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P. Jänne



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    ISS01 - Industry Supported Symposium: Current and Emerging Treatments for Patients with ALK+ NSCLC – ARIAD Pharmaceuticals Inc. (ID 435)

    • Event: WCLC 2016
    • Type: Industry Supported Symposium
    • Track:
    • Presentations: 1
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      ISS01.04 - Will Mutation Testing be Standard in the Resistant Setting? (ID 7138)

      P. Jänne

      • Abstract

      Abstract not provided

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    MA16 - Novel Strategies in Targeted Therapy (ID 407)

    • Event: WCLC 2016
    • Type: Mini Oral Session
    • Track: Chemotherapy/Targeted Therapy/Immunotherapy
    • Presentations: 2
    • Now Available
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      MA16.03 - Global RET Registry (GLORY): Activity of RET-Directed Targeted Therapies in RET-Rearranged Lung Cancers (Now Available) (ID 4325)

      P. Jänne

      • Abstract
      • Presentation
      • Slides

      Background:
      GLORY is a global registry of patients with RET-rearranged non-small cell lung cancer (NSCLC). In order to complement ongoing prospective studies, the registry’s goal is to provide data on the efficacy of RET-directed targeted therapies administered outside the context of a clinical trial. We previously reported results from our first interim analysis (Gautschi, ASCO 2016). Following additional accrual into the registry, updated results are presented here, with a focus on an expanded efficacy analysis of various RET inhibitors.

      Methods:
      A global, multicenter network of thoracic oncologists identified patients with pathologically-confirmed NSCLC harboring a RET rearrangement. Molecular profiling was performed locally via RT-PCR, FISH, or next-generation sequencing. Anonymized data including clinical, pathologic, and molecular features were collected centrally and analyzed by an independent statistician. Response to RET tyrosine kinase inhibition (TKI) administered off-protocol was determined by RECIST1.1 (data cutoff date: April 15, 2016). In the subgroup of patients who received RET TKI therapy, the objectives were to determine overall response rate (ORR, primary objective), progression-free survival (PFS), and overall survival (OS).

      Results:
      165 patients with RET-rearranged NSCLC from 29 centers in Europe, Asia, and the USA were accrued. The median age was 61 years (range 28-89 years). The majority of patients were female (52%), never smokers (63%), with lung adenocarcinomas (98%) and advanced disease (91%). The most frequent metastasic sites were lymph nodes (82%), bone (51%) and lung (32%). KIF5B-RET was the most commonly identified fusion (70%). 53 patients received at least one RET-TKI outside of a clinical protocol, including cabozantinib (21), vandetanib (11), sunitinib (10), sorafenib (2), alectinib (2), lenvatinib (2), nintedanib (2), ponatinib (2) and regorafenib (1). In patients who were evaluable for response (n=50), the ORR was 37% for cabozantinib, 18% for vandetanib, and 22% for sunitinib. Median PFS was 3.6, 2.9, and 2.2 months and median OS was 4.9, 10.2, and 6.8 months for cabozantinib, vandetanib, and sunitinib, respectively. Responses were also observed with nintedanib and lenvatinib. Among patients who received more than one TKI (n=10), 3 partial responses were achieved after prior treatment with a different TKI.

      Conclusion:
      RET inhibitors are active in individual patients with RET-rearranged NSCLC, however, novel therapeutic approaches are warranted with the hope of improving current clinical outcomes. GLORY remains the largest dataset of patients with RET-rearranged NSCLC, and continues to accrue patients.

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      MA16.11 - CNS Response to Osimertinib in Patients with T790M-Positive Advanced NSCLC: Pooled Data from Two Phase II Trials (Now Available) (ID 4920)

      P. Jänne

      • Abstract
      • Presentation
      • Slides

      Background:
      Brain metastases develop in 25–40% of patients with NSCLC. Osimertinib is an oral, potent, irreversible EGFR-TKI, selective for both sensitising (EGFRm) and T790M resistance mutations. Preclinical and early clinical evidence support central nervous system (CNS) penetration and activity of osimertinib. Two Phase II studies (AURA extension [NCT01802632] and AURA2 [NCT02094261]) evaluating the efficacy and safety of osimertinib are ongoing. We present a pre planned subgroup analysis assessing pooled CNS response from these two studies; data cut-off (DCO) was 1 November 2015. An earlier pooled analysis from these two studies (1 May 2015 DCO) showed the objective response rate (ORR) in patients with CNS metastases was consistent with ORR in the overall patient population.

      Methods:
      Patients with advanced NSCLC who progressed following prior EGFR-TKI therapy with centrally-confirmed T790M positive status (cobas® EGFR Mutation Test) received osimertinib 80 mg once daily (n=411). Patients with stable, asymptomatic CNS metastases were eligible for enrolment. CNS efficacy was assessed in an evaluable for CNS response analysis set, which included patients with at least one measurable CNS lesion on baseline brain scan (RECIST v1.1) by blinded independent central neuroradiology review (BICR). Effect of prior radiotherapy on CNS response was assessed.

      Results:
      As of 1 November 2015, 50/192 patients with baseline brain scans had at least one measurable CNS lesion identified by BICR. Baseline demographics were broadly consistent with the overall patient population. Confirmed CNS ORR was 54% (27/50; 95% CI: 39%, 68%), with 12% complete CNS response (6/50 patients). The median CNS duration of response (22% maturity) was not reached (95% CI: not calculable [NC], NC). The estimated percentage of patients remaining in response at 9 months was 75% (95% CI: 53, 88). CNS disease control rate (DCR) was 92% (46/50; 95% CI: 81%, 98%). Median time to first response was 5.7 weeks (range: 5.6–6.6). Median best percentage change from baseline in CNS target lesion size was 53% (range: -100% – +80%). Median follow up for CNS progression-free survival (PFS) was 11 months; the median CNS PFS was not reached (95% CI: 7, NC). At 12 months, 56% (95% CI: 40%, 70%) of patients were estimated to remain on study, alive and CNS progression-free. CNS response was observed regardless of prior radiotherapy to the brain.

      Conclusion:
      Osimertinib demonstrates durable efficacy in patients with T790M NSCLC and measurable CNS metastases, with a CNS response rate of 54% and a DCR of 92%.

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    OA03 - Immunotherapy Checkpoint Inhibitors in Advanced NSCLC (ID 367)

    • Event: WCLC 2016
    • Type: Oral Session
    • Track: Chemotherapy/Targeted Therapy/Immunotherapy
    • Presentations: 1
    • Now Available
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      OA03.02 - Atezolizumab as 1L Therapy for Advanced NSCLC in PD-L1–Selected Patients: Updated ORR, PFS and OS Data from the BIRCH Study (Now Available) (ID 4799)

      P. Jänne

      • Abstract
      • Presentation
      • Slides

      Background:
      Atezolizumab, a humanized anti-PDL1 mAb, inhibits the PD-L1/PD-1 pathway to restore tumor-specific T-cell immunity, resulting in durable anti-tumor effects. BIRCH (NCT02031458) is a single-arm Phase II study of atezolizumab monotherapy in PD-L1–selected advanced NSCLC patients, across multiple therapy lines. Primary analyses (median follow-up, 8.5 months) demonstrated a meaningful ORR with durable response in chemotherapy-naive 1L and 2L+ PD-L1–selected patients. Here we report updated efficacy data in 1L patients.

      Methods:
      1L eligibility criteria included PD-L1–selected, advanced-stage NSCLC with no CNS metastases or prior chemotherapy. PD-L1 was centrally evaluated (VENTANA SP142 IHC assay). Patients expressing PD-L1 on ≥5% of tumor cells (TC) or tumor-infiltrating immune cells (IC), ie, TC2/3 or IC2/3, were enrolled. Patients with EGFR mutation or ALK rearrangement must have had prior TKI treatment. Atezolizumab 1200mg was administered IV q3w until radiographic disease progression or unacceptable toxicity. The primary endpoint was independent review facility(IRF)-assessed ORR. Secondary endpoints included investigator(INV)-assessed ORR, DOR, PFS (RECIST v1.1) and OS.

      Results:
      With a median follow-up of 14.6 months, median OS was not reached in TC3 or IC3 patients and was 20.1 months in TC2/3 or IC2/3 (ITT) patients; INV-assessed ORR was 32% and 24%, respectively (Table). Furthermore, ORR was 31% for mutant EGFR (n=13) vs 20% for wild-type EGFR patients (n=104), and 27% for mutant KRAS (n=33) vs 21% for wild-type KRAS patients (n=67). No new safety signals were observed. Updated efficacy (including IRF ORR), safety and exploratory biomarker analyses will be presented.

      Conclusion:
      With longer follow-up, atezolizumab continued to demonstrate promising efficacy in 1L NSCLC. These results indicate that atezolizumab has durable efficacy in the 1L setting, in EGFR and KRAS mutant and wild-type tumors, and support ongoing Phase III trials evaluating atezolizumab vs chemotherapy in 1L NSCLC.

      Endpoint(95% CI) TC3 or IC3[a](n=65) TC2/3 or IC2/3[b](n=139)
      INV ORR, % 32% (21.2–45.1) 24% (16.9–31.7)
      EGFR mutant/wild-type, % 25%/29% 31%/20%
      KRAS mutant/wild-type, % 38%/27% 27%/21%
      mDOR, mo 13.1 (8.5–NE) 13.1 (9.9–17.5)
      mOS, mo NE (12.0–NE) 20.1 (20.1–NE)
      12-mo OS rate, % 61% (48.8–73.8) 66% (57.9–74.5)
      mPFS, mo 7.3 (4.9–12.0) 7.3 (5.6–9.1)
      12-mo PFS rate, % 36% (23.8–48.8) 32% (24.0–40.7)
      NE, not estimable.[a ]TC ≥50% or IC ≥10% PD-L1–expressing cells.[b ]TC or IC ≥5% PD-L1–expressing cells.

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    P1.02 - Poster Session with Presenters Present (ID 454)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Biology/Pathology
    • Presentations: 1
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      P1.02-054 - Genomic Complexity in KRAS Mutant Non-Small Cell Lung Cancer (NSCLC) by Smoking Status with Comparison to EGFR Mutant NSCLC (ID 6134)

      P. Jänne

      • Abstract

      Background:
      Background: KRAS is the most frequently mutated oncogene in NSCLC and lacks an effective targeted therapy. Notably, KRAS mutations occur in both never/light-smokers and smokers. However, the relationship between smoking status and a KRAS+ tumor’s genomic complexity (mutation burden, copy number changes, concurrent mutations in key oncogenic pathways) is unclear. Similarly, the relationship between genomic complexity in tumors from never/light smokers but with a KRAS v EGFR activating mutation is also unknown.

      Methods:
      Methods: Targeted next-generation sequencing (NGS) data at our institution from 7/13-1/16 was reviewed to identify KRAS+ NSCLC tumors. All patients with a <10 pack-year (py) smoking history (NS) and a subset of heavy smokers (HS) (>40 py) were identified, with clinical and genomic analysis. A comparison cohort of 48 patients with EGFR+ NSCLC was also identified. Fisher’s exact test was used to compare frequency of gene mutations.

      Results:
      Results: 41 NS and 104 HS KRAS patients were evaluated. NS patients were more likely to be female (34/41 v 66/104, p<.01) and diagnosed with Stage I disease (14/41 v 13/104, p<.01). Compared to KRAS NS patients, tumors from KRAS HS patients were also genomically more complex, with increased total nucleotide variants (median=10 v 7, p<.001) and total copy number variations (median=22.5 v 5, p<.01). Intriguingly, in the cohort of EGFR tumors, total nucleotide variants resembled the KRAS NS cohort (median=6.5) but the total copy number variants were more similar to the KRAS HS cohort (median=25). Compared to KRAS NS tumors, KRAS HS tumors were also more likely to have: a) concurrent mutation in TP53 (43/104 v 8/41, p=.012) and b) concurrent mutations/2-copy deletions in >1 tumor suppressor (TS)/tumor (panel of TP53, STK11, APC, CDKN2A/B, RB) (26/104 v 4/41, p=.042). Although the total number of nucleotide variants in the EGFR cohort was most similar to the KRAS NS cohort, TS distribution in these EGFR tumors was closer to the KRAS HS cohort (TP53 variants in 31/48 and multiple TS variants in 14/48). Finally, median OS for KRAS HS patients with Stage IV disease was 9.7m v 28.7m in KRAS NS patients (HR=0.56).

      Conclusion:
      Conclusions: The genomic landscape of KRAS+ NSCLC from HS patients is distinct from NS patients and includes increased total mutations and frequency of TS loss. EGFR mutant tumors share some similarities with KRAS tumors from both NS and HS patients. Overall, NS KRAS+ tumors may be a genetically distinct cohort within the broader context of KRAS+ NSCLC.

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    P2.03b - Poster Session with Presenters Present (ID 465)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
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      P2.03b-031 - Impact of PD-L1 Status on Clinical Response in SELECT-1: Selumetinib + Docetaxel in KRASm Advanced NSCLC (Now Available) (ID 5040)

      P. Jänne

      • Abstract
      • Slides

      Background:
      Anti-PD-1/PD-L1 immunotherapy has delivered clinical benefit for patients with NSCLC, and PD-L1 has emerged as a predictive biomarker. In the Phase III SELECT-1 trial (NCT01933932), selumetinib (AZD6244, ARRY-142886), an oral, potent and selective, allosteric MEK1/2 inhibitor with a short half-life, plus second-line docetaxel did not provide clinical benefit for patients with KRAS-mutant (KRASm) NSCLC compared with placebo plus docetaxel (PBO+DOC). Although no incremental benefit was observed, it is important to evaluate biomarkers, such as PD-L1, to understand more about the biology of patients with KRASm NSCLC.

      Methods:
      In total, 510 patients with a prospectively, centrally confirmed KRAS mutation (cobas® KRAS Mutation Test, Roche Molecular Systems) were randomised 1:1 to selumetinib 75 mg BID, plus docetaxel 75 mg/m[2] q21d (SEL+DOC), or PBO+DOC. Evaluations included progression-free survival (PFS) by investigator assessment (RECIST 1.1; primary endpoint), and overall survival (OS). Association of tumour PD-L1 status with clinical responses was assessed as an exploratory objective. PD-L1 status was centrally determined using the PD-L1 IHC 28-8 pharmDx test (Dako) for all patients with sufficient tumour sample. Samples with a pre-specified cut-off of ≥5% tumour cell staining were considered PD-L1 positive.

      Results:
      SEL+DOC did not improve PFS or OS compared with PBO+DOC. PD-L1 status was determined for 385 (75%) patients: 224 (58%) samples were PD-L1 <5%, and 161 (42%) samples were PD-L1 ≥5%; the remaining 125 patients had unknown PD-L1 status due to insufficient tumour sample. Subgroups were balanced across treatments. PD-L1 subgroup analysis of PFS and OS is presented below.

      Subgroup Events (%) in SEL+DOC group Events (%) in PBO+DOC group HR (95% CI)
      PFS
      PD-L1 <5% 94/112 (84%) 101/112 (90%) 0.89 (0.67, 1.18)
      PD-L1 ≥5% 65/79 (82%) 71/82 (87%) 0.70 (0.50, 0.99)
      PD-L1 unknown 59/63 (94%) 57/62 (92%) 1.24 (0.86, 1.79)
      OS
      PD-L1 <5% 73/112 (65%) 74/112 (66%) 0.94 (0.68, 1.30)
      PD-L1 ≥5% 55/79 (70%) 58/82 (71%) 0.89 (0.61, 1.28)
      PD-L1 unknown 48/63 (76%) 38/62 (61%) 1.57 (1.02, 2.41)


      Conclusion:
      Prevalence of PD-L1 positive status in this KRASm cohort was similar to that reported for a pan-NSCLC cohort (Borghaei, NEJM 2015). No significant PFS or OS differences were observed between treatments in either PD-L1 positive or negative tumours. Additional biomarker analyses are planned for different KRAS codon mutations, and LKB1 and TP53 status.

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    P2.06 - Poster Session with Presenters Present (ID 467)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Scientific Co-Operation/Research Groups (Clinical Trials in Progress should be submitted in this category)
    • Presentations: 2
    • Now Available
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      P2.06-007 - A Phase 1/2 Trial of the Oral EGFR/HER2 Inhibitor AP32788 in Non–Small Cell Lung Cancer (NSCLC) (ID 5047)

      P. Jänne

      • Abstract

      Background:
      Approximately 4%–9% of EGFR-mutated NSCLC tumors have EGFR exon 20 insertion mutations, and no targeted treatment options are currently approved for patients with these mutations. In addition, approximately 2%–4% of patients with NSCLC have HER2 mutations, the majority of which are exon 20 insertion mutations. The irreversible EGFR/HER2 inhibitor AP32788 was designed to selectively inhibit EGFR or HER2 kinases with EGFR/HER2 exon 20 mutations. In preclinical studies, investigational agent AP32788 had potent inhibitory activity against all EGFR and HER2 mutants tested, including exon 20 insertion mutants, while sparing wild-type EGFR.

      Methods:
      This phase 1/2 trial is a first-in-human, open-label, multicenter study to evaluate the safety, tolerability, pharmacokinetics, and antitumor activity of orally administered AP32788 (NCT02716116). The study will be conducted in 2 parts: a dose-escalation phase with a 3+3 design and an expansion phase of 4 histologically and molecularly defined cohorts after the recommended phase 2 dose (RP2D) is determined. Patients (≥18 years) must have locally advanced or metastatic NSCLC. In phase 1, the dose-escalation phase, patients refractory to standard available therapies will be enrolled. The primary endpoint of phase 1 is identification of the RP2D of AP32788. Secondary endpoints include safety, dose-limiting toxicities, maximum tolerated dose, and plasma pharmacokinetics. Expected phase 1 enrollment is 20–30 patients. In phase 2, the expansion phase, 4 cohorts will be enrolled, patients with: 1. EGFR exon 20 activating insertions, without active, measurable CNS metastases; 2. HER2 exon 20 activating insertions or point mutations, without active, measurable CNS metastases; 3. EGFR exon 20 activating insertions or HER2 exon 20 activating insertions or point mutations and active, measurable CNS metastases; 4. other targets against which AP32788 has demonstrated preclinical activity (eg, EGFR exon 19 deletions or exon 21 substitutions [with/without the T790M mutation] and other uncommon activating mutations in EGFR). The primary endpoint of phase 2 is investigator-assessed objective response rate (ORR) per RECIST v1.1 for all expansion cohorts except Expansion Cohort 3, for which the primary endpoint is intracranial ORR. Phase 2 secondary endpoints include safety, pharmacokinetics, and additional efficacy assessments (ORR per independent review committee, best overall response, best target lesion response, duration of response, disease control rate, progression-free survival, and overall survival; for Expansion Cohort 3: duration of intracranial response and intracranial progression-free survival). Expected phase 2 enrollment is 80 patients (total). The first patient was enrolled in phase 1 in June 2016.

      Results:
      Section not applicable.

      Conclusion:
      Section not applicable.

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      P2.06-017 - Amethyst NSCLC Trial: Phase 2 Study of MGCD265 in Patients with Advanced or Metastatic NSCLC with Activating Genetic Alterations in MET (Now Available) (ID 5384)

      P. Jänne

      • Abstract
      • Slides

      Background:
      MGCD265 is a potent, orally available, small molecule RTK inhibitor of MET and Axl, both of which mediate signals for cell growth, survival, and migration. The Amethyst NSCLC trial is designed to evaluate the activity of MGCD265 in patients with NSCLC exhibiting genetic alterations involving MET. Alterations in MET, including gene amplification and/or genetic mutations, occur in approximately 7% of NSCLC cases converting MET to an oncogene capable of driving cancer development and progression. Amplification of MET has been associated with a poor prognosis in NSCLC. In addition, various genetic mutations result in the deletion of exon 14 in MET mRNA (METex14del) and the subsequent loss of the Y1003 regulatory binding site for CBL ubiquitin ligase, required for MET degradation and signal attenuation. Loss of the Y1003 binding site of MET results in sustained MET signaling, which has been implicated as an oncogenic driver in a subset of NSCLC. The importance of MET as a driver is demonstrated in xenograft models of NSCLC with METex14del and MET amplification, and where MGCD265 induces tumor regression. Additionally, confirmed partial responses have been observed in pts with NSCLC characterized by METex14del who were treated with MGCD265 in the Phase 1 setting.

      Methods:
      Pts with platinum pre-treated NSCLC characterized by activating genetic MET alterations identified in tumor tissue or circulating tumor DNA (ctDNA) are eligible for this multi-center, global, Phase 2 trial. Pts are assigned to one of four cohorts based on the type of MET dysregulation and detection method: 1) mutations in tissue, 2) amplification in tissue, 3) mutations in ctDNA, and 4) amplification in ctDNA. The primary endpoint is Objective Response Rate (ORR) in accordance with RECIST 1.1; a Bayesian Predictive Probability Design is applied independently to each cohort. Secondary objectives include safety, tolerability, response duration, survival, correlation between tissue and ctDNA testing, and PK/PD. This study is currently open globally, and recruitment is ongoing.

      Results:
      Section not applicable.

      Conclusion:
      Section not applicable.

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    P3.02a - Poster Session with Presenters Present (ID 470)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Advanced NSCLC
    • Presentations: 1
    • Now Available
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      P3.02a-006 - Immune Recognition of ALK Fusion Proteins in Patients with ALK-Rearranged Non-Small Cell Lung Cancer (Now Available) (ID 6091)

      P. Jänne

      • Abstract
      • Slides

      Background:
      Although several tyrosine kinase inhibitors have potent antitumor activity against ALK-rearranged non-small cell lung cancers (NSCLC), resistance to these small molecules emerges through a number of mechanisms. Preclinical evidence suggests that ALK-positive NSCLCs can also be successfully targeted immunologically using vaccine-based approaches. Immunologic responses against the ALK protein have been reported in ALK-positive anaplastic large cell lymphoma, and we sought to determine whether ALK could be recognized by the immune systems of patients with ALK-positive NSCLC.

      Methods:
      Serum was collected from 32 ALK-positive and 29 ALK-negative NSCLC patients over the course of routine clinical care who had consented to an institutional review board approved translational research protocol. We developed a novel enzyme-linked immunosorbent assay (ELISA) to detect autoantibodies against the ALK cytoplasmic domain in patients with ALK-rearranged NSCLC, and the specificity of these autoantibodies was validated using Western blot analysis. Short peptides spanning the length of the ALK cytoplasmic domain were synthesized to more narrowly define the precise immunogenic peptide sequences.

      Results:
      Among 32 ALK-positive NSCLC patients, very high ALK autoantibody titers were detected in the serum of 3 patients (9%), and ALK autoantibodies were not detected in any of the 29 patients with ALK-negative NSCLC. These autoantibodies specifically recognized only the ALK cytoplasmic domain and not the ALK extracellular domain. Epitope mapping demonstrated that the autoantibodies from each of the 3 patients with high autoantibody titers recognized distinct ALK peptide sequnces within the ALK cytoplasmic domain.

      Conclusion:
      ALK is capable of being recognized by the immune systems in some patients with ALK-positive NSCLC. Further investigation is needed to determine whether the presence of anti-ALK antibodies impacts prognosis in NSCLC. The naturally immunogenic properties of ALK in NSCLC may be able to be exploited using therapeutic ALK vaccines in patients.

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    SC27 - P53 and KRAS Mutations in NSCLC (ID 351)

    • Event: WCLC 2016
    • Type: Science Session
    • Track: Biology/Pathology
    • Presentations: 1
    • Now Available
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      SC27.04 - KRAS-Directed Drug Therapy in Advanced NSCLC (Now Available) (ID 6716)

      P. Jänne

      • Abstract
      • Presentation
      • Slides

      Abstract not provided

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