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Gene Expression Pro...
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Karlsson, AnnaLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine
(author)
Gene Expression Profiling of Large Cell Lung Cancer Links Transcriptional Phenotypes to the New Histological WHO 2015 Classification
- Article/chapterEnglish2017
Publisher, publication year, extent ...
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ELSEVIER SCIENCE INC,2017
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electronicrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:uu-333713
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-333713URI
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https://doi.org/10.1016/j.jtho.2017.05.008DOI
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https://lup.lub.lu.se/record/e5cfb6c0-e8e0-49a2-a0b5-a7373e324b0eURI
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Introduction: Large cell lung cancer (LCLC) and large cell neuroendocrine carcinoma (LCNEC) constitute a small proportion of NSCLC. The WHO 2015 classification guidelines changed the definition of the debated histological subtype LCLC to be based on immunomarkers for adenocarcinoma and squamous cancer. We sought to determine whether these new guidelines also translate into the transcriptional landscape of lung cancer, and LCLC specifically.Methods: Gene expression profiling was performed by using Illumina V4 HT12 microarrays (Illumina, San Diego, CA) on samples from 159 cases (comprising all histological subtypes, including 10 classified as LCLC WHO 2015 and 14 classified as LCNEC according to the WHO 2015 guidelines), with complimentary mutational and immunohistochemical data. Derived transcriptional phenotypes were validated in 199 independent tumors, including six WHO 2015 LCLCs and five LCNECs.Results: Unsupervised analysis of gene expression data identified a phenotype comprising 90% of WHO 2015 LCLC tumors, with characteristics of poorly differentiated proliferatiVe cancer, a 90% tumor protein p53 gene (TP53) mutation rate, and lack of well-known NSCLC oncogene driver alterations. Validation in independent data confirmed aggregation of WHO 2015 LCLCs in the specific phenotype. For LCNEC tumors, the unsupervised gene expression analysis suggested two different transcriptional patterns corresponding to a proposed genetic division of LCNEC tumors into SCLC-like and NSCLC-like cancer on the basis of TP53 and retinoblastoma 1 gene (RB1) alteration patterns.Conclusions: Refined classification of LCLC has implications for diagnosis, prognostics, and therapy decisions. Our molecular analyses support the WHO 2015 classification of LCLC and LCNEC tumors, which herein follow different tumorigenic paths and can accordingly be stratified into different transcriptional subgroups, thus linking diagnostic immunohistochemical staining driven classification with the transcriptional landscape of lung cancer.
Subject headings and genre
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Brunnström, HansLund University,Lunds universitet,Tumörmikromiljö,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Tumor microenvironment,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine,Regional Laboratories Region Skåne(Swepub:lu)med-hsb
(author)
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Micke, PatrickUppsala University,Uppsala universitet,Klinisk och experimentell patologi,Patrick Micke(Swepub:uu)patmi676
(author)
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Veerla, SrinivasLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)klin-sve
(author)
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Mattsson, Johanna Sofia Margareta,1985-Uppsala University,Uppsala universitet,Klinisk och experimentell patologi,Patrick Micke(Swepub:uu)johma961
(author)
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La Fleur, LinneaUppsala University,Uppsala universitet,Klinisk och experimentell patologi,Science for Life Laboratory, SciLifeLab,Johan Botling(Swepub:uu)linla513
(author)
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Botling, JohanUppsala University,Uppsala universitet,Klinisk och experimentell patologi,Johan Botling(Swepub:uu)johanbot
(author)
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Jönsson, MatsLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)medk-mjo
(author)
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Reuterswärd, ChristelLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)med-chr
(author)
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Planck, MariaLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine,Skåne University Hospital(Swepub:lu)onk-mpl
(author)
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Staaf, JohanLund University,Lunds universitet,Bröstcancer-genetik,Sektion I,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Breastcancer-genetics,Section I,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)onk-jst
(author)
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Bröstcancer-genetikSektion I
(creator_code:org_t)
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In:Journal of Thoracic Oncology: ELSEVIER SCIENCE INC12:8, s. 1257-12671556-08641556-1380
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Brunnström, Hans
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Micke, Patrick
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Botling, Johan
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