Oncogenic mutations of the EGFR pathway in lung adenocarcinoma
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1 Oncogenic mutations of the EGFR pathway in lung adenocarcinoma Balazs Hegedus Translational Thoracic Oncology Lab, Medical University of Vienna MTA-SE Molecular Oncology Research Group, Budapest, Hungary
2 Growth factor receptor signaling EGFR KRAS BRAF PI3KCA NF1 (GAP) PTEN Lung adenocarcinoma 8-20% 20-30% 1-3% 3-8%?? 11%
3 Response to Platinum-Based Chemotherapy and Subtype-Specific KRAS Mutations in Advanced Lung Adenocarcinoma
4 The most frequent oncogenic mutations of KRAS in lung adenocarcinoma Nucleotide change Amino acid change Mutation GGT>TGT Glycin Cystein G12C GGT>GTT Glycin Valin G12V GGT>GAT Glycin Aspartat G12D GGT>GCT Glycin Alanin G12A GGT>AGT Glycin Serin G12S GGT>CGT Glycin Arginin G12R GGC>GAC Glycin Aspartat G13D Dogan S, Shen R, Ang DC, Johnson ML, D'Angelo SP, Paik PK, Brzostowski EB,Riely GJ, Kris MG, Zakowski MF, Ladanyi M. Molecular epidemiology of EGFR andkras mutations in 3,026 lung adenocarcinomas: higher susceptibility of women tosmoking-related KRAS-mutant cancers. Clin Cancer Res Nov 16;18(22):
5 Biological effect of the amino acid change Garassino MC, Marabese M, Rusconi P, Rulli E, Martelli O, Farina G, Scanni A, Broggini M. Different types of K-Ras mutations could affect drug sensitivity and tumour behaviour in non-small-cell lung cancer. Ann Oncol Jan;22(1):235-7.
6 Patient population and enrollment criteria Single center study (National Koranyi Institute of Pulmonolgy and TB) 1125 patient with KRAS mutation analysis 01/01/ /12/ patients met the requirements of inclusion criteria: III-IV stage lung adenocarcinoma ECOG: 0-1 platinum based chemotherapy (adjuvant chemo treatment was excluded) Cserepes et al, European Journal of Cancer, 2014
7 KRAS mutation analysis RFLP Detection of wild-type and mutant alleles. samples control wt wt mut wt wt wt mut wt Direct sequencing validation of the mutation and the accurate nucleotide change detection
8 Prevalence of KRAS mutations Entire patient population KRAS status Number % Mutant % Total Wild type KRAS12 mut KRAS13 mut Patients with full clinical follow-up Number of patients 505 Wild type 338 Codon13 mutation 20 Codon12 mutation all 147 G12C 61 G12V 29 G12D 27 G12A 8 G12S 6 G12R 3 Not identified 11 COSMIC* Current cohort G12C 42% 38,61% G12V 20% 18,35% G12D 15% 17,09% G12A 7% 5,06%
9 Prognostic / predictive factors p= p<0.001 p<0.001 p=0.69
10 KRAS mutation subtype and smoking history 50,00% 45,00% 40,00% 35,00% 30,00% 25,00% 20,00% 15,00% Asp Cys Val Other 10,00% 5,00% 0,00% Never smoker Ex smoker Current smoker Ever smoker
11 Comparison of G12V versus all other G12 KRAS mutant
12 Perspective: mutant allele specific imbalance (MASI) VillaruzLC, SocinskiMA, Cunningham DE, ChioseaSI, Burns TF, Siegfried JM, DacicS. The prognostic and predictive value of KRAS oncogenesubstitutions in lung adenocarcinoma. Cancer Jun 15;119(12): doi: /cncr Epub 2013 Mar 22. PubMed PMID:
13 Epidemiology of rare EGFR mutations Lohinai et al, Journal of Thoracic Oncology, 2015
14 Epidemiology of rare EGFR mutations
15 Prognosticators in lung adenocarcinoma
16 EGFR TKI treatment
17 DIRECT database
18
19 EGFR mutation, TKI treatment and immunotherapy
20 Metastatic site-specific variation of KRAS status in lung adenocarcinoma Metastatic site Multiple Single Lung Bone Adrenal Brain Pleura Liver Nonmetastati c Total Age (mean±sd) 60.8± ±9.3 62± ± ± ± ± ± ±8.9 Gender Male 64 (46%) Female 74 (54%) 181 (50%) 181 (50%) 102 (45%) 126 (55%) 74 (56%) 34 (39%) 36 (43%) 38 (49%) 26 (47%) 190(49%) 57 (44%) 53 (61%) 48 (57%) 40 (51%) 29 (53%) 213 (51%) ECOG (92%) 335 (94%) 218 (97%) 115 (91%) 75 (87%) 77 (93%) 71 (91%) 48 (91%) 382 (96%) performan ce status >1 11 (8%) 21 (6%) 7 (3%) 11 (9%) 11 (13%) 6 (7%) 7 (9%) 5 (9%) 15 (4%) Unknown data Neversmoker (12%) 52 (16%) 29 (14%) 18 (16%) 7 (9%) 7 (9%) 20 (27%) 4 (8%) 66 (17%) Smoking status Former smoker Current smoker 37 (30%) 71 (58%) 104 (31%) 179 (53%) 61 (29%) 32 (28%) 20 (25%) 25 (32%) 23 (32%) 20 (41%) 117 (57%) 65 (58%) 52 (66%) 45 (58%) 30 (41%) 25 (51%) 115 (30%) 203 (53%) Unknown data KRAS Wild-type 94 (68%) 263 (73%) 148 (65%) 94 (72%) 58 (67%) 60 (71%) 65 (83%) 46 (84%) Mutant 44 (32%) 99 (27%) 80 (35%) 37 (28%) 29 (33%) 24 (29%) 13 (17%) 9 (16%) 290 (72%) 113 (28%)
21 KRAS status in metastatic lung adenocarcinoma
22 Metastatic site-specific variation of KRAS status in lung adenocarcinoma
23 Repurposing bisphosphonates
24 KRAS mutation and bisphosphonate treatment sensitivity Garay, Lohinai et al, unpublished data
25 Personalised (precision) medicine in lung adenocarcinoma Subtypes of molecular alterations, especially of so-called driver mutations, must be used as markers that determine the selection of patients who most likely can benefit from therapy. The clinical consequence of molecular alterations are context (e.g. metastatic site) dependent. The translation of our knowledge about molecular mechanisms and signaling networks to predict therapeutic consequences is a very delicate task and requires thorough preclinical and clinical investigations.
26 Acknowledgements Medical University of Vienna Dr. Balazs Dome Dr. Bahil Ghanim Dr. Viktoria Laszlo Prof. Walter Berger Dr. Michael Grusch Semmelweis University, Budapest Prof. Jozsef Timar Dr. Erzsebet Raso Tamas Barbai Prof. Ilona Kovalszky Dr. Tamas Garay Eszter Molnar Dr. Istvan Kenessey National Koranyi Institute of Pulmonology, Budapest Dr. Gyula Ostoros Dr. Zoltan Lohinai Mihaly Cserepes Dr. Judit Moldvay Anita Rozsas National Institute of Oncology, Budapest Dr. Jozsef Tovari
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