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Biswas, D., Birkbak, N. J., Rosenthal, R., Hiley, C. T., Lim, E. L., Papp, K., . . . Swanton, C. (2019). A clonal expression biomarker associates with lung cancer mortality. Nature Medicine, 25(10), 1540-1548
Öppna denna publikation i ny flik eller fönster >>A clonal expression biomarker associates with lung cancer mortality
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2019 (Engelska)Ingår i: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 25, nr 10, s. 1540-1548Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

An aim of molecular biomarkers is to stratify patients with cancer into disease subtypes predictive of outcome, improving diagnostic precision beyond clinical descriptors such as tumor stage(1). Transcriptomic intratumor heterogeneity (RNA-ITH) has been shown to confound existing expression-based biomarkers across multiple cancer types(2-6). Here, we analyze multi-region whole-exome and RNA sequencing data for 156 tumor regions from 48 patients enrolled in the TRACERx study to explore and control for RNA-ITH in non-small cell lung cancer. We find that chromosomal instability is a major driver of RNA-ITH, and existing prognostic gene expression signatures are vulnerable to tumor sampling bias. To address this, we identify genes expressed homogeneously within individual tumors that encode expression modules of cancer cell proliferation and are often driven by DNA copy-number gains selected early in tumor evolution. Clonal transcriptomic biomarkers overcome tumor sampling bias, associate with survival independent of clinicopathological risk factors, and may provide a general strategy to refine biomarker design across cancer types.

Nationell ämneskategori
Cancer och onkologi Klinisk laboratoriemedicin
Forskningsämne
Patologi
Identifikatorer
urn:nbn:se:uu:diva-396656 (URN)10.1038/s41591-019-0595-z (DOI)000489166700023 ()31591602 (PubMedID)
Forskningsfinansiär
EU, Europeiska forskningsrådet, FP7-THESEUS-617844EU, Europeiska forskningsrådet, 835297
Tillgänglig från: 2019-11-14 Skapad: 2019-11-14 Senast uppdaterad: 2020-01-08Bibliografiskt granskad
Tsakonas, G., Botling, J., Micke, P., Rivard, C., La Fleur, L., Mattsson, J. S., . . . Ekman, S. (2019). c-MET as a biomarker in patients with surgically resected non-small cell lung cancer. Lung Cancer, 133, 69-74
Öppna denna publikation i ny flik eller fönster >>c-MET as a biomarker in patients with surgically resected non-small cell lung cancer
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2019 (Engelska)Ingår i: Lung Cancer, ISSN 0169-5002, E-ISSN 1872-8332, Vol. 133, s. 69-74Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Background: c-MET protein overexpression has been proposed as a biomarker in non-small cell lung cancer (NSCLC), albeit its role in the clinical setting has not been firmly established yet. Patients and methods: We designed a retrospective cohort study, consisting of 725 patients with surgically removed NSCLC. Immunohistochemistry (IHC) was conducted in tissue microarrays (TMA) from lung tumors and healthy tissue. IHC staining was quantified using H-scores (range 0-300). Association between c-MET H-score and overall survival (OS) as well as progression-free survival (PFS) was explored. Results: c-MET H-score >= 20 had a significant positive impact on OS in the multivariate analysis in the whole study population, HR = 0.79 (95%CI: 0.64 - 0.97). The prognostic effect of c-MET H-score >= 20 was even stronger in patients who received adjuvant treatment with a HR = 0.61 (95% CI: 0.40 - 0.93). In the subgroup of adenocarcinoma and squamous cell carcinoma patients with stage IIA-IIIB disease, the prognostic impact of c-MET was significant in the univariate analysis (HR = 0.60, 95% CI: 0.43 - 0.83). Conclusion: c-MET H-score >= 20 is a positive prognostic biomarker for OS in early stage NSCLC. This benefit seems to be strongly correlated to adjuvant chemotherapy, therefore rendering c-MET H-score >= 20 a possible predictive biomarker for platinum-based adjuvant chemotherapy in early stage NSCLC.

Ort, förlag, år, upplaga, sidor
Elsevier, 2019
Nyckelord
c-MET, Lung cancer, Biomarker, OS, PFS, H-score
Nationell ämneskategori
Cancer och onkologi Klinisk laboratoriemedicin
Forskningsämne
Patologi
Identifikatorer
urn:nbn:se:uu:diva-390909 (URN)10.1016/j.lungcan.2019.04.028 (DOI)000474326700012 ()31200831 (PubMedID)
Forskningsfinansiär
Stockholms läns landsting
Tillgänglig från: 2019-08-16 Skapad: 2019-08-16 Senast uppdaterad: 2020-01-08Bibliografiskt granskad
La Fleur, L. (2019). Mutation and immune profiling of non-small cell lung cancer. (Doctoral dissertation). Uppsala: Acta Universitatis Upsaliensis
Öppna denna publikation i ny flik eller fönster >>Mutation and immune profiling of non-small cell lung cancer
2019 (Engelska)Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
Abstract [en]

Several novel therapies that target molecular alterations and immune checkpoints in lung cancer have been introduced in the last decade. Still, only a minority of patients obtain long term disease control and overall survival remains poor. The aim of this thesis was to characterize the landscape of genetic alterations and immune cell infiltrates in tumor tissues from a large representative patient cohort of non-small cell lung cancer (NSCLC).

The mutational status of 82 genes related to lung cancer development were evaluated, in paper I, by a targeted re-sequencing approach adapted to work on “real-life” samples of mixed quality. We observed a remarkably high prevalence of activating KRAS mutations. Otherwise, the mutation spectrum resembled other western lung cancer populations. Poor survival was linked to subgroups of lung adenocarcinoma with mutations in TP53, STK11 and SMARCA4, independent of concomitant KRAS mutations. In lung squamous cell carcinoma, patients with mutations in CSMD3 had better survival.

The infiltration of tumor-associated immune cells was assessed by immunohistochemical analysis in paper II. Previously described immune response patterns termed “inflamed” and “desert” were confirmed in our dataset. In addition, we discovered a new immune phenotype characterized by overall sparse presence of most immune cell types except for a distinct infiltration of NK and plasma cells. This novel immune class displayed a favorable prognosis and was therefore designated “oasis”.

In paper III, infiltration of macrophage subtypes was evaluated by immunohistochemical analysis of CD68, CD163, MSR1 and MARCO. The majority of macrophages exhibited a tumor promoting phenotype and expression of MARCO, a targetable scavenger receptor, was detected in a distinct subset of NSCLC patients. Further investigation of the functional roles of MARCO in a human NSCLC setting was carried out in paper IV. Here, MARCO expression on cultured myeloid cells could be induced by NSCLC cell lines. The MARCO+ cells displayed an immunosuppressive phenotype and could effectively suppress the cytolytic effect of NK cells and CD8+ T cells. A monoclonal antibody targeting MARCO removed these inhibitory effects of the MARCO+ cells.

In summary, this thesis contributes knowledge on the genetic and immunologic underpinning of lung cancer that forms the basis for current and future treatment strategies in the evolving era of personalized oncology and pathology.

Ort, förlag, år, upplaga, sidor
Uppsala: Acta Universitatis Upsaliensis, 2019. s. 69
Serie
Digital Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 1651-6206 ; 1592
Nyckelord
Non-small cell lung cancer, Tumor microenvironment, Tumor-associated macrophages, Immune infiltrates, PD-L1, Mutation patterns, Immune therapy, MARCO, TP53, STK11, KRAS
Nationell ämneskategori
Medicin och hälsovetenskap
Identifikatorer
urn:nbn:se:uu:diva-390321 (URN)978-91-513-0733-6 (ISBN)
Disputation
2019-10-11, Rudbecksalen, Rudbecklaboratoriet, Dag Hammarskjölds väg 20, Uppsala, 09:00 (Engelska)
Opponent
Handledare
Tillgänglig från: 2019-09-19 Skapad: 2019-08-20 Senast uppdaterad: 2019-10-15
La Fleur, L., Falk-Sörqvist, E., Smeds, P., Berglund, A., Sundström, M., Mattsson, J. S., . . . Botling, J. (2019). Mutation patterns in a population-based non-small cell lung cancer cohort and prognostic impact of concomitant mutations in KRAS and TP53 or STK11. Lung Cancer, 130, 50-58
Öppna denna publikation i ny flik eller fönster >>Mutation patterns in a population-based non-small cell lung cancer cohort and prognostic impact of concomitant mutations in KRAS and TP53 or STK11
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2019 (Engelska)Ingår i: Lung Cancer, ISSN 0169-5002, E-ISSN 1872-8332, Vol. 130, s. 50-58Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

OBJECTIVES: Non-small cell lung cancer (NSCLC) is a heterogeneous disease with unique combinations of somatic molecular alterations in individual patients, as well as significant differences in populations across the world with regard to mutation spectra and mutation frequencies. Here we aim to describe mutational patterns and linked clinical parameters in a population-based NSCLC cohort.

MATERIALS AND METHODS: Using targeted resequencing the mutational status of 82 genes was evaluated in a consecutive Swedish surgical NSCLC cohort, consisting of 352 patient samples from either fresh frozen or formalin fixed paraffin embedded (FFPE) tissues. The panel covers all exons of the 82 genes and utilizes reduced target fragment length and two-strand capture making it compatible with degraded FFPE samples.

RESULTS: We obtained a uniform sequencing coverage and mutation load across the fresh frozen and FFPE samples by adaption of sequencing depth and bioinformatic pipeline, thereby avoiding a technical bias between these two sample types. At large, the mutation frequencies resembled the frequencies seen in other western populations, except for a high frequency of KRAS hotspot mutations (43%) in adenocarcinoma patients. Worse overall survival was observed for adenocarcinoma patients with a mutation in either TP53, STK11 or SMARCA4. In the adenocarcinoma KRAS-mutated group poor survival appeared to be linked to concomitant TP53 or STK11 mutations, and not to KRAS mutation as a single aberration. Similar results were seen in the analysis of publicly available data from the cBioPortal. In squamous cell carcinoma a worse prognosis could be observed for patients with MLL2 mutations, while CSMD3 mutations were linked to a better prognosis.

CONCLUSION: Here we have evaluated the mutational status of a NSCLC cohort. We could not confirm any survival impact of isolated driver mutations. Instead, concurrent mutations in TP53 and STK11 were shown to confer poor survival in the KRAS-positive adenocarcinoma subgroup.

Nyckelord
KRAS, Mutation patterns, Non-small cell lung cancer, STK11, TP53, Targeted resequencing
Nationell ämneskategori
Klinisk laboratoriemedicin
Forskningsämne
Patologi
Identifikatorer
urn:nbn:se:uu:diva-380587 (URN)10.1016/j.lungcan.2019.01.003 (DOI)000463276900008 ()30885352 (PubMedID)
Forskningsfinansiär
Cancerfonden, 2013/711Cancerfonden, 2016/827
Tillgänglig från: 2019-03-29 Skapad: 2019-03-29 Senast uppdaterad: 2020-01-03Bibliografiskt granskad
La Fleur, L., Boura, V. F., Alexeyenko, A., Berglund, A., Ponten, V., Mattsson, J. S., . . . Botling, J. (2018). Expression of scavenger receptor MARCO defines a targetable tumor-associated macrophage subset in non-small cell lung cancer. International Journal of Cancer, 143(7), 1741-1752
Öppna denna publikation i ny flik eller fönster >>Expression of scavenger receptor MARCO defines a targetable tumor-associated macrophage subset in non-small cell lung cancer
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2018 (Engelska)Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 143, nr 7, s. 1741-1752Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Tumor-associated macrophages (TAMs) are attractive targets for immunotherapy. Recently, studies in animal models showed that treatment with an anti-TAM antibody directed against the scavenger receptor MARCO resulted in suppression of tumor growth and metastatic dissemination. Here we investigated the expression of MARCO in relation to other macrophage markers and immune pathways in a non-small cell lung cancer (NSCLC) cohort (n=352). MARCO, CD68, CD163, MSR1 and programmed death ligand-1 (PD-L1) were analyzed by immunohistochemistry and immunofluorescence, and associations to other immune cells and regulatory pathways were studied in a subset of cases (n=199) with available RNA-seq data. We observed a large variation in macrophage density between cases and a strong correlation between CD68 and CD163, suggesting that the majority of TAMs present in NSCLC exhibit a protumor phenotype. Correlation to clinical data only showed a weak trend toward worse survival for patients with high macrophage infiltration. Interestingly, MARCO was expressed on a distinct subpopulation of TAMs, which tended to aggregate in close proximity to tumor cell nests. On the transcriptomic level, we found a positive association between MARCO gene expression and general immune response pathways including strong links to immunosuppressive TAMs, T-cell infiltration and immune checkpoint molecules. Indeed, a higher macrophage infiltration was seen in tumors expressing PD-L1, and macrophages residing within tumor cell nests co-expressed MARCO and PD-L1. Thus, MARCO is a potential new immune target for anti-TAM treatment in a subset of NSCLC patients, possibly in combination with available immune checkpoint inhibitors.

Ort, förlag, år, upplaga, sidor
WILEY, 2018
Nyckelord
lung cancer, MARCO, tumor-associated macrophages, immune therapy, PD-L1
Nationell ämneskategori
Cancer och onkologi Klinisk laboratoriemedicin
Forskningsämne
Patologi
Identifikatorer
urn:nbn:se:uu:diva-364230 (URN)10.1002/ijc.31545 (DOI)000443392100020 ()29667169 (PubMedID)
Forskningsfinansiär
Cancerfonden
Tillgänglig från: 2018-10-24 Skapad: 2018-10-24 Senast uppdaterad: 2019-08-20Bibliografiskt granskad
Isaksson, J., Willen, L., La Fleur, L., Mindus, S., Sundström, M., Branden, E., . . . Botling, J. (2017). Establishing Reflex NGS Testing in NSCLC in a Regional Network of County Hospitals in Central Sweden. Journal of Thoracic Oncology, 12(1), S499-S500
Öppna denna publikation i ny flik eller fönster >>Establishing Reflex NGS Testing in NSCLC in a Regional Network of County Hospitals in Central Sweden
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2017 (Engelska)Ingår i: Journal of Thoracic Oncology, ISSN 1556-0864, E-ISSN 1556-1380, Vol. 12, nr 1, s. S499-S500Artikel i tidskrift, Meeting abstract (Övrigt vetenskapligt) Published
Ort, förlag, år, upplaga, sidor
Elsevier, 2017
Nyckelord
FFPE, next generation sequencing, NSCLC
Nationell ämneskategori
Cancer och onkologi
Identifikatorer
urn:nbn:se:uu:diva-377744 (URN)10.1016/j.jtho.2016.11.605 (DOI)000413055801108 ()
Tillgänglig från: 2019-02-26 Skapad: 2019-02-26 Senast uppdaterad: 2019-02-26Bibliografiskt granskad
Karlsson, A., Brunnström, H., Micke, P., Veerla, S., Mattsson, J. S., La Fleur, L., . . . Staaf, J. (2017). Gene Expression Profiling of Large Cell Lung Cancer Links Transcriptional Phenotypes to the New Histological WHO 2015 Classification. Journal of Thoracic Oncology, 12(8), 1257-1267
Öppna denna publikation i ny flik eller fönster >>Gene Expression Profiling of Large Cell Lung Cancer Links Transcriptional Phenotypes to the New Histological WHO 2015 Classification
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2017 (Engelska)Ingår i: Journal of Thoracic Oncology, ISSN 1556-0864, E-ISSN 1556-1380, Vol. 12, nr 8, s. 1257-1267Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

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.

Ort, förlag, år, upplaga, sidor
ELSEVIER SCIENCE INC, 2017
Nyckelord
Lung cancer, Large cell lung carcinoma, LCNEC, Mutation, Gene expression, WHO classification
Nationell ämneskategori
Cancer och onkologi Klinisk laboratoriemedicin
Forskningsämne
Patologi
Identifikatorer
urn:nbn:se:uu:diva-333713 (URN)10.1016/j.jtho.2017.05.008 (DOI)000407187400009 ()28535939 (PubMedID)
Forskningsfinansiär
CancerfondenGunnar Nilssons cancerstiftelseCrafoordska stiftelsenKonung Gustaf V:s Jubileumsfond
Tillgänglig från: 2017-11-21 Skapad: 2017-11-21 Senast uppdaterad: 2019-03-29Bibliografiskt granskad
La Fleur, L., Falk-Sörqvist, E., Smeds, P., Sundström, M., Mattsson, J. S., Brandén, E., . . . Botling, J. (2017). Mutation Profiling by Targeted Next Generation Sequencing of an Unselected NSCLC Cohort. Journal of Thoracic Oncology, 12(1), S526-S527
Öppna denna publikation i ny flik eller fönster >>Mutation Profiling by Targeted Next Generation Sequencing of an Unselected NSCLC Cohort
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2017 (Engelska)Ingår i: Journal of Thoracic Oncology, ISSN 1556-0864, E-ISSN 1556-1380, Vol. 12, nr 1, s. S526-S527Artikel i tidskrift, Meeting abstract (Övrigt vetenskapligt) Published
Ort, förlag, år, upplaga, sidor
Elsevier, 2017
Nyckelord
Targeted resequencing, Consecutive cohort, NSCLC
Nationell ämneskategori
Cancer och onkologi
Identifikatorer
urn:nbn:se:uu:diva-377745 (URN)10.1016/j.jtho.2016.11.647 (DOI)000413055801149 ()
Tillgänglig från: 2019-02-26 Skapad: 2019-02-26 Senast uppdaterad: 2019-02-26Bibliografiskt granskad
Rao, S., Sigl, V., Wimmer, R. A., Novatchkova, M., Jais, A., Wagner, G., . . . Penninger, J. (2017). RANK rewires energy homeostasis in lung cancer cells and drives primary lung cancer. Genes & Development, 31(20), 2099-2112
Öppna denna publikation i ny flik eller fönster >>RANK rewires energy homeostasis in lung cancer cells and drives primary lung cancer
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2017 (Engelska)Ingår i: Genes & Development, ISSN 0890-9369, E-ISSN 1549-5477, Vol. 31, nr 20, s. 2099-2112Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Lung cancer is the leading cause of cancer deaths. Besides smoking, epidemiological studies have linked female sex hormones to lung cancer in women; however, the underlying mechanisms remain unclear. Here we report that the receptor activator of nuclear factor-kB (RANK), the key regulator of osteoclastogenesis, is frequently expressed in primary lung tumors, an active RANK pathway correlates with decreased survival, and pharmacologic RANK inhibition reduces tumor growth in patient-derived lung cancer xenografts. Clonal genetic inactivation of KRas(G12D) in mouse lung epithelial cells markedly impairs the progression of KRas(G12D)-driven lung cancer, resulting in a significant survival advantage. Mechanistically, RANK rewires energy homeostasis in human and murine lung cancer cells and promotes expansion of lung cancer stem-like cells, which is blocked by inhibiting mitochondrial respiration. Our data also indicate survival differences in KRas(G12D)-driven lung cancer between male and female mice, and we show that female sex hormones can promote lung cancer progression via the RANK pathway. These data uncover a direct role for RANK in lung cancer and may explain why female sex hormones accelerate lung cancer development. Inhibition of RANK using the approved drug denosumab may be a therapeutic drug candidate for primary lung cancer.

Nyckelord
RANK, energy homeostasis, lung cancer, lung cancer stem-like cells
Nationell ämneskategori
Cancer och onkologi Klinisk laboratoriemedicin
Forskningsämne
Patologi
Identifikatorer
urn:nbn:se:uu:diva-342920 (URN)10.1101/gad.304162.117 (DOI)000415923700007 ()29118048 (PubMedID)
Tillgänglig från: 2018-02-26 Skapad: 2018-02-26 Senast uppdaterad: 2019-03-29Bibliografiskt granskad
Grinberg, M., Djureinovic, D., Brunnström, H. R., Mattsson, J. S., Edlund, K., Hengstler, J. G., . . . Micke, P. (2017). Reaching the limits of prognostication in non-small cell lung cancer: an optimized biomarker panel fails to outperform clinical parameters.. Modern Pathology, 30(7), 964-977
Öppna denna publikation i ny flik eller fönster >>Reaching the limits of prognostication in non-small cell lung cancer: an optimized biomarker panel fails to outperform clinical parameters.
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2017 (Engelska)Ingår i: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 30, nr 7, s. 964-977Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Numerous protein biomarkers have been analyzed to improve prognostication in non-small cell lung cancer, but have not yet demonstrated sufficient value to be introduced into clinical practice. Here, we aimed to develop and validate a prognostic model for surgically resected non-small cell lung cancer. A biomarker panel was selected based on (1) prognostic association in published literature, (2) prognostic association in gene expression data sets, (3) availability of reliable antibodies, and (4) representation of diverse biological processes. The five selected proteins (MKI67, EZH2, SLC2A1, CADM1, and NKX2-1 alias TTF1) were analyzed by immunohistochemistry on tissue microarrays including tissue from 326 non-small cell lung cancer patients. One score was obtained for each tumor and each protein. The scores were combined, with or without the inclusion of clinical parameters, and the best prognostic model was defined according to the corresponding concordance index (C-index). The best-performing model was subsequently validated in an independent cohort consisting of tissue from 345 non-small cell lung cancer patients. The model based only on protein expression did not perform better compared to clinicopathological parameters, whereas combining protein expression with clinicopathological data resulted in a slightly better prognostic performance (C-index: all non-small cell lung cancer 0.63 vs 0.64; adenocarcinoma: 0.66 vs 0.70, squamous cell carcinoma: 0.57 vs 0.56). However, this modest effect did not translate into a significantly improved accuracy of survival prediction. The combination of a prognostic biomarker panel with clinicopathological parameters did not improve survival prediction in non-small cell lung cancer, questioning the potential of immunohistochemistry-based assessment of protein biomarkers for prognostication in clinical practice.Modern Pathology advance online publication, 10 March 2017; doi:10.1038/modpathol.2017.14.

Nationell ämneskategori
Cancer och onkologi Medicinsk genetik Klinisk laboratoriemedicin
Forskningsämne
Patologi
Identifikatorer
urn:nbn:se:uu:diva-318128 (URN)10.1038/modpathol.2017.14 (DOI)000404718100006 ()28281552 (PubMedID)
Forskningsfinansiär
Cancerfonden
Tillgänglig från: 2017-03-23 Skapad: 2017-03-23 Senast uppdaterad: 2019-03-29Bibliografiskt granskad
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