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Lung Cancer Treatments 2017Edward S. Kim, MD, FACPChair, Solid Tumor Oncology and Investigational TherapeuticsDonald S. Kim Distinguished Chair for Cancer ResearchMedical Director, Clinical Trials OfficeLevine Cancer Institute, Carolinas HealthCare SystemCharlotte, North Carolina

Organizations

Levine Cancer InstituteCarolinas HealthCare System 20 regional sites across NC, SC15,000 new cancer cases2nd building construction (eta late 2018)Dedicated Phase I Unit (expansion to regional site)Bone Marrow Transplant UnitBiostatistics DepartmentBiospecimen RepositoryPatient NavigationOncology-centric Palliative CareIntegrative MedicineSenior OncologyWeekly Molecular Tumor BoardMobile CT Lung screening unitDerek Raghavan, MDPresident, Levine CancerInstitute

NSCLC: A Major Public Health Problem Estimated 1.6 million deaths each year worldwide fromlung cancer In 2015: Estimated 221,200 new cases of lung cancer expected to bediagnosed in US 158,000 Americans expected to die from lung cancer Leading cause of cancer-related deaths in US men andwomen More deaths from lung cancer than breast, prostate, colon, liver,melanoma, and kidney cancers combined Need for better thought out, patient-driven studiesTorre LA, et al. CA Cancer J Clin. 2015;65(2):87-108.Siegel RL, et al. CA Cancer J Clin. 2015;65(1):5-29.

The Changing and ChallengingLandscape of Oncology New drugs being approved Several new drugs for same indications– Bladder cancer (Immunotherapy)– Lung cancer (EGFR TKIs, Immunotherapy)– Head and neck cancer (Immunotherapy) Same drugs in disease type in different stage or line of therapy– Lung (EGFR TKIs, ALK TKIs, Immunotherapy) Biomarkers for some and not others (PD-L1, level of expression,Mutational Burden, MSI, MMR) Different biomarkers in same family (EGFR: Del19, L858R, T790M)

The Changing and ChallengingLandscape of Oncology 71 Anti-Cancer Drugs approved by the FDA from 2002-2014 for Metastaticand/or Advanced and/or Refractory Solid Tumors for top ten pharmacompanies1 Median PFS improvement was only 2.5 months Median OS improvement was only 2.1 months Cancer treatment is ineffective in 75% of patient population21FojoT, et al, JAMA Otolaryngol Head Neck Surg. 2014; 140 (12):1225-1236.Medicine Coalition 4th Edition 20142Precision

Renaissance in the Field of Lung Cancer Molecular biomarkers determine treatment– We are finally like breast cancer Immunotherapy is the new cornerstone– Melanoma was the front-runner but lung cancer has brought itinto the mainstream Diagnostic comprehensive gene panels Plasma/Serum diagnostic tests– Are we getting closer to PSA, CA-125? New clinical trials in early stage disease Screening and detection

The Beginning: Lung Cancer Milestones 015201520162017Doublets all we gotDocetaxel 2nd lineGefitinib data reportedAdjuvant cisplatin-based chemotherapyEGFR Mutations describedGefitinib wild-type data reportedPemetrexed, ErlotinibBevacizumab approved E4599EGFR mutations incorporated into clinical testingALK inhibitor approvedAfatinib approvedT790MNivolumabPembrolizumab first line, AtezolizumabBrigatinib; BRAF v600E (Trametinib, Dabrafenib)

Lung Cancer Treatment 2000:ECOG 1594 Comparison of 4 First-Line DoubletRegimens in Advanced NSCLCProbability of Survival Nonsquamous andsquamoushistologies No differences Efficacy not soencouraging Easy for providersto “take home amessage” “Treat with anydoublet you wouldlike”Schiller JH, et al. N Engl J Med. 2002;346:92-98.

E4599: Bevacizumab with Chemotherapy in NSCLCOverall SurvivalMedian survival: 12.5 vs 10.2 monthsHR 0.77 (95% CI: .65, .93), P 0.0071-yr Survival: 52% vs 44%2-yr Survival: 22% vs 17%100Patients surviving, %8060Treatment groupCarboplatin and paclitaxelCarboplatin and paclitaxel bevacizumab40200061218MonthsSandler et al. NEJM 2006243036

Erlotinib: NCIC BR.21 Trial2:1 randomization to the experimental armNSCLCFailed 1 or 2Prior Therapies(N 700)Erlotinib 150 mg/d PO best supportive careSurvival QOLvsPlacebo 150 mg/d PO best supportive care90% power to detect a 33% survival benefit, 0.05Shepherd, et al. ASCO. 2004 (abstr 7022).Survival QOL

Not Targeted Therapy 2005:BR.21- Overall Survival1.0042.5% improvement in median survivalSurvival distribution functionTM0.75Tarceva(n 488)Placebo(n 243)Median survival (months)6.74.71-year survival (%)3121HR 0.73, P al time (months)2530*HR and P-value adjusted for stratification factors at randomization plus HER1/EGFR status.Shepherd, et al. ASCO. 2004 (abstr 7022).

The Beginning: Lung Cancer Milestones 015201520162017Doublets all we gotDocetaxel 2nd lineGefitinib data reportedAdjuvant cisplatin-based chemotherapyEGFR Mutations describedGefitinib wild-type data reportedPemetrexed, ErlotinibBevacizumab approved E4599EGFR mutations incorporated into clinical testingALK inhibitor approvedAfatinib approvedT790MNivolumabPembrolizumab first line, AtezolizumabBrigatinib; BRAF v600E (Trametinib, Dabrafenib)

NSCLC Drug Approvals/Indications: 2015 - Present amucirumabAtezolizumabCeritinibBrigatinib Pembrolizumab– PD-L1 (1st, 2nd line)– MSI-H or dMMR solidtumors– NSCLC (Carboplatin Pemetrexed) Crizotinib (ROS1) Dabrafenib, Trametinib

The Changing Landscape of Lung Cancer: 200580 of 100 patients eligible for chemotherapyOnly 15-20% oftumors had a partialresponse

The Changing Landscape of Lung Cancer: 2017Molecular subsets: EGFR Mutations

The Changing Landscape of Lung Cancer: 2017Molecular subsets: ALK

The Changing Landscape of Lung Cancer: 2017Molecular subsets: ROS1

The Changing Landscape of Lung Cancer: 2017Molecular subsets: PD-L1

The Changing Landscape of Lung Cancer: 2017Molecular subsets: BRAFv600E

The Changing Landscape of Lung Cancer: 2017Molecular subsets: 50% of patients candidates for targeted therapy

Lung Cancer HistologyNOS 1–15%Large Cell 10-15%Squamous Cell 25-30%SCLC 13%Adenocarcinoma 40%

Screening for Lung Cancer

American College of Physicians, ASCO,USPSTF Recommendations

The Era of Precision Medicine Genomic sequencing has revolutionized our understanding of the cancergenome Deeper understanding of the cancer genome enabled significant advances in thedevelopment of targeted therapies Molecular profiling of tumor tissue biopsies has enabled targeted therapies to bedirected to patients most likely to benefit Optimizing the utilization of targeted therapies requires effective serial monitoringof treatment response and emergence of resistanceBRAF V600E: VemurafinibALK rearrangement: Crizotinib, Ceretinib, AlectinibEGFR Del 19; L858R: TKls e.g. Erlotinib, GefitinibEGFR T790M: Osimertinib

Lung Cancer Mutation Consortium:Incidence of Driver MutationsPD-L1 andothers nowoverlappingKris MG, et al. JAMA. 2014;311:1998-2006.

Evaluation for Patients with Lung Cancer Confirmed biopsy (histology) Staging from head to toe– intrathoracic, extrathoracic, brain, bones Physical Assessment Biomarker Assessment––––EGFR mutationALKROS 1PD-L1“Molecular assessment is an essential element for theevaluation of patients with lung cancer”

EGFR Mutations:Big Change in Lung Cancer TreatmentEGFR or TGFα EGFR is a cell surface proteinthat dimerizes to activate atyrosine kinase Activating mutations in EGFRyield constitutive activation,resulting in downstream cellproliferation, angiogenesis,and potential metastasisEGFR or otherfamily membersPPTKPTENPSos RasGrb2PRAFPI3KAktEvasion ofApoptosisMEKSTATSignallingMAPKGene TranscriptionCell-Cycle ProgressionProliferationProfileResistance toApoptosisProliferationInvasionAdapted from Bronte G, et al. Crit Rev Oncol Hematol. 2014;89:300-313.MetastasisAngiogenesis

EGFR Mutations Found in 15-18% of adenocarcinoma patients and 50% of neversmoking adenocarcinoma patients Characteristics that enhance chances are low or never-smokers,adenocarcinomas, Asians Predominantly located in EGFR exons 18-21 90% of EGFR mutations are either exon 19 deletions or exon 21point mutations (L858R) All EGFR mutations are not the same Del 19 and L858R are most associated with response Exon 20 insertions and T790M are most associated withresistance

Treatment-Naïve EGFRMUT PatientsEGFR TKIs vs ChemotherapyStudyTreatmentNMedian PFS,monthsMedian OS,monthsMaemondoGefitinib vsCarboplatin/Paclitaxel23010.8 vs 5.4(P 0.001)30.5 vs 23.6(P 0.31)MitsudomiGefitinib vsCisplatin/Docetaxel1779.2 vs 6.3(P 0.0001)36 vs 39(HR: 1.19)OPTIMALErlotinib vsCarboplatin/Gemcitabine16513.1 vs 4.6(P 0.0001)HR: 1.065(P 0.65)EURTACErlotinib vsplat-based Chemotherapy1749.7 vs 5.2(P 0.0001)19.3 vs 19.5(P 0.87)LUX-Lung 3Afatinib vsCDDP/Pemetrexed307*13.6 vs 6.9(P 0.0001)31.6 vs 28.2(P 0.1090)LUX-Lung 6Afatinib vsCisplatin/Gemcitabine324*11.0 vs 5.6(P 0.0001)23.6 vs 23.5(P 0.1756)*Common mutations only.Maemondo M, et al. N Engl J Med. 2010;362:2380-2388; Mitsudomi T, et al. Lancet Oncol. 2010;11:121-128;Mitsudomi T, et al. 2012 ASCO. Abstract 7521; Zhou C, et al. Lancet Oncol. 2011;12:735-742;Zhang C, et al. 2012 ASCO. Abstract 7520; Rosell R, et al. Lancet Oncol. 2012;13:239-246;Sequist, et al. J Clin Oncol 2013;31:3327-3334;Yang JC-H, et al. J Clin Oncol. 2014;32(suppl 15). Abstract 8004.

EGFR Mutations: TKI vs Chemotherapy

EGFR Mutations: TKI vs Chemotherapy

First-Line EGFR TKI Demonstrates Efficacy inEGFR Mutation-Positive NSCLC100EGFR TKI group (n 68)Best Change From Baseline (%)806040200-20-40-60-80-100Adapted from Rosell R, et al. Lancet Oncol. 2012;13:239-246.Mutation exon 21Deletion exon 19

Patient With Del19 EGFR MutationDecember 2000December 2002

Afatinib OS in Del 19 Subgroup:Type of mutation mattersLUX-Lung 3LUX-Lung 61.0Median,monthsPem/Cisn 5733.321.11.0Median,months0.8HR (95%CI),p-value0.6AfatinibCis/Pem0.40No of patients9 12 15 18 21 24 27 30 33 36 39 42 45 48 51Time (months)31.418.40.64 (0.44–0.94),p 0.02290.406Gem/Cisn 62AfatinibCis/Gem0.23Afatinibn 1240.60.20HR (95%CI),p-value0.54 (0.36–0.79),p 0.0015Estimated OS probabilityEstimated OS probability0.8Afatinibn 1120369 12 15 18 21 24 27 30 33 36 39 42 45Time (months)No of patientsAfatinib112 108 105 102 96 93 83 80 72 62 58 51 34 30 21610Afatinib124 122 118 115 106 9990807369593916810Pem/Cis57 55 50 46 43 37 33 27 25 22 20 16 10100Gem/Cis623028262118114300Yang et al. ASCO 2014. Abstract 8004.Yang, et al. Lancet Oncol. 2015;16:141-151.615853494435

Afatinib OS in L858R SubgroupL858R/LUX-Lung 3Median, monthsHR (95% CI)P valueEstimated OS probability0.8Afatinib(n 91)Cis/Pem(n 47)27.640.31.0Median, months1.30 (0.80–2.11)P 0.2919AfatinibCis/Pem0.60.400No. of patients:69 12 15 18 21 24 27 30 33 36 39 42 45 48 51Time (months)19.624.31.22 (0.81–1.83)P 0.3432AfatinibCis/Gem0.40.23Cis/Gem(n 46)0.60.20Afatinib(n 92)HR (95% CI)P value0.8Estimated OS probability1.0L858R/LUX-Lung 6036912 15 18 21 24 27 30 33 36 39 42 45Time (months)No. of patients:Afatinib91 89 83 79 75 69 60 53 49 46 43 39 24 19 11300Afatinib9292 847566595138312421123100Cis/Pem47 43 42 40 38 34 30 28 27 25 20 19 16 14410Cis/Gem4643 40383735312723151264000Yang, et al. Lancet Oncol. 2015;16:141-151.9

Mechanisms of Resistance to EGFR TKIFig. 1 The frequency of observed drug resistance mechanisms.Novel Mechanisms T790M Mutation – 49% MET amplification – 5% PI3KCA Mutation - 5% EMT Changes – 5% SCLC Features – 14% Unknown – 30%Sequist LV, et al. Sci Transl Med. 2011;3(75):75ra26.

T790M Blocks Erlotinib Binding and Leads toResistance to First-Generation InhibitorsMichalczyk A, et al. Bioorganic & Medicinal Chemistry. 2008;6(7):3482-3488.

Third Generation EGFR TKIs“3rd”GenerationNRR*T790M-RRT790M PFSRociletinib(CO-1686)25637%53% 8.0 mo HyperglycemiaOsimertinib(AZD9291)25321%61% 8.2 mo DiarrheaHM61713(800 mg)6212%(300 mg)55%NRDyspnea/rashEGF816X*53 60%NRRashASP8273*47 33%61%NRHyponatremia/diarrheaMultiple other agents earlier in developmentToxicity*T790M subgroups are very small.RR, response rate; PFS, progression-free survival.Sequist L, et al. J Clin Oncol. 2015;33(suppl). Abstract 8001; Jänne PA, et al. N Engl J Med. 2015;372(18):1689-1699; Park K,et al. J Clin Oncol. 2015;33(suppl). Abstract 8084; Tan DS-W, et al. J Clin Oncol. 2015;33(suppl). Abstract 8013; Goto Y, et al. JClin Oncol. 2015;33(suppl). Abstract 8014.

Osimertinib (AZD9291) in Patients With AcquiredResistance to EGFR TKI and EGFR T790MResponse Rate 61%Jänne PA, et al. N Engl J Med. 2015;372(18):1689-1699.

Osimertinib vs. Pemetrexed Platinum inT790M Positive EGFR mutant NSCLC

Osimertinib vs. Pemetrexed Platinum in T790MPositive EGFR mutant NSCLC

CNS response to osimertinib in patients with T790M-positive advanced NSCLC: data from a randomized Phase III trial (AURA3) br / Presented By Maria Garrassino at 2017 ASCO Annual Meeting

Tumor response in CNS – evaluable for br / response setPresented By Maria Garrassino at 2017 ASCO Annual Meeting

FLAURA: Phase III, Double-Blind, RandomizedStudy of TAGRISSO as 1L Therapy1,2TAGRISSO(80 mg orally once daily)Patients Biopsy-confirmed,aEGFRm NSCLC Treatment-naïvefor advancedNSCLCErlotinib 150 mg once dailybORGefitinib 250 mg once dailybKey inclusion criteria: Age 18 yearsPrimary endpoint: PFSSecondaryendpoints: ORR PFS in T790M( /–)patients OS PROs CNS efficacy analysis is planned Locally advanced or metastatic NSCLC No prior therapy for advanced diseasec Patients must have EGFR-TKI-sensitizingmutation (ex19del or L858R) Mandatory tumor sample of sufficient quantity toallow central analysis of EGFR mutation statusProprietary and confidential AstraZeneca document – for internal use only.47

Resistance to Third Generation EGFR TKIsThress KS, et al. Nat Med. 2015;21(6):560-562.

Summary: Acquired Resistance to EGFR TKIs First-line EGFR TKIs should be continued at least until initiation ofnext line of therapy and beyond progressive disease in“smoldering progression” Local therapy should be considered in patients with isolatedmetastases or oligometastases with continuation of the originalEGFR TKI The T790M mutation is responsible for 60% of all acquiredresistance to frontline EGFR TKIs Osimertinib FDA approved after EGFR-TKI– Recent data positive in 1st line treatment in EGFR mutations

EML4-ALK Translocations in NSCLCEML4-ALK frequency: 4% (64/1709)Primarily lungadenocarcinomaSoda et al. Nature 2007

43yo Male Never Smoker with Stage IV NSCLC( ) for EML4-ALKPre-TreatmentAfter 1 cyclePF-02341066

Tumor Responses to Crizotinib for Patientswith ALK-positive NSCLCShaw et al. NEJM 371(21): 1963-71, 2014

Response Rate Crizotinib vs. Chemotherapy

Ceritinib in Crizotinib-Naïve, ALK NSCLCFelip et al., ESMO 2014

There Are Multiple Secondary Resistance Mutationsa0ALK Kinase DomainaF1174V.Adapted from Lovly CM, et al. Sci Transl Med. 2012;4:120ps2.2468Number of Patients10

About One-Third of Resistant Tumors HarborALK Resistance Mutations or Camidge DR, et al. Nat Rev Clin Oncol.2014;11:473-481.

ALK Inhibitor Therapy in ALK-Rearranged NSCLCDrug/StudyN Alectinib incrizotinib-resistantNSCLC (AF-002JG) Phase I/II doseescalation47 Alectinib crizotinib naïveNSCLC (AF-001JP) Phase II46 Brigatinib inadvanced malignancies Post-hoc analysis137DoseOutcomesAdverseEvents ORR 59.5% Median PFS not yetreached Activity againstbrain mets in 2/4 pts Fatigue Myalgia Peripheraledema300 mg bid ORR 93.5% 2 yr PFS 76% 2 yr OS 79% Increased AST Dysgeusia Increased ALT90 mg/day,90 mg/day 180 mg/day,or 180 mg/day ORR 79% 90 mg 81% 90 180 mg 68% 180 mg Median PFS 12.9 mo 90 mg 11.1 mo 180 mg Not reached in 90 180 Nausea Diarrhea FatiguePhase I:300-900 mg bidPhase II:600 mg bid(recommended)Of 137, 79 ptsALK and 71 priorcrizotinib txbid, twice daily; ORR, overall response rate; PFS, progression-free survival; pts, patients, mets, metastases; tx, treatment; mo,months.Gadgeel SM, et al. Lancet Oncol. 2014;15:1119-1128; Tamura T, et al. International Journal of Radiation Oncology Biology Physics.2014;90(suppl 5):S6; Rosell R, et al. ELCC. 2015. Abstract 99O.

Alectinib vs crizotinib in treatment-naïve advanced ALK NSCLC: primary results of the global phase III ALEX study (LBA9008)Presented By Alice Shaw at 2017 ASCO Annual Meeting

Primary endpoint: PFS, investigator-assessedPresented By Alice Shaw at 2017 ASCO Annual Meeting

PFS by baseline CNS metastases status*Presented By Alice Shaw at 2017 ASCO Annual Meeting

Secondary endpoint: OSPresented By Alice Shaw at 2017 ASCO Annual Meeting

Leptomeningeal carcinomatosis responded toalectinibPre-alectinibPre-alectinibCSF cytologyOu, S et al., WCLC 20136 weeks on alectinib

ROS1 NSCLC treated with Crizotinib

BRAF V600E: Dabrafenib and Trametinib

Entrectinib (RXDX-101)Most potent, orally available pan-TRK inhibitor in clinical developmentTargetIC50* (nM)TrkATrkBTrkCROS1ALK1.70.10.10.21.6* Biochemical kinase assay69

46M with SQSTM1-NTRK1 NSCLCOngoing response at 15.1 monthsBaselineDay 26: - 47% response15-20 CNS metsImages courtesy of A. Shaw, MD, PhD and A. Farago, MD, PhD (MGH)CRDay 317: - 79% responseCR

STARTRK-2Entrectinib Global Phase 2 Basket Study

Improving Clinical Trial Accrual

Recommended Approach to Eligibility CriteriaConsiderationCategoryQuestion for ConsiderationDoes the eligibility criterion support the scientific hypothesis?Relationship to scientificobjectiveCould the scientific goal be achieved without including this particular eligibilitycriterion?Will the results of the study be applicable to a patient not enrolled on the study?GeneralizabilityAre the eligibility criteria too restrictive for practical clinical use?Is patient safety being adequately protected and does this eligibility criterion contributeto this?Patient safety and drugtoxicityContinual review on a regularbasisAre potential drug toxicities and mechanism of action being accounted for and doeslimiting or including this criterion support or hinder the scientific goal?At what point should eligibility criteria be re-justified during protocol development andduring enrollment?Should a trial close due to poor accrual or be allowed to reduce/relax eligibility criteriaas a first step?Kim ES. ASCO 2016

Importance to Cancer MoonshotStrategic Goal 3– Accelerate Bringing NewTherapies to Patients: Plans for Year 2 &Beyond1. Modernize eligibility criteria for clinical trials“In coordination with the American Society of ClinicalOncology, Friends of Cancer Research, and otherstakeholders, FDA will evaluate clinical trial entrancecriteria that may unnecessarily restrict clinical trialaccess—such as brain metastases, HIV status, organdysfunction, and age restrictions (e.g., pediatrics)—tobetter assess when restrictions are warranted for specificclinical trials to protect patient safety. Moving forward,FDA will work with sponsors to improve the use ofscience‐based, clinically relevant eligibility criteria to allowgreater patient access to clinical trials while maintainingpatient safety.”

ASCO-Friends Project Overview Prioritized assessment of four eligibility criteria– Brain Metastases; Minimum Age; HIV/AIDS; & OrganDysfunction, Prior Malignancies, and Comorbidities Formed multi-stakeholder working groups–––––––Patient advocatesClinical investigatorsFDA medical reviewersDrug and biotech manufacturersNCIBiostatisticiansPharmacologists

ASCO-Friends Project LeadershipASCOEdward S. Kim, MD, FACPRichard L. Schilsky, MD,FACP, FASCOSuanna Bruinooge, MPHCaroline Schenkel, MScFriends of CancerResearchEllen Sigal, PhDJeff Allen, PhDSamantha Roberts, PhDMarina Kozak, PhDFDARichard Pazdur, MDGwynn Ison, MDJulia Beaver, MDTatiana Prowell, MDRaji Sridhara, PhDPlanning CommitteeEric Rubin, MD (Merck)Nancy Roach (FightColorectal Cancer)Elizabeth Garret-Mayer(Medical Univ. of SC)Working Group ChairsStuart Lichtman, MD(MSKCC)Nancy Lin, MD (Harvard &RANO Group)Thomas Uldrick, MD (NCI)Lia Gore, MD (Univ. of CO)

ASCO-Friends Project Overview 6 manuscripts submitted for publication to JCO– Accepted July 2017 Implementation of current recommendations– Templates Next eligibility criteria in discussion

Targeted Agent and Profiling UtilizationRegistry (TAPUR) Study Pragmatic phase 2 study with FDA-approved, targetedagents Incorporates general and drug-specific eligibility criteria Prior Malignancy:– No exclusion or time limit for patients with prior malignancies HIV – General Criteria – included except where clinician decides toexclude– Drug-specific – pembrolizumab and olaparib exclude Performance Status (PS):– General eligibility: 0-2 per general eligibility– Drug-specific: pembrolizumab or regorafenib must have PS 0-1

TAPUR Study Eligibility Criteria (cont’d) Brain Metastases – eligible, so long as the patient is:– Not progressive and not on treatment– Has not experienced a seizure or had a clinically significant change inneurological status within the 3 months– Off steroids for at least one month prior to enrollment. Patients must have acceptable organ function as defined below:– AST (SGOT) and ALT(SGPT) 2.5 x institutional ULN (or 5 x ULNin patients with known hepatic metastases)– Serum creatinine 1.5 ULN or calculated or measured creatinineclearance 50 mL/min/1.73 m2 Pediatric Population:– Current TAPUR study eligibility criteria requires 18 years– Plans to lower minimum age to 12 years where pediatric dose defined

Levine Cancer Institute first site to register100th patient for TAPURLCI-Main (34)LCI-Cleveland (0)LCI-University (4)LCI-Mallard Creek (1)LCI-Rutherford (0)LCI-NorthEast (9)14 1LCI-Lincolnton (1)LCI-South Tryon (7)LCI-Pineville (2)LCI-AnMed (0)7 342 56LCI-Rock Hill (0)LCI-Carolina Lakes (0)92LCI-Stanly (2)LCI-Southpark (5)LCI-Matthews (0)5LCI-Union (5)LCI-Ballantyne (6)LCI-RSF (pending)LCI-Whiteville (0)

The Fight Against Lung Cancer

The Fight Against Lung Cancer

“Why wefight theBATTLE !” 52 yr woman Stage 4 lungcancer Brain mets April 2002

Thank you for your ncolnAnMedCMCCMC-UnionCMC-MercyBlue RidgeCMC-UniversityCleveland RegionalStanly RegionalRoper St. Francis

EGFR Mutations Found in 15-18% of adenocarcinoma patients and 50% of never-smoking adenocarcinoma patients Characteristics that enhance chances are low or never-smokers, adenocarcinomas, Asians Predominantly located in EGFR exons 18-21 90% of EGFR mutations are either exon 19 deletions or exon 21 point mutations (L858R)

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