BACKGROUND:Dipeptidyl peptidase IV (DPP4) is a cell surface receptor that possesses numerous substrates implicated in tumor growth and metastasis. Prior studies have suggested an association between DPP4 inhibition and increased progression-free survival (PFS) and overall survival (OS) in colorectal and lung cancers but no benefit in breast or pancreatic cancers. However, no studies to date have explored the impact of DPP4 inhibitors (DPP4i) in patients with metastatic renal cell carcinoma (mRCC). In this study we present a first-time analysis examining the impact of DPP4i use on PFS and OS in patients with mRCC and type 2 diabetes mellitus. METHODS:We performed a retrospective analysis of patients with diabetes and mRCC at the University of Virginia. The study group comprised those whose diabetic regimen included a DPP4i during mRCC treatment. The control group comprised patients whose diabetic regimen did not include a DPP4i during treatment. Cox regression analysis was utilized to determine the hazard ratios of progression and death between groups. RESULTS:Fifty-nine patients were eligible for the study, with 11 in the DPP4i group and 48 in the control group. Cancer progression occurred in 81.8% of patients in the DPP4i group and 66.7% in the control group. No statistically significant differences on PFS (HR: 1.60 [95% CI, 0.75-3.43]) or OS (HR: 0.69 [95% CI, 0.28-1.70]) were found between groups. CONCLUSIONS:This retrospective study explored the effect of DPP4i on outcomes in patients with mRCC and diabetes. DPP4i have been shown to have favorable effects on PFS and OS in some cancers but not in others. The results of this study suggest that DPP4i do not confer clinical benefit in patients with mRCC. Larger studies are warranted to better elucidate the effect of DPP4i in mRCC and the mechanisms underlying differential tumor response to these agents in different malignancies.

426 Background: Dipeptidyl peptidase IV (DPP4) is a cell surface receptor with exopeptidase activity that is expressed on most cell types, and possesses numerous substrates including growth factors, chemokines, and vasoactive peptides. These effects have implicated DPP4 in tumor growth and metastasis. Prior SEER-Medicare and retrospective studies have suggested an association between DPP4 inhibition and increases in both progression-free survival (PFS) and overall survival (OS) in patients with colorectal and lung cancers. Similar studies have shown no associated OS benefit from DPP4 inhibition in breast or pancreatic cancers, and increased OS but not PFS in prostate cancer. However, no studies to date have explored the impact of DPP4 inhibitors (DPP4i) in renal cell carcinoma (RCC). Thus, in this study we present a first-time analysis examining the impact of DPP4i use on PFS in patients with metastatic RCC and type 2 diabetes mellitus. Methods: We performed a single-center retrospective analysis of patients with diabetes and metastatic RCC at University of Virginia. The control group included patients who were on metformin, a sulfonylurea or SGLT2 inhibitor during treatment for metastatic RCC, while the study group included those who were taking a DPP4i with or without metformin and other diabetes medications during treatment. The primary and secondary endpoints of this study were PFS and OS, respectively. Results: Fifty-nine patients were eligible for the study, 11 of whom were taking a DPP4i with or without other diabetic medications during RCC treatment, while 48 were taking metformin with or without other non-DPP4i medications. Cancer progression occurred in 81.8% of patients in the DPP4i group compared to 66.7% of patients in the control group with an odds ratio of 1.58 (95% CI: 0.672-3.71), p = 0.57. No statistically significant difference on PFS (HR: 1.60; 95% CI: 0.75-3.43; p = 0.24) or OS (HR of death: 0.73; 95% CI: 0.27-1.97; p = 0.52) was found in this study. Conclusions: This retrospective study explored the effect of DPP4i on outcomes in patients with metastatic RCC and diabetes. While DPP4i have been shown in previous SEER-Medicare and retrospective studies to have favorable effects on PFS and OS in certain cancers such as colorectal and lung, the results of this study suggest that DPP4i do not confer clinical benefit in patients with RCC, similar to pancreatic and breast cancers. Given the small sample size in this study, larger studies are warranted to better elucidate the effect of DPP4i in metastatic RCC as well as the mechanisms underlying differential tumor response to these agents.

424 Background: The renin-angiotensin system (RAS), traditionally associated with blood pressure regulation and fluid balance, also plays a role in tumor development and growth among several cancer types. Renin-angiotensin system inhibitors (RASI), such as angiotensin converting enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARBs), have been shown in studies of various malignant neoplasms to be associated with improved outcomes. In metastatic urothelial cancer, the use of ACEI and ARBs has been associated with higher rates of tumor regression among patients (pts) receiving immunotherapy (IO) with PD1/L1 inhibitors. One potential mechanistic explanation is RASI-induced downregulation of TGF-beta, for which high expression is a known mechanism of PD1/L1 inhibitor resistance. While the development of novel IO therapies has changed the treatment landscape for mRCC, only one study to date has examined the impact of RAS inhibition in pts with mRCC receiving IO. We hypothesized that concurrent RASI in pts with mRCC receiving IO is associated with increased tumor regression. Methods: We conducted a retrospective analysis of pts with mRCC receiving immunotherapy as a first or second line of treatment from 2016-2023 at the University of Virginia. A logistic regression model was used to evaluate the impact of concurrent RASI on tumor regression. The primary endpoint in this study was any regression of tumor on imaging. Results: Data were available for 147 pts with mRCC who received IO as a first- (n=104, 70.7%) or second- (n=43, 29.3%) line treatment. 52 pts (35.4%) received ACEI/ARBs during IO; 42 pts (40.4%) who received IO as first-line treatment were on ACEI/ARBs and 10 patients (23.2%) who received IO as a second-line treatment were on ACEI/ARBs. Analysis showed that pts who received ACEI or ARBs during IO were more likely to have tumor regression compared to pts who were not on concurrent RASI (OR 7.43 [95% CI 2.70-23.53], p=0.0002). This held true regardless if pts received IO as a first-line (OR 6.02 [95% CI 1.84-23.38], p=0.005) or second-line (OR 9.71 [95% CI 1.51-122], p=0.032) treatment. Conclusions: Our hypothesis generating study suggests that in our RCC population the concurrent use of RASI in pts with mRCC receiving IO was associated with a significantly increased likelihood of tumor regression. These findings highlight the potential therapeutic advantage of RASI in combination with IO for mRCC pts. Further exploration of this association is warranted in prospective studies to improve treatment outcomes for this patient population.[Table: see text]

e17036 Background: Poly (ADP-ribose) polymerase (PARP) inhibition exhibits an enhanced cytotoxic effect in cancers with DDR alterations, but as monotherapy has little activity for those without DDR defects. A variety of combinatorial methods utilizing PARP inhibitors are under investigation to determine if a multimodal approach could benefit patients without DDR alterations. Supported by pre-clinical models, we hypothesized that the PARP inhibitor talazoparib in combination with the chemotherapy temozolomide could induce DNA damage leading to cell death and tumor response. Methods: This is a single arm Phase 1b/2 study of escalating doses of intermittent talazoparib (Day (D) 1-6) plus temozolomide (D2-8) in 28D cycles in patients with mCRPC without DDR mutations. Patients must have failed at least one androgen receptor signaling inhibitor and may have received chemotherapy in the hormone sensitive setting. Response is determined by a composite endpoint of overall response per RECIST v1.1, PSA50% decline, and CTC conversion from >1 to 0. Pharmacokinetic samples were collected, and the mTPI-2 method was used in escalation. Results: 13 patients were enrolled across 4 dose levels in escalation. The most common adverse events were anemia (any grade (Gr) 31%, Gr3 23%), thrombocytopenia (any Gr 54%, Gr3+ 30.7%), fatigue (Gr≤2, 62%), and nausea (Gr1 46%). There was one patient with a DLT (Gr3 neutropenic fever, Gr4 thrombocytopenia). The identified RP2D was talazoparib 1 mg (D1-6) and temozolomide 75mg/m 2 (D2-8). 4 (30.8%) patients met the efficacy endpoint (3 CTC responses, 1 PR, 0 PSA50% decline). While there were no PSA50 responses, 2 (15.4%) patients had a PSA30% decline. Median duration on trial was 20 weeks with 4 (30.8%) patients on trial for ≥6mos, 2 of whom also met the efficacy endpoint. Conclusions: Hematologic toxicity was dose limiting in this combination strategy using intermittent dosing of talazoparib and temozolomide in patients with mCRPC without DDR alterations. A reduction in CTCs to 0 was identified at several dose levels, and PSA30% declines were seen in 2 patients. With identification of the RP2D, enrollment in the Phase 2 study is currently underway. Clinical trial information: NCT04019327 .

TPS5106 Background: Bavdegalutamide (ARV-110) is a novel, oral PROteolysis TArgeting Chimera (PROTAC) protein degrader that targets wild-type androgen receptor (AR) and clinically relevant mutants. Bavdegalutamide demonstrated tumor growth inhibition in multiple xenograft models (eg, AR gene amplification, AR mutation, enzalutamide resistance, and enzalutamide insensitivity). In a phase 1/2 study (NCT03888612), bavdegalutamide showed clinical activity in patients with metastatic castration-resistant prostate cancer (mCRPC) who had previously received 1–2 prior novel hormonal agents (eg, abiraterone and/or enzalutamide), including heavily pretreated patients. Abiraterone is approved, in combination with a corticosteroid, to treat patients with mCRPC or with high-risk castration-sensitive prostate cancer (CSPC). Up to a third of patients treated with abiraterone develop primary resistance to this drug and nearly all patients experience disease progression. Here we describe a phase 1b study that will evaluate the combination of bavdegalutamide with abiraterone at the initiation of progression on abiraterone (prostate-specific antigen [PSA] progression without radiographic progression) to test if the addition of bavdegalutamide will overcome resistance to abiraterone and re-establish the AR pathway blockade in patients with prostate cancer. Methods: Eligible patients are men ≥18 years of age with histologically, pathologically, or cytologically confirmed adenocarcinoma of the prostate and Eastern Cooperative Oncology Group performance status of 0 or 1. Patients must be receiving ongoing treatment with stable doses of abiraterone and a concomitant corticosteroid for mCRPC or CSPC and have PSA progression ≥16 weeks after initiation of abiraterone, ≥2 rising PSA values measured ≥1 week apart, and no radiographic evidence of disease progression while receiving abiraterone. Ongoing androgen deprivation therapy with a gonadotropin-releasing hormone analogue or inhibitor or orchiectomy is required. Prior treatment with enzalutamide, apalutamide, darolutamide, or experimental AR-directed therapies is not permitted. Bavdegalutamide, abiraterone, and a corticosteroid will be administered daily in 28-day cycles. Primary objectives are to evaluate the safety and tolerability of bavdegalutamide plus abiraterone and determine the recommended phase 2 dose and schedule of this combination (based on the incidence of first-cycle dose-limiting toxicities and the frequency and severity of adverse events and laboratory abnormalities). Clinical trial information: NCT05177042.

88 Background: Men with metastatic, castration resistant prostate cancer (mCRPC) harboring DNA repair defects (̃20%) achieve a radiographic progression free survival of 7.4 months with PARP inhibitors (PARPi). Preclinical studies combining a PARPi (olaparib) and DNA damage checkpoint inhibitor (ATR inhibitor, ceralasertib) show synergy, providing the rationale to test this combination in men with mCRPC, including where single agent olaparib has been shown to be active. Methods: Two cohorts were accrued to a trial combining ceralasertib with olaparib in men a) with or b) without DNA repair defects. All patients progressed on ≥1 prior mCRPC therapy with no prior PARPi or platinum chemotherapy. The primary endpoint was disease response (confirmed PSA decline ≥50% and/or RECIST response), while disease progression was defined per Prostate Cancer Working Group 3 definition. Each cohort is analyzed independently for disease endpoints, while both groups were combined for toxicity assessments. Results: The 12 person DNA repair-deficient (DRDef) cohort allowed patients with germline BRCA2 loss (n = 4), somatic BRCA2 loss (n = 1) and ATM loss (n = 1 germline, n = 5 somatic and n = 1 somatic with unknown germline). 35 men without BRCA2/BRCA1 or ATM genomic loss were accrued to the DNA repair-proficient (DRPro) cohort. These men had next-generation sequencing (NGS) on contemporary biopsies (prior to enrolment without intervening therapy, 12), prior NGS on metastatic tissue (10), prior NGS on primary prostatic tissue (n = 3), or cell-free analyses (5). Five patients have incomplete cell-free analyses. At data cutoff (October 2021), in the DRDef cohort, the response rate by confirmed ≥50% PSA decline was 4/10 (40%) including 3 of 4 BRCA2 patients, and another is awaiting sufficient follow up; 1 of 6 ATM-deficient patients responded and another is awaiting sufficient follow up. All 4 DRDef responders remain on therapy (median of 8 months). For patients in the DRPro cohort who have completed therapy and response assessment (n = 21), 3 responded, one with a duration of 12 months, two with 6 months. An updated analysis will be presented. Conclusions: This analysis suggests potential activity of the doublet for DRDef (BRCA2 mainly) and DRPro mCRPC. Ongoing biomarker analysis (e.g. ATM IHC, contemporaneous cell-free DNA analysis rather than archived tissue) may help guide selection of patients most likely to benefit. Clinical trial information: NCT03787680.

447 Background: While ICI prolong OS after platinum chemotherapy in aUC, outcomes vary based on clinical confounders. We aimed to develop a prognostic model in pts receiving ICI in a non-clinical trial setting. Methods: We used a hypothesis driven approach of clinician selected covariates to develop a new prognostic model. Data source was a retrospective cohort of pts treated with ICI at 19 institutions. Demographics, clinicopathologic data, treatment patterns, and OS were collected. Univariate (UVA) Cox regression was done on 24 variables hypothesized to be associated with OS. Variables were retained for multivariate analysis (MVA) if they had statistical relationship with OS (p<0.2) and were included in the final model if p<0.05 on MVA. Each retained covariate was assigned 1 point in the final prognostic model. Stratified median OS and c-statistic were calculated. Results: 415 pts with mean age 69, 26% female, 66% ever smokers, 69% pure UC, 15% upper tract UC, 54% with prior extirpative surgery, Bellmunt risk factors 17%, 51%, 28% and 4% for 0, 1, 2, 3, respectively were included. Non-White race, ECOG PS≥1, albumin<3.5g/dL (lower limit of normal), hemoglobin<10g/dL, absolute neutrophil count (ANC)>8x106/ul (upper limit of normal), and presence of bone or liver metastases (mets) were all associated with worse OS on UVA Cox regression; albumin<3.5 g/dL, ANC>8x106/uL, presence of bone or liver mets remained significant on MVA and were included in the prognostic model. Median (m)OS by new model and Bellmunt are shown in table. C-statistic of the new model was 0.67. Conclusions: Albumin<3.5 g/dL, ANC >8x106/ul, presence of bone or liver mets were negative prognostic factors in pts with aUC treated with ICI. This has comparable features to recently reported 5-factor model using clinical trial data, including LDH (unavailable in our cohort). External validation is being pursued. The proposed model may be used for prognostication, clinical trial design, eligibility and stratification. [Table: see text]

TPS254 Background: Inhibition of poly(ADP-ribose) polymerase (PARP) shows promise in prostate cancer, but is limited to the ~20% of men with defects in genes encoding for DNA repair proteins BRCA1, BRCA2 or ATM (homologous recombination defect positive, HRD+). The effect is modest for HRD+ patients with a progression free survival of ~7 months. Pharmacologically simulating genetic DNA repair defects may expand who benefits to homologous recombination defect negative (HRD-) patients and improve HRD+ response. The ataxia telangiectasia and Rad3-related protein (ATR) is ideal with its roles in cell cycle regulation, replication fork resolution and both single and double strand break repair. Preclinical studies on HRD-/HRD+ cell lines support this. We hypothesize co-inhibition of ATR and PARP will respond regardless of HRD status. Methods: TRAP is a prospective, multi-institutional, phase 2 clinical trial testing AZD6738 combined with olaparib in HRD+ and HRD- mCRPC patients. Primary endpoint is the response rate (RR) by RECIST radiographic response or PSA decline ≥50% in 35 HRD- patients, with a secondary objective of RR in 12 HRD+ patients. HRD+ is mono/biallelic loss of ATM or biallelic loss of BRCA1/2. Tissue based sequencing is done unless completed prior in mCRPC, known BRCA germline loss, treating provider deems biopsy unsafe or biopsy fails. Those unable or failing biopsy are designated as HRD-, but BRCA1/2 and ATM are tested via circulating tumor DNA in a commercial test. Eligible patients must progress after ≥1 line of mCRPC therapy. Progression on a second generation anti-androgen (e.g. apalutamide), abiraterone or within 6 months of docetaxel in hormone sensitive disease are eligible. Treatment entails 160 mg PO daily of AZD6738 on days 1-7 and 300 mg PO BID of olaparib on days 1-28 of a 28-day cycle. Statistical analysis will provide RR with 95% binomial confidence intervals. Analysis of tumor specimens, circulating tumor cells and DNA will be performed for predictors of response and acquired resistance. The study is at four sites in the US, participates in the Prostate Cancer Clinical Trials Consortium, LLC, is managed by the University of Michigan and funded by AstraZeneca. Clinical trial information: NCT03787680.

495 Background: Urinary tract cancer can be pure urothelial carcinoma (PUC) or variant UC (VUC, defined here as pure non-UC or mixed UC + non-UC); VUC often has a worse prognosis. Little is known about outcomes for patients (pts) with VUC receiving ICI. We hypothesized that VUC does not compromise ICI efficacy in pts with aUC. Methods: We performed a retrospective cohort study across 18 institutions. Demographic, clinicopathologic, treatment and outcomes data was collected for pts with aUC who received ICI. Pts were stratified to PUC vs VUC; VUC was further divided by histologic subtype, i.e. squamous, neuroendocrine (NE), etc. We compared overall response rate (ORR) using logistic regression, progression free survival (PFS) and overall survival (OS) using Kaplan-Meier and Cox proportional hazards; p<0.05 was significant. Results: 519 consecutive pts were identified; 405, 414 and 411 included in ORR, OS and PFS analyses, respectively. Demographics included mean age 69, 27% female, 66% ever smokers, 15% upper tract disease, 54% with extirpative surgery. ORR to ICI between pts with PUC and VUC was comparable (both 28%, p=0.86) without significant differences for individual subtypes vs PUC. Median OS for pts with PUC was 11.0 vs 9.9 mo for VUC (p=0.45), but only 3.7 mo for those with NE features (HR=3.01 [95% CI 1.63-5.57] vs PUC, p<0.001). Median PFS was 4.1 vs 5.2 mo for PUC vs VUC (p=0.46) and 2.8 mo for NE (HR=1.85 [95% CI 0.94-3.61] vs PUC, p=0.07). Conclusions: ORR to ICI and OS were comparable across histologic types; however, OS was shorter for tumors with NE features. VUC should not exclude pts from receiving ICI in routine practice and clinical trials.[Table: see text]

4525 Background: Anti-PD(L)1 immune checkpoint inhibitors (ICI) prolong overall survival (OS) after platinum chemotherapy in mUC. However, clinical outcomes in pts with poor PS at time of ICI initiation are unknown. We hypothesized that ICI initiation in pts with ECOG PS 2-3 would be associated with worse outcomes vs. pts with ECOG PS < 2, and impact death location. Methods: A retrospective cohort study in 8 institutions identified pts with mUC who received ICI. Demographic, clinicopathologic, treatment (tx) patterns, tx response, and outcomes were collected. Primary endpoint: overall response rate (ORR). Secondary endpoints: median (m) OS in pts receiving ICI as 1st and 2nd line (1L, 2L); odds of dying in hospital (vs elsewhere) for pts receiving ICI (vs no tx) within 30 days of death; and estimated drug cost for pts with ICI within 30 days of death based on average wholesale price. Unadjusted logistic regression was used to assess association between ORR and ECOG PS (2-3 vs < 2) and wald test was used to compare mOS between ECOG PS (2-3 vs < 2). Results: 194 consecutive pts (30% women, 41% never smokers, median age at diagnosis 69) treated with ICI for mUC were identified. Median number of total tx lines was 2; all pts received ≥1 ICI line (6 pts received 2 ICI lines); 97, 79, 17 and 7 pts received ICI in 1L, 2L, 3L and 4L, respectively; 26% pts with ICI in 1L and 2L had ECOG PS 2-3. ORR and mOS are shown in table. Among 106 pts who died, 96 had available death location; of those, 8% received ICI within 30 days of death. Starting ICI within 30 days of death (vs no tx) was associated with higher odds of hospital death (OR 6.05, 95%CI 1.3-27.6). Estimated average ICI cost/pt within 30 days of death was $1400.58. Conclusions: Pts with ECOG PS 2-3 at time of ICI initiation had similar ORR vs ECOG PS < 2 but worse mOS. ICI initiation within 30 days from death was associated with higher likelihood of hospital death. ICI may not circumvent the negative prognostic role of poor PS, so biomarker-based pt selection is critical. Limitations include lack of adjustment for selection bias and other confounders at time of ICI initiation; data validation is ongoing. [Table: see text]

2010 Background: CPIs are widely used in the treatment of both metastatic melanoma and NSCLC. BM frequently occur and are treated with CNS-RT. Since both CNS-RT and CPIs can cause neuro-inflammation, we tested the hypothesis that concomitant treatment with CPIs and CNS-RT results in an increased risk of CNS-AEs. Methods: We identified patients with melanoma and NSCLC with BM treated with CNS-RT and seen at our institution between 2014 and 2016. Concomitant treatment with CPIs and CNS-RT was defined as administration of CPIs within 3 months before or after CNS-RT. CNS-AEs were defined as new or worsening edema on brain MRI without disease progression, new or worsening neurological deficit, or need to start or increase corticosteroids. A generalized linear model incorporated significant variables from a univariate analysis to model the incidence of CNS-AEs. Variables considered included the use of CPIs within 3 months of CNS-RT, cancer type, type of CNS-RT (gamma knife [GKRS] versus whole brain radiation therapy [WBRT]), number of metastases, and maximum metastasis size. Results: We identified 213 cases of CNS-RT (NSCLC 167 [78%], GKRS 147 [69%], WBRT 63 [30%], median 2 BM [1 to > 20], median 17 mm max diameter [2 mm-74 mm]). Patients were 52% female with median age 61 (range 21-87), and ECOG 0-2 in 93% at time of CNS-RT. CNS-AEs occurred in 40 (19%) cases. Receipt of CPIs within 3 months of CNS-RT was the only factor associated with an increased risk of CNS-AEs (odds ratio 3.9, 95% CI 1.6-9.2, p-value 0.002). The rates of CNS-AEs were 11 of 28 (39%) in cases which received CPIs within 3 months of CNS-RT and 29 of 184 (16%) in cases which did not. The characteristics of the 11 cases with CPI exposure and CNS-AEs were: 73% underwent GKRS, 45% were NSCLC, 18% received CTLA4 alone, 55% PD-(L)1 alone, 27% combined CTLA4/PD-1, and 55% had a neuro deficit as part of their CNS-AE. Conclusions: This retrospective analysis demonstrates that the use of CPIs within 3 months of CNS-RT is associated with an increased risk of CNS-AEs. CNS-RT modality, cancer type, and metastasis size or number were not associated with an increased risk of CNS-AEs.

155 Background: Platinum-doublet chemotherapy (chemo) is routinely used for treatment of early stage and metastatic NSCLC. Immunotherapy is a proven treatment in these patients as well. The presence of tumor infiltrating lymphocytes (TILs) has been shown to be prognostic of this disease; however, the effect of chemo on TILs and the tumor immune microenvironment in NSCLC has not been well studied. We tested the hypothesis that chemo results in a decrease in the presence of TILs in NSCLC. Methods: We retrospectively identified patients treated with neo-adjuvant platinum-doublet chemo who underwent surgical resection from 2007-2015 at the University of Virginia. The specimens were sectioned and IHC stained for CD8, FoxP3, and PD-L1. Two independent investigators assessed a central and a peripheral high power field of tumor for number of CD8 and FoxP3 positive TILs. An independent pathologist assessed tumor cell PD-L1 expression. The nonparametric Wilcoxon Mann Whitney test was used to compare measurements of TILs in chemo-exposed tissue to a control cohort from a database of NSCLC surgical specimens that had not received pre-operative therapy. Results: Of the 17 patients who met eligibility criteria, 11 had sufficient tissue for evaluation. Results are shown in Table 1. There was a significant decrease in CD8 and FoxP3 TILs in both the center and periphery in patients exposed to chemo. There was no difference in PD-L1 expression. Conclusions: These data suggest that platinum-doublet chemo significantly decreases the presence of cytotoxic and regulatory subsets of TILs without effecting PD-L1 expression. This study is limited by the lack of pre-treatment tumor samples to compare pre- and post-treatment TILs in individual patients. Further studies are warranted to evaluate the impact of decreased TILs in the setting of concurrent or sequential immunotherapy treatment with chemo in NSCLC. [Table: see text]