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20. Immune checkpoint blockade in the treatment of advanced non-small cell lung cancer – predictors of response and impact of previous radiotherapy.

Author

Öjlert, Åsa Kristina, Nebdal, Daniel, Lund-Iversen, Marius, Åstrøm Ellefsen, Renée, Brustugun, Odd Terje, Gran, Jon Michael, Halvorsen, Ann Rita, and Helland, Åslaug

Subjects
LUNG cancer prognosis, LUNG cancer, C-reactive protein, IMMUNE checkpoint inhibitors, CONFIDENCE intervals, RETROSPECTIVE studies, REGRESSION analysis, TREATMENT effectiveness, CANCER patients, NEUTROPHILS, DESCRIPTIVE statistics, COMBINED modality therapy, IMMUNOTHERAPY, PROPORTIONAL hazards models, LYMPHOCYTE count, THERAPEUTICS
Abstract

The implementation of immune checkpoint inhibitors (ICI) into the standard care of advanced non-small cell lung cancer (NSCLC) has improved prognosis for this group of patients. However, long-term survival is rare. The aim of the study was to identify predictors of response and, especially, to investigate the impact radiotherapy might have on duration of response. The association between pretreatment patient/tumor characteristics and progression-free survival (PFS), overall survival (OS), and lung cancer-specific survival was investigated in 78 patients receiving an ICI as ≥2nd line treatment for advanced NSCLC, using Cox regression analysis. Due to competing risk, cause-specific deaths were also examined with cumulative incidence plots. Median OS was 12.6 months (95% CI 7.8–18.2) and median PFS 4.1 months (95% CI 3.0–6.2), after median follow-up time of 49.7 months (range 20.9–51.5). Increasing CRP and neutrophil/lymphocyte ratio (NLR), were associated with poor PFS (CRP: HR 1.49, 95% CI 1.12–1.98; NLR: HR 1.59, 95% CI 1.22–1.85) and OS (CRP: HR 1.94, 95% CI 1.47–2.56; NLR: HR 1.54, 95% CI 1.27–1.87). Radiotherapy prior to immunotherapy was not significantly associated with patient outcome. However, when the dataset was split at 6 months of follow-up, to be able to identify early and late predictors of prognosis, we found that patients receiving radiotherapy <6 months prior to immunotherapy had better PFS (HR: 0.27, 95% CI 0.09–0.84) and lung cancer-specific survival (HR: 0.41, 95% CI 0.18–0.95) after the first 6 months of follow-up, while increasing CRP (PFS: HR1.61, 95% CI 1.21–2.14; OS: HR2.04, 95% CI 1.51–2.74) and NLR (PFS: HR 1.57, 95% CI 1.29–1.91; OS: HR 1.63, 95% CI 1.35–1.97) were predictors of poor short-term prognosis. Radiotherapy may be of importance to achieve a long-lasting response to immunotherapy, while indicators of systemic inflammation can help in identifying patients with poor short-term prognosis. [ABSTRACT FROM AUTHOR]

Published
2021
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21. Circulating microRNAs; biomarkers for early detection, prediction of therapy response and prognosis in cancer patients

Author

Halvorsen, Ann Rita

Abstract

In order to optimize the treatment and outcome for cancer patients, biomarkers for early detection, prediction of treatment and estimation of prognosis are needed. The aim of this thesis was to investigate if microRNAs in circulation could be used as biomarkers for cancer patients. Serum or plasma from lung, breast, ovarian cancer patients, and controls were used for RNA extraction and microRNA quantification. The combination of six specific microRNAs was able to distinguish lung cancer patients from healthy individuals and COPD. This signature was further tested in serum from a lung cancer screening cohort. With sensitivity of 88 % and specificity of 71 % lung cancer patients could be discriminated from those without cancer. Further, a set of seven microRNAs could identify lung cancer patients treated with immune therapy with prolonged overall survival. In ovarian cancer patients, one microRNA associated with good response to bevacizumab was identified, confirming the predictive potential of microRNAs in circulation. Three microRNAs were associated with prognosis of the disease. In a study of breast cancer patients, the levels of microRNAs in tumor cells, the tumor interstitium, the normal interstitium, and serum were investigated. This revealed that certain microRNAs seem to be secreted from the cell and into the microenvironment and some of these further into circulation. This may be a unique method to identify tumor specific microRNAs. In addition, 23 microRNAs in the interstitium were associated with the presence of tumor infiltration lymphocytes supporting microRNAs role in communication between cells. Earlier studies have shown that microRNAs are very stable in circulation, making them attractive as biomarkers. In addition, blood as a base for biomarkers is less invasive to acquire. The findings from this study show that microRNAs in circulation can be an important tool as markers for cancer patients.

Published
2017

22. High number of kinome-mutations in non-small cell lung cancers associated with reduced immune response and poor relapse-free survival

Author

Helland, Åslaug, Brustugun, Odd Terje, Nakken, Sigve, Halvorsen, Ann Rita, Dønnem, Tom, Bremnes, Roy M., Busund, Lill-Tove, Sun, Jinchang, Lorenz, Susanne, Solberg, Steinar, Jørgensen, Lars Hilmar, Vodak, Daniel, Myklebost, Ola, Hovig, Eivind, and Meza, Leonardo Zepeda

Subjects
VDP::Medisinske Fag: 700::Klinisk medisinske fag: 750::Onkologi: 762, VDP::Medical disciplines: 700::Clinical medical disciplines: 750::Oncology: 762
Abstract

Source at https://doi.org/10.1002/ijc.30726 Lung cancer is the leading cause of cancer related death, and the past years’ improved insight into underlying molecular events has significantly improved outcome for specific subsets of patients. In particular, several new therapies that target protein kinases have been implemented, and many more are becoming available. We have investigated lung cancer specimens for somatic mutations in a targeted panel of 612 human genes, the majority being protein kinases. The somatic mutation profiles were correlated to profiles of immune cell infiltration as well as relapse‐free survival. Targeted deep sequencing was performed on 117 tumour/normal pairs using the SureSelect Human Kinome kit (Agilent Technologies), with capture probes targeting 3.2 Mb of the human genome, including exons and untranslated regions of all known kinases, kinase receptors and selected cancer‐related genes (612 genes in total). CD8 staining was determined using Ventana Benchmark. Survival analyses were performed using SPSS. The number of mutations per sample ranged from 0 to 50 (within the 612 genes tested), with a median of nine. The prognosis was worse for patients with more than the median number of mutations. A significant correlation was found between mutations in one of selected DNA‐repair genes and the total number of mutations in that tumour (p

Published
2017

25. Serum cytokine profiles and metabolic tumor burden in patients with non-small cell lung cancer undergoing palliative thoracic radiation therapy

Author

Eide, Hanne A., primary, Knudtsen, Ingerid Skjei, additional, Sandhu, Vandana, additional, Løndalen, Ayca M., additional, Halvorsen, Ann Rita, additional, Abravan, Azadeh, additional, Kure, Elin H., additional, Bogsrud, Trond V., additional, Brustugun, Odd Terje, additional, Kyte, Jon Amund, additional, Malinen, Eirik, additional, and Helland, Åslaug, additional

Published
2018
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26. Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking

Author

Weischenfeldt, Joachim, Dubash, Taronish, Drainas, Alexandros P., Mardin, Balca R., Chen, Yuanyuan, Stuetz, Adrian M., Waszak, Sebastian M., Bosco, Graziella, Halvorsen, Ann Rita, Raeder, Benjamin, Efthymiopoulos, Theocharis, Erkek, Serap, Siegl, Christine, Brenner, Hermann, Brustugun, Odd Terje, Dieter, Sebastian M., Northcott, Paul A., Petersen, Iver, Pfister, Stefan M., Schneider, Martin, Solberg, Steinar K., Thunissen, Erik, Weichert, Wilko, Zichner, Thomas, Thomas, Roman, Peifer, Martin, Helland, Aslaug, Ball, Claudia R., Jechlinger, Martin, Sotillo, Rocio, Glimm, Hanno, Korbel, Jan O., Weischenfeldt, Joachim, Dubash, Taronish, Drainas, Alexandros P., Mardin, Balca R., Chen, Yuanyuan, Stuetz, Adrian M., Waszak, Sebastian M., Bosco, Graziella, Halvorsen, Ann Rita, Raeder, Benjamin, Efthymiopoulos, Theocharis, Erkek, Serap, Siegl, Christine, Brenner, Hermann, Brustugun, Odd Terje, Dieter, Sebastian M., Northcott, Paul A., Petersen, Iver, Pfister, Stefan M., Schneider, Martin, Solberg, Steinar K., Thunissen, Erik, Weichert, Wilko, Zichner, Thomas, Thomas, Roman, Peifer, Martin, Helland, Aslaug, Ball, Claudia R., Jechlinger, Martin, Sotillo, Rocio, Glimm, Hanno, and Korbel, Jan O.

Abstract

Extensive prior research focused on somatic copy-number alterations (SCNAs) affecting cancer genes, yet the extent to which recurrent SCNAs exert their influence through rearrangement of cis-regulatory elements (CREs) remains unclear. Here we present a framework for inferring cancer-related gene overexpression resulting from CRE reorganization (e.g., enhancer hijacking) by integrating SCNAs, gene expression data and information on topologically associating domains (TADS). Analysis of 7,416 cancer genomes uncovered several pan-cancer candidate genes, including IRS4, SMARCA1 and TERT. We demonstrate that IRS4 overexpression in lung cancer is associated with recurrent deletions in cis, and we present evidence supporting a tumor promoting role. We additionally pursued cancer-type-specific analyses and uncovered IGF2 as a target for enhancer hijacking in colorectal cancer. Recurrent tandem duplications intersecting with a TAD boundary mediate de novo formation of a 3D contact domain comprising IGF2 and a lineage-specific super-enhancer, resulting in high-level gene activation. Our framework enables systematic inference of CRE rearrangements mediating dysregulation in cancer.

Published
2017

27. Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking

Author

Weischenfeldt, Joachim Lütken, Dubash, Taronish, Drainas, Alexandros P, Mardin, Balca R, Chen, Yuanyuan, Stütz, Adrian M, Waszak, Sebastian M, Bosco, Graziella, Halvorsen, Ann Rita, Raeder, Benjamin, Efthymiopoulos, Theocharis, Erkek, Serap, Siegl, Christine, Brenner, Hermann, Brustugun, Odd Terje, Dieter, Sebastian M, Northcott, Paul A, Petersen, Iver, Pfister, Stefan M, Schneider, Martin, Solberg, Steinar K, Thunissen, Erik, Weichert, Wilko, Zichner, Thomas, Thomas, Roman, Peifer, Martin, Helland, Aslaug, Ball, Claudia R, Jechlinger, Martin, Sotillo, Rocio, Glimm, Hanno, Korbel, Jan O, Weischenfeldt, Joachim Lütken, Dubash, Taronish, Drainas, Alexandros P, Mardin, Balca R, Chen, Yuanyuan, Stütz, Adrian M, Waszak, Sebastian M, Bosco, Graziella, Halvorsen, Ann Rita, Raeder, Benjamin, Efthymiopoulos, Theocharis, Erkek, Serap, Siegl, Christine, Brenner, Hermann, Brustugun, Odd Terje, Dieter, Sebastian M, Northcott, Paul A, Petersen, Iver, Pfister, Stefan M, Schneider, Martin, Solberg, Steinar K, Thunissen, Erik, Weichert, Wilko, Zichner, Thomas, Thomas, Roman, Peifer, Martin, Helland, Aslaug, Ball, Claudia R, Jechlinger, Martin, Sotillo, Rocio, Glimm, Hanno, and Korbel, Jan O

Abstract

Extensive prior research focused on somatic copy-number alterations (SCNAs) affecting cancer genes, yet the extent to which recurrent SCNAs exert their influence through rearrangement of cis-regulatory elements (CREs) remains unclear. Here we present a framework for inferring cancer-related gene overexpression resulting from CRE reorganization (e.g., enhancer hijacking) by integrating SCNAs, gene expression data and information on topologically associating domains (TADs). Analysis of 7,416 cancer genomes uncovered several pan-cancer candidate genes, including IRS4, SMARCA1 and TERT. We demonstrate that IRS4 overexpression in lung cancer is associated with recurrent deletions in cis, and we present evidence supporting a tumor-promoting role. We additionally pursued cancer-type-specific analyses and uncovered IGF2 as a target for enhancer hijacking in colorectal cancer. Recurrent tandem duplications intersecting with a TAD boundary mediate de novo formation of a 3D contact domain comprising IGF2 and a lineage-specific super-enhancer, resulting in high-level gene activation. Our framework enables systematic inference of CRE rearrangements mediating dysregulation in cancer.

Published
2017

31. Profiling of microRNAs in tumor interstitial fluid of breast tumors - a novel resource to identify biomarkers for prognostic classification and detection of cancer

Author

Halvorsen, Ann Rita, primary, Helland, Åslaug, additional, Gromov, Pavel, additional, Wielenga, Vera Timmermans, additional, Talman, Maj-Lis Møller, additional, Brunner, Nils, additional, Sandhu, Vandana, additional, Børresen-Dale, Anne-Lise, additional, Gromova, Irina, additional, and Haakensen, Vilde D., additional

Published
2016
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32. DNA methylation signature (SAM40) identifies subgroups of the Luminal A breast cancer samples with distinct survival

Author

Fleischer, Thomas, primary, Klajic, Jovana, additional, Aure, Miriam Ragle, additional, Louhimo, Riku, additional, Pladsen, Arne V., additional, Ottestad, Lars, additional, Touleimat, Nizar, additional, Laakso, Marko, additional, Halvorsen, Ann Rita, additional, Alnæs, Grethe I. Grenaker, additional, Riis, Margit L.H., additional, Helland, Åslaug, additional, Hautaniemi, Sampsa, additional, Lønning, Per Eystein, additional, Naume, Bjørn, additional, Børresen-Dale, Anne-Lise, additional, Tost, Jörg, additional, and Kristensen, Vessela N., additional

Published
2016
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33. Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking

Author

Weischenfeldt, Joachim, primary, Dubash, Taronish, additional, Drainas, Alexandros P, additional, Mardin, Balca R, additional, Chen, Yuanyuan, additional, Stütz, Adrian M, additional, Waszak, Sebastian M, additional, Bosco, Graziella, additional, Halvorsen, Ann Rita, additional, Raeder, Benjamin, additional, Efthymiopoulos, Theocharis, additional, Erkek, Serap, additional, Siegl, Christine, additional, Brenner, Hermann, additional, Brustugun, Odd Terje, additional, Dieter, Sebastian M, additional, Northcott, Paul A, additional, Petersen, Iver, additional, Pfister, Stefan M, additional, Schneider, Martin, additional, Solberg, Steinar K, additional, Thunissen, Erik, additional, Weichert, Wilko, additional, Zichner, Thomas, additional, Thomas, Roman, additional, Peifer, Martin, additional, Helland, Aslaug, additional, Ball, Claudia R, additional, Jechlinger, Martin, additional, Sotillo, Rocio, additional, Glimm, Hanno, additional, and Korbel, Jan O, additional

Published
2016
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34. Non-small cell lung cancer is characterised by a distinct inflammatory signature in serum compared with chronic obstructive pulmonary disease

Author

Eide, Hanne Astrid, primary, Halvorsen, Ann Rita, additional, Sandhu, Vandana, additional, Fåne, Anne, additional, Berg, Janna, additional, Haakensen, Vilde Drageset, additional, Kure, Elin H, additional, Brustugun, Odd Terje, additional, Kiserud, Cecilie Essholt, additional, Kyte, Jon Amund, additional, and Helland, Åslaug, additional

Published
2016
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35. A unique set of 6 circulating microRNAs for early detection of non-small cell lung cancer

Author

Halvorsen, Ann Rita, primary, Bjaanæs, Maria, additional, LeBlanc, Marissa, additional, Holm, Are M., additional, Bolstad, Nils, additional, Rubio, Luis, additional, Peñalver, Juan Carlos, additional, Cervera, José, additional, Mojarrieta, Julia Cruz, additional, López-Guerrero, Jose Antonio, additional, Brustugun, Odd Terje, additional, and Helland, Åslaug, additional

Published
2016
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37. Genome-wide DNA methylation analyses in lung adenocarcinomas: Association with EGFR, KRAS and TP53 mutation status, gene expression and prognosis

Author

Bjaanaes, Maria Moksnes, primary, Fleischer, Thomas, additional, Halvorsen, Ann Rita, additional, Daunay, Antoine, additional, Busato, Florence, additional, Solberg, Steinar, additional, Jørgensen, Lars, additional, Kure, Elin, additional, Edvardsen, Hege, additional, Børresen-Dale, Anne-Lise, additional, Brustugun, Odd Terje, additional, Tost, Jörg, additional, Kristensen, Vessela, additional, and Helland, Åslaug, additional

Published
2015
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38. Profiling of micro RNAs in tumor interstitial fluid of breast tumors - a novel resource to identify biomarkers for prognostic classification and detection of cancer.

Author

Halvorsen, Ann Rita, Helland, Åslaug, Gromov, Pavel, Wielenga, Vera Timmermans, Talman, Maj‐Lis Møller, Brunner, Nils, Sandhu, Vandana, Børresen‐Dale, Anne‐Lise, Gromova, Irina, and Haakensen, Vilde D.

Abstract

It has been hypothesized based on accumulated data that a class of small noncoding RNAs, termed micro RNAs, are key factors in intercellular communication. Here, micro RNAs present in interstitial breast tumor fluids have been analyzed to identify relevant markers for a diagnosis of breast cancer and to elucidate the cross-talk that exists among cells in a tumor microenvironment. Matched tumor interstitial fluid samples ( TIF, n = 60), normal interstitial fluid samples ( NIF, n = 51), corresponding tumor tissue specimens ( n = 54), and serum samples ( n = 27) were collected from patients with breast cancer, and detectable micro RNAs were analyzed and compared. In addition, serum data from 32 patients with breast cancer and 22 healthy controls were obtained for a validation study. To identify potential serum biomarkers of breast cancer, first the micro RNA profiles of TIF and NIF samples were compared. A total of 266 micro RNAs were present at higher level in the TIF samples as compared to normal counterparts. Sixty-one of these micro RNAs were present in > 75% of the serum samples and were subsequently tested in a validation set. Seven of the 61 micro RNAs were associated with poor survival, while 23 were associated with the presence of immune cells and adipocytes. To our knowledge, these data demonstrate for the first time that profiling of micro RNAs in TIF can identify novel biomarkers for the prognostic classification and detection of breast cancer. In addition, the present findings demonstrate that micro RNAs may represent the cross-talk that occurs between tumor cells and their surrounding stroma. [ABSTRACT FROM AUTHOR]

Published
2017
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39. Mutations in NSCLC.

Author

Helland, Åslaug, primary, Brustugun, Odd Terje, additional, Nakken, Sigve, additional, Halvorsen, Ann Rita, additional, Sun, Jinchang, additional, Lorenz, Susanne., additional, Vodak, Daniel, additional, Myklebost, Ola, additional, Hovig, Eivind, additional, and Meza-Zepeda, Leonardo A., additional

Published
2014
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41. Osteopontin is a prognostic biomarker in non-small cell lung cancer

Author

Rud, Ane Kongsgaard, primary, Boye, Kjetil, additional, Øijordsbakken, Miriam, additional, Lund-Iversen, Marius, additional, Halvorsen, Ann Rita, additional, Solberg, Steinar K, additional, Berge, Gisle, additional, Helland, Åslaug, additional, Brustugun, Odd Terje, additional, and Mælandsmo, Gunhild M, additional

Published
2013
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45. DNA methylation signature (SAM40) identifies subgroups of the Luminal A breast cancer samples with distinct survival.

Author

Fleischer T, Klajic J, Aure MR, Louhimo R, Pladsen AV, Ottestad L, Touleimat N, Laakso M, Halvorsen AR, Grenaker Alnæs GI, Riis ML, Helland Å, Hautaniemi S, Lønning PE, Naume B, Børresen-Dale AL, Tost J, and Kristensen VN

Subjects
Breast Neoplasms pathology, Cluster Analysis, Epigenesis, Genetic, Epigenomics methods, Female, Gene Dosage, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Kaplan-Meier Estimate, Prognosis, Biomarkers, Tumor, Breast Neoplasms genetics, Breast Neoplasms mortality, DNA Methylation, Transcriptome
Abstract

Breast cancer patients with Luminal A disease generally have a good prognosis, but among this patient group are patients with good prognosis that are currently overtreated with adjuvant chemotherapy, and also patients that have a bad prognosis and should be given more aggressive treatment. There is no available method for subclassification of this patient group. Here we present a DNA methylation signature (SAM40) that segregates Luminal A patients based on prognosis, and identify one good prognosis group and one bad prognosis group. The prognostic impact of SAM40 was validated in four independent patient cohorts. Being able to subdivide the Luminal A patients may give the two-sided benefit of identifying one subgroup that may benefit from a more aggressive treatment than what is given today, and importantly, identifying a subgroup that may benefit from less treatment.

Published
2017
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46. Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking.

Author

Weischenfeldt J, Dubash T, Drainas AP, Mardin BR, Chen Y, Stütz AM, Waszak SM, Bosco G, Halvorsen AR, Raeder B, Efthymiopoulos T, Erkek S, Siegl C, Brenner H, Brustugun OT, Dieter SM, Northcott PA, Petersen I, Pfister SM, Schneider M, Solberg SK, Thunissen E, Weichert W, Zichner T, Thomas R, Peifer M, Helland A, Ball CR, Jechlinger M, Sotillo R, Glimm H, and Korbel JO

Subjects
Genetic Association Studies, Genetic Predisposition to Disease, Humans, Promoter Regions, Genetic, DNA Copy Number Variations genetics, Enhancer Elements, Genetic genetics, Gene Expression Regulation, Neoplastic, Insulin Receptor Substrate Proteins genetics, Insulin-Like Growth Factor II genetics, Neoplasms genetics
Abstract

Extensive prior research focused on somatic copy-number alterations (SCNAs) affecting cancer genes, yet the extent to which recurrent SCNAs exert their influence through rearrangement of cis-regulatory elements (CREs) remains unclear. Here we present a framework for inferring cancer-related gene overexpression resulting from CRE reorganization (e.g., enhancer hijacking) by integrating SCNAs, gene expression data and information on topologically associating domains (TADs). Analysis of 7,416 cancer genomes uncovered several pan-cancer candidate genes, including IRS4, SMARCA1 and TERT. We demonstrate that IRS4 overexpression in lung cancer is associated with recurrent deletions in cis, and we present evidence supporting a tumor-promoting role. We additionally pursued cancer-type-specific analyses and uncovered IGF2 as a target for enhancer hijacking in colorectal cancer. Recurrent tandem duplications intersecting with a TAD boundary mediate de novo formation of a 3D contact domain comprising IGF2 and a lineage-specific super-enhancer, resulting in high-level gene activation. Our framework enables systematic inference of CRE rearrangements mediating dysregulation in cancer.

Published
2017
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47. Unique microRNA-profiles in EGFR-mutated lung adenocarcinomas.

Author

Bjaanaes MM, Halvorsen AR, Solberg S, Jørgensen L, Dragani TA, Galvan A, Colombo F, Anderlini M, Pastorino U, Kure E, Børresen-Dale AL, Brustugun OT, and Helland A

Subjects
Adenocarcinoma genetics, Adenocarcinoma mortality, Adenocarcinoma of Lung, Aged, Cohort Studies, DNA Mutational Analysis, Female, Humans, Kaplan-Meier Estimate, Lung Neoplasms genetics, Lung Neoplasms mortality, Male, MicroRNAs metabolism, Middle Aged, Mutation, Oligonucleotide Array Sequence Analysis, Proportional Hazards Models, Proto-Oncogene Proteins genetics, Proto-Oncogene Proteins p21(ras), ras Proteins genetics, Adenocarcinoma metabolism, ErbB Receptors genetics, Lung Neoplasms metabolism, MicroRNAs genetics, Transcriptome
Abstract

The findings of mutations and the development of targeted therapies have improved lung cancer management. Still, the prognosis remains poor, and we need to know more about the genetic and epigenetic alterations in lung cancer. MicroRNAs are involved in crucial biological processes like carcinogenesis by regulating gene expression at the post-transcriptional level. In this project, we have studied the microRNA expression of lung adenocarcinomas and corresponding normal lung tissue and correlated the expression with clinical data and EGFR- and KRAS-mutational status. Agilent microarrays have been used, examining microRNA expression in 154 surgically resected lung adenocarcinomas and 20 corresponding normal lung tissue samples. Findings were confirmed by RT-qPCR in the same cohort and in an independent cohort of 103 lung cancer patients. EGFR and KRAS mutation analyses were also performed. 129 microRNAs were significantly differentially expressed in lung adenocarcinomas compared with normal lung tissue, and 17 microRNAs were differentially expressed between EGFR-mutated and EGFR wildtype tumors. We identified microRNAs associated with time to progression. We have identified several aberrantly expressed microRNAs that discriminate lung adenocarcinomas from normal lung tissue, and hence may be potential biomarkers for early detection. We have found microRNAs that are differentially expressed between EGFR-mutated and EGFR wildtype lung adenocarcinomas, suggesting that microRNAs can be used as molecular biomarkers in classification. We hypothesize that microRNA expression can be used as biomarkers for clinical course., (© 2014 The Authors. Published by Wiley Periodicals, Inc. on behalf of UICC.)

Published
2014
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