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Suresh S Ramalingam
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MA 18 - Global Tobacco Control and Epidemiology II (ID 676)
- Event: WCLC 2017
- Type: Mini Oral
- Track: Epidemiology/Primary Prevention/Tobacco Control and Cessation
- Presentations: 1
- Moderators:H. Kawai, Christian Klaus Manegold
- Coordinates: 10/17/2017, 15:45 - 17:30, Room 511 + 512
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MA 18.06 - Clinical Prognostic Model for Older Patients with Advanced Non-Small Cell Lung Cancer (ID 8113)
15:45 - 17:30 | Author(s): Suresh S Ramalingam
- Abstract
- Presentation
Background:
The median age at diagnosis of lung cancer is 70 years. Older patients are often not prescribed standard therapy. Due to multiple competing causes of death, older patients often do not demonstrate a benefit in overall survival (OS). It is important to know which older patients would actually be candidates for aggressive therapy based on their prognosis, and to develop a simple prognostic model that can help clinicians determine individual prognosis.
Method:
Data on patients enrolled on 38 NCI-sponsored cooperative group clinical trials of advanced non-small cell lung cancer (NSCLC) from 1991 to 2011 were analyzed. Multivariable Cox PH model was built with a stepwise procedure with all potential predictors: age, sex, race, ethnicity (Hispanic or non-Hispanic), performance status, initial stage, BMI, and weight loss in the past 3/6 months. We derived a prognostic score using the estimated Cox PH regression coefficient in the training set. To assess the performance of our prognostic model, we calculated the area under receiver operating characteristic (ROC) curve of 1- and 2-year survival in the testing set.
Result:
The final analysis included 1454 NSCLC patients ≥70 years of age. These patients were randomly divided into a training set (n=962) and a testing set (n=492). The prognostic risk score was calculated as: 3 (if male) + 3 (if PS=1) + 8 (if PS=2) + 11 (if initial stage=IV) + 4 (if weight loss). Patients were classified into three prognostic groups by tertiles: good (0-6), intermediate (7-14) and poor (≥15). The median OS in the three groups in the testing set were: 14.6 months (95% CI, 12.2-18.5); 12.2 months (95% CI, 10.7-14.4) and 7.0 months (95% CI, 5.6-8.9), respectively. Despite its simplicity, the present model had area under the 1-year and 2-year ROCs (0.63 and 0.68, respectively) that were higher than existing models.
Conclusion:
Male gender, poor performance status, distant metastases and weight loss immediately prior to diagnosis predict for poor OS in older patients with advanced NSCLC. This study proposes a simple prognostic model for older adults with advanced NSCLC based on basic clinical characteristics that are part of the routine evaluation process for every patient with NSCLC.
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OA 01 - The New Aspect of Radiation Therapy (ID 652)
- Event: WCLC 2017
- Type: Oral
- Track: Radiotherapy
- Presentations: 1
- Moderators:M. Hiraoka, S.H. Kim
- Coordinates: 10/16/2017, 11:00 - 12:30, F201 + F202 (Annex Hall)
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OA 01.06 - Radiation Therapy is Associated with an Increased Incidence of Cardiac Events in Small Cell Lung Cancer Patients (ID 8469)
11:00 - 12:30 | Author(s): Suresh S Ramalingam
- Abstract
- Presentation
Background:
Radiation (RT) dose to the heart was a predictor of inferior overall survival (OS) in the non-small cell lung cancer trial RTOG 0617, but little data quantifies cardiac morbidity for small cell lung cancer (SCLC) patients treated with RT.
Method:
The Surveillance, Epidemiology, and End Results (SEER) Program database and Medicare claims data were queried to establish rates of cardiac events (CE) among SCLC patients treated with chemotherapy (CTX) +/- RT. CE were defined as any new cardiac diagnosis including ischemic disease, cardiomyopathy, dysrhythmia, heart failure, and pericarditis. Chronic/pre-existing diagnoses were not counted as events. CTX-only patients were matched to CTX + RT patients to account for start date of RT. Second phase of propensity score matching (PSM) balanced demographical and clinical differences. Multivariate analysis (MVA) determined effect of tumor and RT covariates on CE and OS. Kaplan-Meier and cumulative incidence (CI) function curves were generated.
Result:
From 2000 – 2011, 7,060 patients were available: 2,892 (40.9%) limited-stage and 4,168 (59.0%) extensive-stage. As expected, CTX + RT patients had better OS (p < 0.001). OS for the CTX + RT and CTX-only groups: 35.0 vs. 21.4% at 12 months, and 6.6 vs 2.3% at 60 months, respectively. RT was associated with CE (p = 0.008), with CI as follows for the CTX + RT and CTX-only groups: 36.4 vs. 35.4% at 12 months, and 44.1 vs 39.0% at 60 months, respectively. MVA demonstrated higher hazard ratio of CE for extensive-stage patients (p < 0.001), black race (p < 0.001), and increased Charlson-Deyo score (p = 0.001). After PSM, 5,286 patients were included. Again, CTX + RT patients had better OS (p < 0.0001). OS for the CTX + RT and CTX-only groups: 30.6 vs. 22.5% at 12 months, and 5.3 vs 2.7% at 60 months, respectively. RT was still associated with CE (p = 0.033) after PSM, with CI of CE for the CTX + RT and CTX-only groups: 36.3 vs. 34.8% at 12 months, and 43.0 vs 38.6% at 60 months, respectively. Tumor laterality (p = 0.84) and RT modality (p = 0.62) were not associated with CE, though low numbers were treated with intensity-modulated versus 3D conformal RT (1:15 ratio).
Conclusion:
In this large database study we demonstrated RT is associated with an absolute increase in the rate of CE at 5-years of approximately 5%. Further evaluation of cardiac sparing radiation techniques should be evaluated for patients with SCLC.
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OA 05 - Next Generation TKI (ID 657)
- Event: WCLC 2017
- Type: Oral
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:James Chih-Hsin Yang, Fiona Blackhall
- Coordinates: 10/16/2017, 15:45 - 17:30, Room 301 + 302
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OA 05.02 - Osimertinib vs SoC EGFR-TKI as First-Line Treatment in Patients with EGFRm Advanced NSCLC (FLAURA): Plasma ctDNA Analysis (ID 8978)
15:45 - 17:30 | Author(s): Suresh S Ramalingam
- Abstract
- Presentation
Background:
FLAURA (NCT02296125) is a Phase III, double-blind, randomized study assessing efficacy and safety of osimertinib vs standard of care (SoC) EGFR-TKI as first-line treatment for patients with EGFRm advanced NSCLC. Concordance between tissue and plasma testing for EGFRm (Ex19del/L858R), and progression-free survival (PFS) by baseline plasma EGFRm status were evaluated.
Method:
Eligible patients: ≥18 years (Japan ≥20 years); Ex19del/L858R mutation-positive lung adenocarcinoma; no prior systemic anti-cancer/EGFR-TKI therapy for advanced NSCLC. Randomization: 1:1 to osimertinib 80 mg once daily (qd) orally (po) or SoC (gefitinib 250 mg or erlotinib 150 mg, qd po). At baseline, patients provided tumor tissue samples for central analysis of EGFRm status (cobas EGFR Mutation Test) and blood samples for retrospective analysis of EGFRm status by plasma ctDNA (cobas EGFR Mutation Test v2). PFS by baseline plasma EGFRm status was assessed. Comparison of EGFRm status between baseline tumor tissue and evaluable ctDNA samples was an exploratory endpoint.
Result:
Globally, 556 patients were randomized: osimertinib, n=279; SoC, n=277. Good concordance was observed between central laboratory tissue and plasma testing for EGFRm in the screened population (see table). In plasma EGFRm-positive patients (n=359), osimertinib (n=183) reduced the risk of progression or death by 56% vs SoC (n=176), hazard ratio (HR) 0.44 (95% CI 0.34, 0.57). This was consistent with the overall PFS result observed with osimertinib vs SoC in the full analysis set (FAS; tumor tissue EGFRm-positive by local/central testing), HR 0.46 (95% CI 0.37, 0.57); p<0.0001 and in plasma EGFRm-negative patients (n=124: osimertinib, n=60; SoC, n=64), HR 0.48 (95% CI 0.28, 0.80).Figure 1
Conclusion:
In the subgroup of plasma EGFRm-positive patients, clinical benefit of osimertinib was superior to SoC, consistent with the overall FLAURA FAS. These results, and good concordance between tissue and plasma testing for EGFRm, support the utility of plasma EGFRm testing for selecting patients eligible for first-line osimertinib treatment.
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OA 08 - Neuroendocrine Carcinoma: Translational (ID 667)
- Event: WCLC 2017
- Type: Oral
- Track: SCLC/Neuroendocrine Tumors
- Presentations: 1
- Moderators:David S Ettinger, S. Zöchbauer-Müller
- Coordinates: 10/17/2017, 11:00 - 12:30, Room 311 + 312
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OA 08.06 - Exploratory Analysis for Predictors of Benefit of PARP Inhibitor Therapy in Extensive Stage Small Cell Lung Cancer: ECOG-ACRIN 2511 Study (ID 10321)
11:00 - 12:30 | Author(s): Suresh S Ramalingam
- Abstract
- Presentation
Background:
Veliparib, a potent inhibitor of Poly (ADP) ribose polymerase (PARP) enzyme potentiates standard chemotherapy against small cell lung cancer (SCLC) in preclinical studies. The combination of veliparib (V) with cisplatin/etoposide (CE) doublet as first-line therapy of extensive stage SCLC (ES-SCLC) showed significant signal of efficacy with adjusted PFS HR: 0.63 1-sided p=0.01. There was strata by treatment interaction indicating different efficacy benefit in patient subsets (adjusted treatment HR comparing CE+V: CE: 0.34; 80% CI: 0.22 - 0.51; 1-sided p<0.001 for male patients with high tumor burden versus adjusted HR: 0.81 80% CI: 0.60 - 1.09; 1-sided p=0.18 for other patients subsets). We explored clinical and tissue-based biomarkers as predictors of benefit from this treatment strategy.
Method:
Post-hoc analysis of clinical data was conducted to identify clinical differences in patients who derived significant benefit from the experimental therapy. Clinical differences were compared between patients in the control and experimental arms within the patient stratum with significant clinical benefit. Similarly, comparison was performed between the strata. Archival tissue samples collected from patients with ES-SCLC enrolled and treated on E2511 study was employed for biomarker analysis using immunohistochemistry to assessSLFN11 and DNA-PK expression. The study has 88% power to detect a PFS hazard ratio of 0.5 comparing biomarker positive to negative patients using a one-sided 0.025 level logrank test.
Result:
There was an imbalance between control and experimental arms in the Male/abnormal LDH stratum (in strata) with respect to Age: p=0.006; malignant pleural effusion: p=0.095 and T stage: p=0.02. Median PFS was 5.1 mos on CE (95% CI 4.1-6.1) vs. 6.2 mos on CE+V (95% CI 5.9-8.8); HR=0.32, p=0.002 (unadjusted); median OS on CE was 8.8 mos (95% CI 6.6-11.1) vs. 9.5 mos on CE+V (95% CI 7.8-12.8); HR=0.76, p=0.39. Mutivariable analysis controlling for these imbalances still showed a benefit of veliparib (HR=0.26, p=0.001). Comparison of “in strata” group (N=46) to the “not in strata” group (N=82) showed significant imbalance in pleural effusion (p=0.058); elevated AST (p=0.0099) and bilirubin (p=0.0447). Median PFS was identical at 5.9 mos for both groups while median OS was 10.7 mos (95% CI 8.9-13.2) for “not in strata” subsests vs. 8.8 mos (95% CI 7.8-10.8) for “in strata” with a HR of 1.57 (p=0.027) comparing “in strata” to “not in strata”. Outcome differences based on SLFN11 and DNA-PK expression will be presented at the meeting.
Conclusion:
PFS benefit of PARP inhibitor therapy in extensive stage SCLC patients with elevated LDH and male gender was not associated with any other clinical characteristics.
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OA 09 - EGFR TKI Resistance (ID 663)
- Event: WCLC 2017
- Type: Oral
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:Thanyanan Reungwetwattana, Lecia V Sequist
- Coordinates: 10/17/2017, 11:00 - 12:30, Room 301 + 302
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OA 09.01 - Characterizing the Genomic Landscape of EGFR C797S in Lung Cancer Using ctDNA Next-Generation Sequencing (ID 10213)
11:00 - 12:30 | Author(s): Suresh S Ramalingam
- Abstract
- Presentation
Background:
Osimertinib is a third-generation EGFR tyrosine kinase inhibitor (TKI) active in T790M-positive lung cancer. Acquired resistance to osimertinib is driven by EGFR C797S in ~20-30% of cases. Next-generation sequencing (NGS) of circulating tumor DNA (ctDNA) can be used to identify resistance mechanisms. The allelic configuration (cis vs. trans) of C797S with respect to T790M has therapeutic implications, but the relative frequency of each and other co-occurring genomic alterations are not well defined in clinical samples.
Method:
We queried the Guardant Health database for lung adenocarcinoma patients and an EGFR C797S mutation. All patients had comprehensive ctDNA testing using the Guardant360 NGS assay between June 2015 and June 2017. Cis/trans configuration for T790M and C797S was determined using Integrated Genomics Viewer software.
Result:
We identified 50 unique patients with a total of 66 samples which were C797S positive. All had a co-existent EGFR activating mutation (del19 74%, L858R 24%, other 2%). 60/66 (91%) C797S+ samples were also T790M+. In the 6 samples with C797S but without T790M in ctDNA, 4 were from patients who were T790M+ on a prior Guardant360 assay, 1 never had T790M in blood or tissue and developed C797S while on 1[st]-line afatinib, and 1 had no further clinical details available. T790M and C797S were on the same allele (cis configuration) in 44/46 evaluable patients (98%); 1 (2%) was in trans. One sample had two different C797S mutations, one cis and one trans to T790M. 13 C797S+/T790M+ samples (22%) had multiple C797X mutations detected and 12 samples carried other mutations in or adjacent to the EGFR ATP-binding pocket (e.g. L792, F795, G796, etc). The most common non-EGFR mutations co-occurring with C797S were BRAF amplification/mutation (20%), MET amplification (17%), PIK3CA mutation/amplification (15%), CCNE1 amplification 14% and MYC amplification (14%).
Conclusion:
Understanding EGFR TKI resistance mechanisms is critical to developing more effective therapies. ctDNA offers a non-invasive method to characterize the resistance landscape. Our data suggests C797S most commonly occurs with T790M in cis (98%), a state associated with resistance to all currently available EGFR TKIs. The trans configuration, which may respond to combined 1[st]/3[rd]-gen EGFR TKIs, is rare (2%). Moreover, C797S is frequently detected along with other resistance mechanisms in ctDNA, underscoring the heterogeneity of resistant cancers. New treatments targeting C797S/T790M are needed, as is a deeper understanding of therapeutic targeting of heterogeneity in resistant cancers.
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P1.08 - Locally Advanced NSCLC (ID 694)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Locally Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 10/16/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P1.08-003 - Concomitant Chemotherapy and Radiotherapy with SBRT Boost for Unresectable, Stage III Non-Small Cell Lung Cancer: A Phase I Study (ID 8181)
09:30 - 16:00 | Author(s): Suresh S Ramalingam
- Abstract
Background:
Stereotactic Body Radiation Therapy (SBRT) is now the standard of care in medically inoperable stage I non-small cell lung cancer, yielding high rates of local control. It is unknown if SBRT can be safely utilized in the locally advanced NSCLC setting. This multi-institution phase I study evaluated the safety of 44 Gy conventionally fractionated thoracic radiation with concurrent chemotherapy plus a dose escalated SBRT boost to both the primary tumor and involved mediastinal lymph nodes. The primary endpoint of this study was to establish the maximum tolerated dose (MTD) of the SBRT boost.
Method:
Inclusion criteria included unresectable stage IIIA or IIIB disease, primary tumor ≤8 cm, and N1 or N2 lymph nodes ≤5 cm. Tumors were staged with PET/CT while four dimensional CT simulation was employed for radiation planning. The treatment schema was 44 Gy thoracic radiation (2 Gy/day) with weekly carboplatin and paclitaxel chemotherapy. A second CT simulation was obtained after 40 Gy was delivered, and a SBRT boost was planned to the remaining gross disease at the primary site and involved lymph nodes. Four SBRT boost dose cohorts were tested: Cohort 1 (9 Gy x 2); cohort 2 (10 Gy x 2); cohort 3 (6 Gy x 5); and cohort 4 (7 Gy x 5). Patients were treated in cohorts of three patients and using Bayesian Escalation with Overdose Control (EWOC) method to determine Maximum tolerated dose of the SBRT boost. Dose limiting toxicities (DLT) were defined as any grade 3 or higher toxicities within 30 days of treatment attributed to treatment, not including hematologic toxicity, or any grade 5 toxicity attributed to treatment.
Result:
The study enrolled 19 patients from 11/2012-12/2016. There were 4 screen failures and 15 patients were treated on study. There were no DLTs in dose cohort 1 (n = 3) and 2 (n = 6). One patient in dose cohort 3 (n = 3) developed a DLT, and 2 patients in dose cohort 4 (n = 3) developed a DLT. The calculated MTD was 6 Gy x 5. The DLT observed at this dose level was a tracheoesophageal fistula; given this substantial toxicity, there was investigator reluctance to enroll further patients in this dose level. Thus the calculated MTD is 6 Gy x5, however 10 Gy x 2 is felt to be a reasonable dose as well given no grade 5 toxicities occurred with this dose.
Conclusion:
The MTD of a SBRT boost combined with 44 Gy thoracic chemoradiation is 6 Gy x 5. A SBRT boost dose of 10 Gy x 2 could be considered very safe with no grade 3 or higher toxicities observed at this dose level.
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P3.03 - Chemotherapy/Targeted Therapy (ID 719)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Chemotherapy/Targeted Therapy
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.03-007 - LCMC2: Expanded Profiling of Lung Adenocarcinomas Identifies ROS1 and RET Rearrangements and TP53 Mutations as a Negative Prognostic Factor (ID 8338)
09:30 - 16:00 | Author(s): Suresh S Ramalingam
- Abstract
Background:
The Lung Cancers Mutation Consortium (LCMC) is a multi-institutional effort where 16 sites identify oncogenic drivers and pool data to assess the impact of targeted therapies in patients with lung adenocarcinomas. We now report the results of the second patient cohort (LCMC2) with an expanded multiplex molecular panel to include RET and ROS1 and tumor suppressors.
Method:
904 patients with centrally confirmed stage IV lung adenocarcinomas who were candidates for therapy had at least one of 14 oncogenic drivers assessed in a CLIA-compliant laboratory using genotyping, FISH, massively parallel sequencing (NGS), and immunohistochemistry (IHC) analyses.
Result:
Among 423 patients tested for all 14 targets, we found a driver in 65%. Mutated KRAS was found in 31%, sensitizing EGFR in 14%, MET amplification in 5%, ALK rearrangements in 4%, BRAF V600E in 3%, and HER2 in 3%. Rearrangements in RET and ROS1 were each found in 2% (CI 1 to 3%). Using IHC, PTEN loss was found in 8% (CI 6 to 11%) and MET expression in 58% (CI 55 to 61%). Use of targeted therapies in patients with EGFR, HER2, or BRAF mutations, ALK, ROS1, or RET rearrangements, and MET amplification was associated with a gain in overall survival of 1.5 years relative to those with the same drivers not receiving targeted therapy and a gain of 1 year relative to those without an actionable driver. Current and former cigarette smokers derived a survival benefit from targeted therapies similar to never smokers (p=0.975). Among 154 patients who had all drivers assessed and NGS testing in addition, any TP53 mutation was associated with poorer survival among those with EGFR, ALK, or ROS1 (p=0.014). STK11 was detected in 11%, all in patients with KRAS mutations.
Conclusion:
Using an expanded testing panel, LCMC2 demonstrates the survival benefit of matching targeted treatments to oncogenic drivers in patients with lung adenocarcinomas, identifies additional prognostic factors, and supports the performance of multiplex molecular testing on specimens from all individuals with lung adenocarcinomas irrespective of clinical characteristics. We detected either MET amplifications or HER2 mutations in 7%, together more than the 4% with ALK. A targeted drug is available in the United States for 35% of patients with lung adenocarcinomas. The routine use of massively parallel sequencing (NGS) detects both targetable drivers and tumor suppressor genes that have significance for therapy selection and prognosis. Supported by Free to Breathe
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P3.04 - Clinical Design, Statistics and Clinical Trials (ID 720)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Clinical Design, Statistics and Clinical Trials
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.04-008 - A Phase 1b/2 Study of Atezolizumab With or Without Daratumumab in Advanced or Metastatic Non-small Cell Lung Cancer (NSCLC) (ID 10214)
09:30 - 16:00 | Author(s): Suresh S Ramalingam
- Abstract
Background:
Daratumumab (DARA), a human CD38 monoclonal antibody, is approved for the treatment of patients with relapsed/refractory multiple myeloma (RRMM). DARA produces deep clinical responses in RRMM and induces T-cell expansion through the reduction of immune suppressive cell populations, such as CD38[+] myeloid-derived suppressor cells and regulatory T and B cells. Atezolizumab (atezo) is a humanized programmed death-ligand 1 (PD-L1) monoclonal antibody that blocks the interaction between PD-L1 and the programmed death-1 and B7.1 receptors, reinvigorating anticancer immune responses. Atezo was recently approved for patients with metastatic NSCLC that progressed on or during platinum therapy based on data showing improved overall survival (OS) in the atezo vs docetaxel treatment arm in two clinical trials. The combination of DARA and atezo may improve clinical responses in NSCLC by enhancing anti-tumor T-cell responses facilitated by checkpoint inhibition. This study will assess the anti-tumor activity and safety profile of DARA plus atezo vs atezo alone in patients (pts) with previously treated advanced or metastatic NSCLC.
Method:
This is an ongoing phase 1b/2 randomized, open-label, multicenter study of DARA (16 mg/kg intravenous [IV] weekly for 3 cycles [Days 1, 8, and 15] and then Day 1 of each 21-day cycle thereafter) in combination with atezo (1200 mg IV; Day 2 of Cycle 1 and Day 1 of each 21-day cycle thereafter) versus atezo alone (1200 mg IV; Day 1 of Cycle 1 of each 21-day cycle). Eligible pts (≥18 years) must have advanced or metastatic NSCLC and have received 2 or more cycles of standard platinum-based therapy with disease progression or intolerance to therapy. Eastern Cooperative Oncology Group performance status of ≤1 and known PD-L1 tumor status are required. Pts previously treated with anti-CD38 therapy, including DARA, CD137 agonists, or immune checkpoint inhibitors are excluded. The primary endpoint is overall response rate. Secondary outcomes include safety, duration of response, clinical benefit rate (≥16 weeks duration), progression-free survival, OS, and pharmacokinetics and immunogenicity of DARA and atezo when given in combination. Approximately 96 pts will be enrolled; 6 pts will receive combination therapy in a safety run-in cohort for evaluation of dose-limiting toxicity followed by 90 pts randomly (1:1) assigned to the 2 treatment arms. ClinicalTrials.gov number, NCT03023423.
Result:
Section not applicable
Conclusion:
Section not applicable
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P3.13 - Radiology/Staging/Screening (ID 729)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Radiology/Staging/Screening
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.13-027 - Utilization of PET Scan in Advanced Stage Non-Small Cell Lung Cancer in the United States (ID 10031)
09:30 - 16:00 | Author(s): Suresh S Ramalingam
- Abstract
Background:
PET scans are used during diagnosis and staging of lung cancer. The role of PET scan in guiding therapy for advanced stage non-small cell lung cancer (NSCLC) is not proven, but it continues to be used during the treatment course at many centers. We studied the Surveillance, Epidemiology, and End Results (SEER) Program database and Medicare claims data to evaluate the use of PET scan in advance stage NSCLC patients in the United States and the impact on patient outcome.
Method:
The SEER-Medicare database was queried to capture patients with stage IV non-small cell lung cancer diagnosed between the years 2000-2011. The cohort of patients that received PET scan after diagnosis were analyzed and compared with the cohort that did not receive PET. The univariate (UV) association between covariates and overall survival (OS) were compared by log-rank tests. Time dependent Cox Model was used in multivariable (MV) analysis, with time from diagnosis to first PET scan as time-dependent variable, while the other covariates as time-independent. All analyses were performed using SAS Version 9.4.
Result:
A total of 52,712 eligible patients with stage IV NSCLC were identified between 2000-2011, out of which 13,873 (26.3%) had received PET scan. Characteristics of PET cohort: median age 74 years, 53% male, 87% white and 82% from metro locations. 87% of the patients that received PET were diagnosed between 2006-2011. In the first year after diagnosis, 70% of the patients had 1 PET, 16% had 2 PETs and 14% had 3 or more PETs. About 64% of the patients had received their first PET scan within 2 months of diagnosis and 19% had it between 2 to 6 months. The average Medicare cost associated with patients that received PET was significantly higher than that of patients that did not receive PET scan ($60,417 vs. $34,287; p<0.001). Chemotherapy and radiation were given in a higher proportion of patients that received PET versus those that did not receive it (56% and 45% versus 26% and 36% respectively; p<0.001). Though univariate analysis revealed that a PET scan within a year of diagnosis was associated with better 1-year survival (HR 0.87, P<0.001), this did not translate into overall survival advantage on multivariable analysis (HR 0.99, P=0.56).
Conclusion:
The utilization of PET scan in stage IV NSCLC patients was associated with higher cost, but without a tangible improvement in survival compared to those that did not have a PET scan.
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SH 01 - WCLC 2017 Highlights of the Previous Day (ID 627)
- Event: WCLC 2017
- Type: Scientific Highlights
- Track: Advanced NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 10/17/2017, 07:00 - 08:00, Room 502
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SH 01.01 - Advanced NSCLC, Clinical Design, Statistics and Clinical Trials, Immunology and Immunotherapy and Patient Advocacy (ID 10745)
07:00 - 08:00 | Presenting Author(s): Suresh S Ramalingam
- Abstract
- Presentation
Abstract not provided
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