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Mor Tal Moskovitz
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EP1.14 - Targeted Therapy (ID 204)
- Event: WCLC 2019
- Type: E-Poster Viewing in the Exhibit Hall
- Track: Targeted Therapy
- Presentations: 1
- Now Available
- Moderators:
- Coordinates: 9/08/2019, 08:00 - 18:00, Exhibit Hall
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EP1.14-12 - KRAS Exon 2 Mutation - A Resistance Pathway to 1st and 2nd Generation EGFR TKIs (Now Available) (ID 1353)
08:00 - 18:00 | Presenting Author(s): Mor Tal Moskovitz
- Abstract
Background
The most common resistance pathway to first and second generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) in advanced non-small cell lung cancer (aNSCLC) is acquired EGFR T790M mutation. Other resistance mechanisms composed of amplifications of MET, HER-2 and small cell transformation. Acquired KRAS mutation is known as resistance mechanism to 3rd generation EGFR TKIs, but not to 1st or 2nd generation.
Method
Patients with EGFR positive NSCLC had molecular profiling done upon resistance to 1st or 2nd generation EGFR TKIs, done by next generation sequencing on FFPE tissue or cfDNA from plasma including EGFR exons 19, 20, 21, KRAS exon 2 and BRAF exon 15. Treatment outcomes and prognosis data were taken from the medical records.
Result
Fifty-three EGFR positive NSCLC patients had molecular profiling done upon resistance to 1st or 2nd generation EGFR TKIs since August 2017, of them 48 had KRAS exon 2 mutation tested. Six (12.5%) patients had KRAS exon 2 mutation, found on plasma in 5 patients and in tissue in 1 patient. Of the 6 patients, the original EGFR mutation was found in 3 patients (50%), and 2 had concurrent EGFR T790M mutation. One patient had KRAS mutation on the initial EGFR testing, although had prolong response to EGFR TKIs.
All patients responded to 1st line EGFR TKIs. Upon progression- the 3 patients tested positive for EGFR T790M mutation were treated with osimertinib, although only 1 patient with concurrent KRAS and EGFR T790M mutation responded, and 2 patients with no EGFR T790M mutation were treated with chemotherapy with progressive disease.
Conclusion
We found acquired KRAS mutation as resistance mechanism for EGFR TKIs in 12.5% of patients with EGFR positive NSCLC treated with 1st or 2nd generation EGFR TKIs.
The patients with NSCLC tested positive for KRAS as resistance mechanism for EGFR TKIs were characterized by poor response to either TKIs or chemotherapy. Therefore, testing for KRAS exon 2 mutation is advised upon disease progression during EGFR TKI therapy.
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OA11 - Decomplexifying Molecular Targets, Immunotherapy and Treatment Settings in the Real World (ID 137)
- Event: WCLC 2019
- Type: Oral Session
- Track: Treatment in the Real World - Support, Survivorship, Systems Research
- Presentations: 1
- Now Available
- Moderators:Kumar Prabhash, Jyoti D Patel
- Coordinates: 9/09/2019, 14:00 - 15:30, Interlaken (1988)
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OA11.06 - Alternative Nivolumab (N) Duration and Scheduling in Advanced Non-Small Cell Lung Cancer (aNSCLC): Real-Life Data (Now Available) (ID 1921)
14:00 - 15:30 | Author(s): Mor Tal Moskovitz
- Abstract
- Presentation
Background
Little is known regarding the optimal scheduling and treatment (Tx) duration of N in aNSCLC. Stopping N after 1 year of Tx negatively affects outcomes.
Method
45 consecutive aNSCLC patients (pts) receiving N for ≥2 years (y) were identified in the electronic databases of 4 Israeli cancer centers. These were divided into Groups A (N continued for >2y at a dose 3mg/kg q2w/240mg q2w; n-21), B (N continued for >2y at a dose 3mg/kg q3w-q8w/480mg q4w; n-17), and C (N stopped at 2y for reason other than progressive disease or intolerable toxicity; n-7). PFS (RECIST 1.1) and safety since 2y after N initiation were assessed.
Result
Baseline, treatment characteristics and outcomes are presented in the Table and the Picture. Allocation to Group B and C was associated with HR for PFS-2.4 (95%CI, 0.3-18.8, p-0.4) and HR for PFS-3.3 (95%CI, 0.3-30.9, p-0.3), respectively. After 2y since N initiation, new N-related toxicity developed in 24%, 18%, and 28% of pts in Groups A, B, and C, respectively (p-NS).
Conclusion
A trend for worse outcomes was observed with alternative N scheduling/N quitting 2y after initiation. So far, continuing N at a standard dose until disease progression/ intolerable toxicity remains the standard treatment option.
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P2.06 - Mesothelioma (ID 170)
- Event: WCLC 2019
- Type: Poster Viewing in the Exhibit Hall
- Track: Mesothelioma
- Presentations: 1
- Now Available
- Moderators:
- Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall
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P2.06-14 - BAP1 Mutant Malignant Pleural Mesothelioma (MPM): Outcomes with Chemotherapy, ICPi and PARPi (Now Available) (ID 1244)
10:15 - 18:15 | Author(s): Mor Tal Moskovitz
- Abstract
Background
Little is known regarding the outcomes of systemic treatments (Tx) in BAP1 altered MPM.
Method
45 patients (pts) with advanced MPM (Group A: 8 MPM with a BAP1 inactivating mutation/copy number loss (FoundationOne CDx/TEMPUSxT), selected from the electronic databases (eD) of 4 Israeli cancer centers (ICC); Group B: 37 consecutive (years 2016-2018) MPM without a BAP1 alteration/not tested, selected from the eD of 2 ICC) were analyzed for ORR, PFS (mRECIST 1.1) and OS with platinum/pemetrexed+/-bevacizumab/nintedanib (CT, n-28), immune check-point inhibitors (ICPi, n-16) and poly (ADP-ribose) polymerase inhibitors (PARPi, n-4). OS since diagnosis (OSDx) was assessed.
Result
Pt and Tx characteristics are presented in the Table. There were no differences in ORR, mPFS or mOS with CT between the Groups: ORR-50% in both Groups, mPFS-9.1mo (95%CI, 1.2-16.1) vs 9.2mo (95%CI, 2.9-17.8) (log-rank-0.01, p-0.9), mOS-NR (95%CI, 6.6-NR) vs 18.5mo (95%CI, 5.4-46.3) (log-rank-1.1, p-0.3), in Groups A and B, respectively. There were no differences in ORR, mPFS or mOS with ICPi between the Groups: ORR- 33% vs 50% (p>0.5), mPFS-2.5mo (95%CI, 1.4-3.7) vs 3.0mo (95%CI, 0.3-10.5) (log-rank-0.5, p-0.4), mOS-NR (95%CI, 4.0-NR) vs 5.8mo (95%CI, 0.3-13.2) (log-rank-0.1, p-0.7), in Groups A and B, respectively. In Group A, no responses were seen with PARPi; PFS with PARPi was 1.8mo (95%CI, 1.8-1.9). OSDx was NR (95%CI, 9.7-NR) vs 19.5mo (95%CI, 9.7-82.2) in Groups A and B, respectively (log-rank-1.6, p-0.2). In the univariate analysis, sex (p-0.04), histology (p-0.002), ECOG PS (p-0.03), but not BAP1 mutation (p-0.3) correlated with OSDx.
Conclusion
Outcomes with CT and ICPi in BAP1 mutant MPM are similar to non-selected MPM. No responses were seen so far with PARPi. According to our data, presence of BAP1 mutation does not affect OS. Additional follow-up is needed.
