of the study online. For nominal and ordinal variable percentage with 95% CI was provided. Factors impacting the accessibility of immunotherapy were identified. Results: A total of 15,674 patients were identified who required immunotherapy; out of them only 444 (2.83%, 95% CI, 2.58-3.1) received it. The distribution of patients eligible as per cancer disease management group and time period is shown in the Table. Among head and neck cancer patients 4.5% (156 out of 3,435) received immunotherapy versus 2.35% (288 out of 12,239) among thoracic cancer patients (p < 0.0001). Among the general category (low socioeconomic), 0.29% (28 out of 9,405) versus 6.6% (416 out of 6,269) among the private category (high socioeconomic) received immunotherapy (p < 0.0001). While 3.7% (361 out of 9,737) among males versus 1.39% (83 out of 5,937) females received immunotherapy (p < 0.0001). There was also a temporal trend seen in the accessibility of immunotherapy (p < 0.0001, Table). Conclusions: The accessibility of immunotherapy is below 3% in India. Patients with head and neck cancers, those with private category and with male gender had higher access to this therapy. There was also a temporal trend observed suggesting increased accessibility over the years. [Table: see text]
Phase 1/1b study of telisotuzumab vedotin (Teliso-V) + osimertinib (Osi), after failure on prior Osi, in patients with advanced, c-Met overexpressing, EGFR-mutated non-small cell lung cancer (NSCLC).
Authors: Goldman Jonathan W. , Horinouchi Hidehito , Cho Byoung Chul , Tomasini Pascale , Dunbar Martin , Hoffman David , Parikh Apurvasena , Blot Vincent , Camidge D. Ross 
Published: June 2022

9013 Background: Osi (third-generation tyrosine kinase inhibitor) is a standard frontline treatment (Tx) for advanced/metastatic EGFR-mutated NSCLC. However, tumors invariably progress after an initial response, with c-Met protein overexpression (OE) often associated with acquired resistance. Second- and third-line Tx options are limited to chemotherapy-based regimens with limited efficacy and significant toxicities. Teliso-V (ABBV-399), an anti–c-Met antibody-drug conjugate, delivers a cytotoxic payload (monomethyl auristatin E) into c-Met OE tumor cells. In a phase 1/1b study (NCT02099058) in patients (pts) with c-Met OE NSCLC, Teliso-V alone or in combination with erlotinib demonstrated an acceptable safety profile and antitumor activity. Interim safety and efficacy data from the Teliso-V + Osi cohort (arm E) of this trial are presented. Methods: Pts (≥18 yr) with metastatic EGFR-mutated, c-Met OE (by central immunohistochemistry) NSCLC who had progressed on a prior Osi regimen were eligible. Pts received Teliso-V (IV Q2W) + Osi (oral; 80 mg QD). Teliso-V was evaluated at 1.6 mg/kg and, after review of safety data, escalated to 1.9 mg/kg (safety evaluation). An expansion cohort was opened at 1.9 mg/kg for pts who had received ≤2 prior lines of systemic therapy. Pharmacokinetics (PK) were assessed throughout the study. Pts received study Tx until disease progression, unacceptable toxicity, or for up to 24 months. Results: As of 20 Dec 2021, 25 pts received Teliso-V (1.6 mg/kg, n = 7; 1.9 mg/kg, n = 18) + Osi. Median age was 60.0 yr; 14 (58%) pts were on prior Tx with Osi for > 12 mo. No dose-limiting toxicities (grade [Gr] ≥3 non-hematologic or Gr 4 hematologic Tx-related adverse events [AEs]) were reported during the safety lead-in or evaluation phases. All-Gr AEs considered possibly related to Teliso-V occurred in 22/25 (88%) pts: the most common (≥20%) were peripheral sensory neuropathy (36%), nausea, and peripheral edema (20% each); Gr ≥3 AEs (> 5%) were anemia (12%) and peripheral motor neuropathy (8%). No Gr 5 events related to Tx were reported. PK of Teliso-V + Osi was similar to single-agent Teliso-V. Efficacy data (19/25 pts) are in the table. The overall objective response rate (ORR) was 58% (67% at 1.9 mg/kg). Conclusions: Teliso-V + Osi is well tolerated with an ORR of 58% (67% at 1.9 mg/kg) in pts with c-Met OE NSCLC who progressed on prior Osi. Clinical trial information: NCT02099058. [Table: see text]
Phase I trial of the RAF/MEK clamp VS-6766 in combination with everolimus using an intermittent schedule with expansion in NSCLC across multiple KRAS variants.
Authors: Minchom Anna Rachel , Sanchez Perez Vicky , Morton Cienne , Manickavasagar Thubeena , Nintos George , Lai-Kwon Julia Elizabeth , Guo Christina , Tunariu Nina , Parker Tom , Prout Toby , Parmar Mona , Turner Alison Joanne , Finneran Laura , Hall Emma , Pachter Jonathan A. , Denis Louis J. , Spicer James F. , Banerji Udai 
Published: June 2022

9018 Background: VS-6766 is a small molecule RAF/MEK clamp that results in the reduction of p-MEK and p-ERK. Preclinical data show synergy of VS-6766 with the mTOR inhibitor everolimus across a panel of KRAS mutated (mt) NSCLC cell lines. This clinical trial evaluated the safety and efficacy of a novel intermittent regimen of VS-6766 and everolimus with an expansion in KRAS mt NSCLC (NCT02407509). Methods: The trial used a 3+3 dose escalation design with an intermittent once a week schedule A, and if tolerated, twice a week schedule B (Mon-Thu or Tue-Fri) for both drugs on a 3 weeks on/1 week off, 28 day cycle. Patients with RAS or RAF mt cancers were eligible for the dose escalation cohort, and 20 patients with KRAS mt NSCLC will be treated in the dose expansion cohort. Toxicity was evaluated by NCI CTC V4 and efficacy was evaluated using RECIST 1.1. Results: A total of 28 patients have been treated; median age 60 yrs (range 36-78), and median lines of previous treatment 3 (range 0-7). Sixteen patients have been treated in the dose escalation (3 in schedule A and 13 in the schedule B). The doses of 4 mg of VS-6766 and 5 mg everolimus (once weekly) were tolerated with no dose limiting toxicities (DLTs) and the dose intensity escalated to schedule B (twice weekly). At 4 mg VS-6766 twice weekly, DLTs were observed in two out of six patients and included grade 4 CPK elevation and grade 3 rash. Thus, the dose in schedule B (twice weekly) was de-escalated to 3.2 mg VS-6766 and the dose of everolimus was kept at 5 mg. No DLTs were reported in 6 patients and thus this was declared as the recommended phase 2 dose (RP2D). At the RP2D, the grade 3-4 drug related AE were rash (18%) and pruritus (7%). In the dose escalation cohorts, 3 partial responses (PRs) were reported (2 KRAS G12D low grade serous ovarian cancer and 1 NRAS Q61K mt thyroid cancer). In the KRAS mt NSCLC expansion cohort, 10 patients are evaluable for efficacy and 2 confirmed responses were reported ( KRAS mutations G12V and G13A) with an objective response rate (ORR) 20% to date. The disease control rate (PR + SD) at the first scheduled evaluation was 90%. The median progression free survival (PFS) in the KRAS mt NSCLC cohort is 6.35 months (95% CI 3.52 – not reached). Updated ORR and PFS data will be presented. Conclusions: A tolerable intermittent dosing schedule targeting both the MAPK and PI3K pathways has been established. The combination of VS-6766 with everolimus has shown activity in patients with a variety of KRAS mutation variants including responses in KRAS mt NSCLC.
A phase Ib/II study of AK112, a PD-1/VEGF bispecific antibody, as first- or second-line therapy for advanced non–small cell lung cancer (NSCLC).
Authors: Zhou Caicun , Ren Shengxiang , Luo Yongzhong , Wang Lei , Xiong Anwen , Su Chunxia , Zhang Zhihong , Li Wei , Zhou Jin , Yu Xinmin , Hu Yanping , Zhang Xiaodong , Dong Xiaorong , Hou Xiaoming , Dai Yuanrong , Song Weifeng , Li Baiyong , Wang Zhongmin Maxwell , Xia Yu 
Published: June 2022

9040 Background: Besides the well-known antiangiogenic effects, anti-VEGF agents also modulate the tumor immune micro-environment, leading to synergic anti-tumor effects. AK112 is a humanized IgG1 bispecific antibody against PD-1 and VEGF. Here, we reported results of an ongoing phase Ib/II trial of AK112 in advanced NSCLC pts. Methods: Pts with stage IIIB/IIIC/IV NSCLC, ECOG PS 0-1 and negative oncogenic drivers were enrolled and given AK112 (10 mg/kg Q3W, 20 mg/kg Q2W, 20 mg/kg Q3W or 30 mg/kg Q3W) intravenously. The primary endpoints were ORR per RECIST v1.1 and safety. Results: At data cutoff (January 5, 2022), 94 pts were enrolled: median age 66.0 years (range: 48-75), PS 1 90.4%, male 85.1%, non-squamous 48.9%, PD-L1 positive (TPS ≥1%) 70.2% and treatment-naïve 84.0%. Of 83 pts evaluable for efficacy, ORR (unconfirmed, similarly hereinafter) and DCR were 22.2%/88.9%, 44.0%/92.0%, 37.9%/93.1% and 100%/100% at doses of 10 mg/kg Q3W, 20 mg/kg Q2W, 20 mg/kg Q3W and 30 mg/kg Q3W, respectively. When doses of AK112 > 10mg/kg Q3W, ORR and DCR were 42.9% (24/56) and 92.9% (52/56) in 56 evaluable pts, 56.3% (18/32) and 100% (32/32) in pts with TPS≥1% at 1st line setting, and 23.5% (4/17) and 76.5% (13/17) in pts with PD-L1 TPS < 1%, respectively. Grade≥3 treatment-related adverse events (TRAEs) occurred in 10.6% (10/94) pts, in which the most common event (occurring in > 1 pt) was pneumonia (2.1%, 2/94). No TRAEs led to permanent treatment discontinuation. Most frequent TRAEs (incidence ≥10%) were proteinuria (17.0%), hypertension (16.0%), lipase increase (12.8%), alanine aminotransferase increase (12.8%), blood urea increase (10.6%), apolipoprotein E increase (10.6%) and hyperglycaemia (10.6%). No significant difference in the incidences of TRAEs were observed between non-squamous and squamous pts. Conclusions: In advanced NSCLC, AK112 was well-tolerated and presented remarkable anti-tumor efficacy. Further phase III studies are planned to validate the findings of this study. Clinical trial information: NCT04900363.
Impact of STK11 copy loss on clinical outcomes to PD-(L)1 blockade in non–small cell lung cancer.
Authors: Gutierrez Catherine , Ricciuti Biagio , Alessi Joao Victor Machado , Pecci Federica , Barrichello Adriana Paula de Castro , Vaz Victor R. , Sholl Lynette M. , Awad Mark M. 
Published: June 2022

9059 Background: STK11 is among the most commonly altered genes in non-squamous lung cancers. While STK11 mutation is associated with diminished efficacy of immune checkpoint inhibition (ICI), particularly in KRAS mutated tumors, it is not known whether STK11 copy deletion influences outcomes to ICI. Methods: Patients with advanced non-squamous non-small cell lung cancer (NSCLC) treated with ICI whose tumors underwent genomic profiling were included. Clinical outcomes to ICI were analyzed according to KRAS mutation and STK11 deletions. STK11 copy number variations (CNVs) were determined using an internal informatic pipeline. Kaplan-Meier methodology was used to estimate event-time distributions. Results: Of 559 patients with non-squamous NSCLCs (Nsq-NSCLC), 40.4% (N = 226) had a KRAS mutation ( KRASmut), 18.4% (N = 103) had an oncogenic STK11 mutation ( STK11mut), and 22.5% had either single (N = 123), or bi-allelic (N = 3) deletion ( STK11del). Given that 32.5% of STK11del cases had a concurrent oncogenic STK11 mutation in our cohort, to isolate the impact of STK11del on ICI outcomes we excluded samples with STK11mut from this analysis. In all comers with NSCLC, STK11del had no impact on objective response rate (22.2% versus 23.8%, P = 0.8), progression-free (PFS, HR 0.90, P = 0.30), and overall survival (OS, HR 0.96, P = 0.79) to ICI. When we examined the impact of STK11del on clinical outcomes to PD-(L)1 blockade among KRASmut cases we found that STK11del was associated with a numerically lower ORR (13.3% versus 30.0%, P = 0.12), and a significantly shorter PFS (HR 0.57, P = 0.018) compared to cases without STK11del. No difference in OS were observed between these groups (HR 0.77, P = 0.39). Among KRASwt NSCLCs, STK11del cases had a similar ORR (22.6% versus 22.9%, P = 0.99), PFS (HR 0.92, P = 0.63), and OS (HR 1.18, P = 0.32) to PD-(L)1 inhibition compared to cases without STK11del. Among KRASmut but not KRASwt NSCLCs, cases with STK11del had significantly lower PD-L1 expression compared to those without STK11 deletions (27.5% versus 70%, P = 0.01). Conclusions: STK11 deletion is associated with low response rate and short progression-free survival among KRAS mutant NSCLCs. Future analyses will incorporate additional cases to increase sample size and immunopathologic findings to assess impact of mono and bi-allelic deletion on protein expression.
Clinicopathologic and mutational landscape of BRAFV600E-mutant non–small cell lung carcinoma.
Authors: Sui Jane Sze Yin , Ladanyi Marc , Rudin Charles M. , Drilon Alexander E. , Riely Gregory J. , Kris Mark G. , Offin Michael 
Published: June 2022

9084 Background: BRAF mutations (mts) occur in 2-5% of non-small cell lung cancers (NSCLC) with approximately 50% being BRAFV600E. Limited data is known regarding the mutational landscape (ML) and prognostic role of co-mutations in BRAFV600E NSCLC. We performed this study to evaluate clinicopathological characteristics and the impact of ML in BRAFV600E NSCLC. Methods: Patients (pts) with BRAFV600Emutant NSCLC were identified using MSK-IMPACT at Memorial Sloan Kettering Cancer Center between January 2014 to October 2021. Baseline clinicopathological characteristics and treatment outcomes were annotated. Due to the enrichment of SETD2 in BRAFV600E NSCLC, we conducted further analyses using cbioportal to identify co-mutations of SETD2 with other actionable mutations in NSCLC. Overall survival (OS) was assessed from the date of metastatic disease until death using the log-rank test. Results: BRAF mutations were detected in 5% of NSCLC samples (512/10220) with 22% (97/435 pts) being BRAFV600E. Of the 97 pts with BRAFV600E NSCLC identified: 57 pts (59%) were females, median age of 68 (range: 38-93 years), 58 pts (60%) were former smokers. All BRAFV600E tumors were adenocarcinoma and the median tumor mutational burden was 5 mt/Mb (range: 0-40). 46 pts (48%) with BRAFV600E NSCLC were diagnosed with de novo metastatic disease. Pts receiving targeted therapy at first, second, and subsequent lines of therapy numbered 17 (29%), 18 (31%), and 10 (17%) respectively. Co-alterations of BRAFV600E with TP53 and SETD2 were found in 45% (44/97) and 42% (41/97), respectively. There is a much lower prevalence of concurrent inactivating SETD2 mutations than with other actionable alterations in NSCLC: ROS1 (9%), ALK (8%), RET (8%), HER2 (6%), MET (5%), KRAS (5%), EGFR (2.9%) and BRAFnon-V600E (2%). Median OS in BRAFV600E+/ TP53+ vs BRAFV600E+/ SETD2+ were 35 vs 36 mos (HR 0.88m 95% CI 0.45-1.75, P= 0.71) and BRAFV600E+/ TP53+/ SETD2+ vs BRAFV600E+/ TP53-/ SETD2- were 19 vs 39 mos (HR 0.37, 95% CI 0.09-1.50, P= 0.06). Conclusions: Among the BRAFV600E lung adenocarcinomas, concurrent TP53 mutation and SETD2 inactivation define a patient subset with significantly shorter overall survival. Further studies are warranted to investigate the role of SETD2 mutations in the context of BRAFV600E in NSCLC pts.