Change search
Link to record
Permanent link

Direct link
BETA
Alternative names
Publications (10 of 430) Show all publications
Turanli, B., Grotli, M., Boren, J., Nielsen, J., Uhlén, M., Arga, K. Y. & Mardinoglu, A. (2018). Drug Repositioning for Effective Prostate Cancer Treatment. Frontiers in Physiology, 9, Article ID 500.
Open this publication in new window or tab >>Drug Repositioning for Effective Prostate Cancer Treatment
Show others...
2018 (English)In: Frontiers in Physiology, ISSN 1664-042X, E-ISSN 1664-042X, Vol. 9, article id 500Article, review/survey (Refereed) Published
Abstract [en]

Drug repositioning has gained attention from both academia and pharmaceutical companies as an auxiliary process to conventional drug discovery. Chemotherapeutic agents have notorious adverse effects that drastically reduce the life quality of cancer patients so drug repositioning is a promising strategy to identify non-cancer drugs which have anti-cancer activity as well as tolerable adverse effects for human health. There are various strategies for discovery and validation of repurposed drugs. In this review, 25 repurposed drug candidates are presented as result of different strategies, 15 of which are already under clinical investigation for treatment of prostate cancer (PCa). To date, zoledronic acid is the only repurposed, clinically used, and approved non-cancer drug for PCa. Anti-cancer activities of existing drugs presented in this review cover diverse and also known mechanisms such as inhibition of mTOR and VEGFR2 signaling, inhibition of PI3K/Akt signaling, COX and selective COX-2 inhibition, NF-kappa B inhibition, Wnt/beta - Catenin pathway inhibition, DNMT1 inhibition, and GSK-3 beta inhibition. In addition to monotherapy option, combination therapy with current anti-cancer drugs may also increase drug efficacy and reduce adverse effects. Thus, drug repositioning may become a key approach for drug discovery in terms of time- and cost-efficiency comparing to conventional drug discovery and development process.

Place, publisher, year, edition, pages
Frontiers Media S.A., 2018
Keywords
prostate cancer, drug repositioning, non-cancer therapeutics, repurposing, approved drugs
National Category
Physiology
Identifiers
urn:nbn:se:kth:diva-229015 (URN)10.3389/fphys.2018.00500 (DOI)000432407100001 ()2-s2.0-85047004631 (Scopus ID)
Funder
Science for Life Laboratory - a national resource center for high-throughput molecular bioscienceKnut and Alice Wallenberg Foundation
Note

QC 20180531

Available from: 2018-05-31 Created: 2018-05-31 Last updated: 2018-05-31Bibliographically approved
Zieba, A., Ponten, F., Uhlén, M. & Landegren, U. (2018). In situ protein detection with enhanced specificity using DNA-conjugated antibodies and proximity ligation. Modern Pathology, 31(2), 253-263
Open this publication in new window or tab >>In situ protein detection with enhanced specificity using DNA-conjugated antibodies and proximity ligation
2018 (English)In: Modern Pathology, ISSN 0893-3952, E-ISSN 1530-0285, Vol. 31, no 2, p. 253-263Article in journal (Refereed) Published
Abstract [en]

Antibodies are important tools in anatomical pathology and research, but the quality of in situ protein detection by immunohistochemistry greatly depends on the choice of antibodies and the abundance of the targeted proteins. Many antibodies used in scientific research do not meet requirements for specificity and sensitivity. Accordingly, methods that improve antibody performance and produce quantitative data can greatly advance both scientific investigations and clinical diagnostics based on protein expression and in situ localization. We demonstrate here protocols for antibody labeling that allow specific protein detection in tissues via bright-field in situ proximity ligation assays, where each protein molecule must be recognized by two antibodies. We further demonstrate that single polyclonal antibodies or purified serum preparations can be used for these dual recognition assays. The requirement for protein recognition by pairs of antibody conjugates can significantly improve specificity of protein detection over single-binder assays.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018
Keywords
antibody conjugate, APEX 1 protein, calvasculin, DNA conjugated antibody, immunoglobulin G antibody, polyclonal antibody, protein, protein A, protein G, rabbit antiserum, reagent, trefoil factor 1, unclassified drug, animal tissue, antibody affinity, antibody labeling, antibody specificity, Article, assay, click chemistry, controlled study, DNA strand, genetic transcription, immunohistochemistry, in situ proximity ligation assay, limit of detection, mRNA expression level, nonhuman, priority journal, protein analysis, protein expression, protein expression level, protein purification, tissue microarray, tissue section
National Category
Biological Sciences
Identifiers
urn:nbn:se:kth:diva-227448 (URN)10.1038/modpathol.2017.102 (DOI)000424761400003 ()2-s2.0-85041805855 (Scopus ID)
Note

Export Date: 9 May 2018; Article; CODEN: MODPE; Correspondence Address: Landegren, U.; Department of Immunology, Genetics and Pathology, Science for Life Laboratory, BMC, Uppsala University, Husargatan 3, Sweden; email: Ulf.Landegren@igp.uu.se; Funding details: VINNOVA; Funding details: 222635; Funding details: 241481; Funding details: NCI, National Cancer Institute; Funding details: #2008:0143, Knut och Alice Wallenbergs Stiftelse; Funding details: FP5, Fifth Framework Programme; Funding details: FP/2007– 2013, FP7, Seventh Framework Programme; Funding details: ERC, European Research Council; Funding details: TRC, The Research Council; Funding details: 294409, ERC, European Research Council; Funding details: IngaBritt och Arne Lundbergs Forskningsstiftelse; Funding details: Uppsala Universitet; Funding text: This work was supported by the Knut and Alice Wallenberg Foundation (#2008:0143), the European Community's 7th Framework Program (FP7/2007–2013) under grant agreement n° 222635 (AffinityProteome) 241481 (Affinomics), The Swedish Research Council, Swedish Governmental Agency for Innovation Systems, IngaBritt and Arne Lundberg Foundation, the European Research Council under the European Union's Seventh Framework Programme (FP/2007– 2013) / ERC Grant Agreement n. 294409 (ProteinSeq), and Uppsala University. UL holds stock in Olink, having rights to the in situ proximity ligation assay technology. We would also like to thank Tara Hiltke at the National Cancer Institute for providing mAbs for in situ proximity ligation assay experiments. QC 20180528

Available from: 2018-05-28 Created: 2018-05-28 Last updated: 2018-05-28Bibliographically approved
Persson, M., Zandian, A., Wingard, L., Nilsson, H., Sjostedt, E., Johansson, D., . . . Nilsson, P. (2018). Searching for Novel Autoantibodies with Clinical Relevance in Psychiatric Disorders. Paper presented at 6th Biennial Conference of the Schizophrenia-International-Research-Society (SIRS), APR 04-08, 2018, Florence, Italy. Schizophrenia Bulletin, 44, S120-S121
Open this publication in new window or tab >>Searching for Novel Autoantibodies with Clinical Relevance in Psychiatric Disorders
Show others...
2018 (English)In: Schizophrenia Bulletin, ISSN 0586-7614, E-ISSN 1745-1701, Vol. 44, p. S120-S121Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
Oxford University Press, 2018
National Category
Biochemistry and Molecular Biology
Identifiers
urn:nbn:se:kth:diva-226780 (URN)000429541800296 ()
Conference
6th Biennial Conference of the Schizophrenia-International-Research-Society (SIRS), APR 04-08, 2018, Florence, Italy
Funder
EU, European Research Council, 670821
Note

QC 20180522

Available from: 2018-05-22 Created: 2018-05-22 Last updated: 2018-05-22Bibliographically approved
Mardinoglu, A., Boren, J., Smith, U., Uhlén, M. & Nielsen, J. (2018). Systems biology in hepatology: approaches and applications. Nature Reviews. Gastroenterology & Hepatology, 15(6), 365-377
Open this publication in new window or tab >>Systems biology in hepatology: approaches and applications
Show others...
2018 (English)In: Nature Reviews. Gastroenterology & Hepatology, ISSN 1759-5045, E-ISSN 1759-5053, Vol. 15, no 6, p. 365-377Article, review/survey (Refereed) Published
Abstract [en]

Detailed insights into the biological functions of the liver and an understanding of its crosstalk with other human tissues and the gut microbiota can be used to develop novel strategies for the prevention and treatment of liver-associated diseases, including fatty liver disease, cirrhosis, hepatocellular carcinoma and type 2 diabetes mellitus. Biological network models, including metabolic, transcriptional regulatory, protein-protein interaction, signalling and co-expression networks, can provide a scaffold for studying the biological pathways operating in the liver in connection with disease development in a systematic manner. Here, we review studies in which biological network models were used to integrate multiomics data to advance our understanding of the pathophysiological responses of complex liver diseases. We also discuss how this mechanistic approach can contribute to the discovery of potential biomarkers and novel drug targets, which might lead to the design of targeted and improved treatment strategies. Finally, we present a roadmap for the successful integration of models of the liver and other human tissues with the gut microbiota to simulate whole-body metabolic functions in health and disease.

Place, publisher, year, edition, pages
Nature Publishing Group, 2018
National Category
Gastroenterology and Hepatology
Identifiers
urn:nbn:se:kth:diva-230482 (URN)10.1038/s41575-018-0007-8 (DOI)000433166800010 ()29686404 (PubMedID)2-s2.0-85045834478 (Scopus ID)
Funder
Knut and Alice Wallenberg FoundationScience for Life Laboratory - a national resource center for high-throughput molecular bioscience
Note

QC 20180613

Available from: 2018-06-13 Created: 2018-06-13 Last updated: 2018-06-13Bibliographically approved
Mardinoglu, A., Boren, J., Smith, U., Uhlén, M. & Nielsen, J. (2018). Systems biology in hepatology: approaches and applications. Nature Reviews. Gastroenterology & Hepatology, 15(6), 365-377
Open this publication in new window or tab >>Systems biology in hepatology: approaches and applications
Show others...
2018 (English)In: Nature Reviews. Gastroenterology & Hepatology, ISSN 1759-5045, E-ISSN 1759-5053, Vol. 15, no 6, p. 365-377Article, review/survey (Refereed) Published
Abstract [en]

Detailed insights into the biological functions of the liver and an understanding of its crosstalk with other human tissues and the gut microbiota can be used to develop novel strategies for the prevention and treatment of liver-associated diseases, including fatty liver disease, cirrhosis, hepatocellular carcinoma and type 2 diabetes mellitus. Biological network models, including metabolic, transcriptional regulatory, protein-protein interaction, signalling and co-expression networks, can provide a scaffold for studying the biological pathways operating in the liver in connection with disease development in a systematic manner. Here, we review studies in which biological network models were used to integrate multiomics data to advance our understanding of the pathophysiological responses of complex liver diseases. We also discuss how this mechanistic approach can contribute to the discovery of potential biomarkers and novel drug targets, which might lead to the design of targeted and improved treatment strategies. Finally, we present a roadmap for the successful integration of models of the liver and other human tissues with the gut microbiota to simulate whole-body metabolic functions in health and disease.

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2018
National Category
Bioinformatics and Systems Biology
Identifiers
urn:nbn:se:kth:diva-230414 (URN)10.1038/s41575-018-0007-8 (DOI)000433166800010 ()29686404 (PubMedID)2-s2.0-85045834478 (Scopus ID)
Funder
Science for Life Laboratory - a national resource center for high-throughput molecular bioscience
Note

QC 20180619

Available from: 2018-06-19 Created: 2018-06-19 Last updated: 2018-06-20Bibliographically approved
Azimi, A., Caramuta, S., Seashore-Ludlow, B., Boström, J., Robinson, J. L., Edfors, F., . . . Maddalo, G. (2018). Targeting CDK2 overcomes melanoma resistance against BRAF and Hsp90 inhibitors. Molecular Systems Biology, 14(3), Article ID e7858.
Open this publication in new window or tab >>Targeting CDK2 overcomes melanoma resistance against BRAF and Hsp90 inhibitors
Show others...
2018 (English)In: Molecular Systems Biology, ISSN 1744-4292, E-ISSN 1744-4292, Vol. 14, no 3, article id e7858Article in journal (Refereed) Published
Abstract [en]

Novel therapies are undergoing clinical trials, for example, the Hsp90 inhibitor, XL888, in combination with BRAF inhibitors for the treatment of therapy-resistant melanomas. Unfortunately, our data show that this combination elicits a heterogeneous response in a panel of melanoma cell lines including PDX-derived models. We sought to understand the mechanisms underlying the differential responses and suggest a patient stratification strategy. Thermal proteome profiling (TPP) identified the protein targets of XL888 in a pair of sensitive and unresponsive cell lines. Unbiased proteomics and phosphoproteomics analyses identified CDK2 as a driver of resistance to both BRAF and Hsp90 inhibitors and its expression is regulated by the transcription factor MITF upon XL888 treatment. The CDK2 inhibitor, dinaciclib, attenuated resistance to both classes of inhibitors and combinations thereof. Notably, we found that MITF expression correlates with CDK2 upregulation in patients; thus, dinaciclib would warrant consideration for treatment of patients unresponsive to BRAF-MEK and/or Hsp90 inhibitors and/or harboring MITF amplification/overexpression. 

Place, publisher, year, edition, pages
Blackwell Publishing Ltd, 2018
Keywords
CDK2, Hsp90 and BRAF inhibitors, melanoma, MITF, proteomics
National Category
Medical Biotechnology
Identifiers
urn:nbn:se:kth:diva-227407 (URN)10.15252/msb.20177858 (DOI)000429006500002 ()2-s2.0-85044744573 (Scopus ID)
Note

Export Date: 9 May 2018; Article; Correspondence Address: Maddalo, G.; Science for Life Laboratory, School of Biotechnology, KTH Royal Institute of TechnologySweden; email: gianluca.maddalo@scilifelab.se; Funding details: IHC, Idaho Humanities Council; Funding details: 154202, Cancerfonden; Funding details: 5310-7132, O. E. och Edla Johanssons Vetenskapliga Stiftelse; Funding details: MTA, Mount Allison University; Funding text: We acknowledge Prof. Sonia Lain and Prof. David Lane and their groups for technical support and for granting us permission to access their Orbitrap Fusion. The cell line pairs M026.X1.CL and M026R.X1.CL, and M029.X1.CL and M029.R.X1.CL have been used according to the Material Transfer Agreement (MTA) for academic institutions V01 13 and V08 16, respectively. GM has been awarded grants from: O. E. och Edla Johanssons foundation (5310-7132); Swedish Cancer Society (Radiumhemmets; 154202); and Lars Hiertas Minne. The authors acknowledge the entire staff of the Protein Atlas Project for the IHC images. We acknowledge Prof. Janne Lehtiö and Rozbeh Jafari for support with TPP. QC 20180529

Available from: 2018-05-29 Created: 2018-05-29 Last updated: 2018-05-29Bibliographically approved
Lee, S., Zhang, C., Arif, M., Liu, Z., Benfeitas, R., Bidkhori, G., . . . Mardinoglu, A. (2018). TCSBN: A database of tissue and cancer specific biological networks. Nucleic Acids Research, 46(D1), D595-D600
Open this publication in new window or tab >>TCSBN: A database of tissue and cancer specific biological networks
Show others...
2018 (English)In: Nucleic Acids Research, ISSN 0305-1048, E-ISSN 1362-4962, Vol. 46, no D1, p. D595-D600Article in journal (Refereed) Published
Abstract [en]

Biological networks provide new opportunities for understanding the cellular biology in both health and disease states. We generated tissue specific integrated networks (INs) for liver, muscle and adipose tissues by integrating metabolic, regulatory and protein-protein interaction networks. We also generated human co-expression networks (CNs) for 46 normal tissues and 17 cancers to explore the functional relationships between genes as well as their relationships with biological functions, and investigate the overlap between functional and physical interactions provided by CNs and INs, respectively. These networks can be employed in the analysis of omics data, provide detailed insight into disease mechanisms by identifying the key biological components and eventually can be used in the development of efficient treatment strategies. Moreover, comparative analysis of the networks may allow for the identification of tissue-specific targets that can be used in the development of drugs with the minimum toxic effect to other human tissues. These context-specific INs and CNs are presented in an interactive website http://inetmodels.com without any limitation. 

Place, publisher, year, edition, pages
Oxford University Press, 2018
Keywords
fatty acid synthase, lipid, adipose tissue, Article, cancer research, case study, coexpression network, comparative study, data base, drug targeting, gene, gene expression, human, integrated network, lipogenesis, liquid chromatography-mass spectrometry, liver tissue, muscle tissue, omics, priority journal, protein protein interaction, protein protein interaction network, RNA sequence, tissue cancer specific biological network, tissue specificity
National Category
Biological Sciences
Identifiers
urn:nbn:se:kth:diva-223201 (URN)10.1093/nar/gkx994 (DOI)000419550700090 ()2-s2.0-85040915985 (Scopus ID)
Funder
Knut and Alice Wallenberg FoundationScience for Life Laboratory - a national resource center for high-throughput molecular bioscience
Note

Export Date: 13 February 2018; Article; CODEN: NARHA; Correspondence Address: Mardinoglu, A.; Science for Life Laboratory, KTH-Royal Institute of TechnologySweden; email: adilm@scilifelab.se QC 20180228

Available from: 2018-02-28 Created: 2018-02-28 Last updated: 2018-02-28Bibliographically approved
Danielsson, F., Fasterius, E., Sullivan, D., Hases, L., Sanli, K., Zhang, C., . . . Lundberg, E. (2018). Transcriptome profiling of the interconnection of pathways involved in malignant transformation and response to hypoxia. OncoTarget, 9(28), 19730-19744
Open this publication in new window or tab >>Transcriptome profiling of the interconnection of pathways involved in malignant transformation and response to hypoxia
Show others...
2018 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 9, no 28, p. 19730-19744Article in journal (Refereed) Published
Abstract [en]

In tumor tissues, hypoxia is a commonly observed feature resulting from rapidly proliferating cancer cells outgrowing their surrounding vasculature network. Transformed cancer cells are known to exhibit phenotypic alterations, enabling continuous proliferation despite a limited oxygen supply. The four-step isogenic BJ cell model enables studies of defined steps of tumorigenesis: the normal, immortalized, transformed, and metastasizing stages. By transcriptome profiling under atmospheric and moderate hypoxic (3% O2) conditions, we observed that despite being highly similar, the four cell lines of the BJ model responded strikingly different to hypoxia. Besides corroborating many of the known responses to hypoxia, we demonstrate that the transcriptome adaptation to moderate hypoxia resembles the process of malignant transformation. The transformed cells displayed a distinct capability of metabolic switching, reflected in reversed gene expression patterns for several genes involved in oxidative phosphorylation and glycolytic pathways. By profiling the stage-specific responses to hypoxia, we identified ASS1 as a potential prognostic marker in hypoxic tumors. This study demonstrates the usefulness of the BJ cell model for highlighting the interconnection of pathways involved in malignant transformation and hypoxic response.

Place, publisher, year, edition, pages
Impact Journals LLC, 2018
Keywords
Hypoxia, Malignant transformation, Transcriptomics
National Category
Cell and Molecular Biology
Identifiers
urn:nbn:se:kth:diva-227616 (URN)10.18632/oncotarget.24808 (DOI)2-s2.0-85045315705 (Scopus ID)
Funder
Science for Life Laboratory - a national resource center for high-throughput molecular bioscience
Note

QC 20180522

Available from: 2018-05-22 Created: 2018-05-22 Last updated: 2018-05-22Bibliographically approved
Karnevi, E., Dror, L. B., Mardinoglu, A., Elebro, J., Heby, M., Olofsson, S.-E. -., . . . Jirström, K. (2018). Translational study reveals a two-faced role of RBM3 in pancreatic cancer and suggests its potential value as a biomarker for improved patient stratification. OncoTarget, 9(5), 6188-6200
Open this publication in new window or tab >>Translational study reveals a two-faced role of RBM3 in pancreatic cancer and suggests its potential value as a biomarker for improved patient stratification
Show others...
2018 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 9, no 5, p. 6188-6200Article in journal (Refereed) Published
Abstract [en]

Periampullary adenocarcinoma, including pancreatic cancer, is a heterogeneous group of tumors with dismal prognosis, partially due to lack of reliable targetable and predictive biomarkers. RNA-binding motif protein 3 (RBM3) has previously been shown to be an independent prognostic and predictive biomarker in several types of cancer. Herein, we examined the prognostic value of RBM3 in periampullary adenocarcinoma, as well as the effects following RBM3 suppression in pancreatic cancer cells in vitro. RBM3 mRNA levels were examined in 176 pancreatic cancer patients from The Cancer Genome Atlas. Immunohistochemical expression of RBM3 was analyzed in tissue microarrays with primary tumors and paired lymph node metastases from 175 consecutive patients with resected periampullary adenocarcinoma. Pancreatic cancer cells were transfected with anti-RBM3 siRNA in vitro and the influence on cell viability following chemotherapy, transwell migration and invasion was assessed. The results demonstrated that high mRNA-levels of RBM3 were significantly associated with a reduced overall survival (p = 0.026). RBM3 protein expression was significantly higher in lymph node metastases than in primary tumors (p = 0.005). High RBM3 protein expression was an independent predictive factor for the effect of adjuvant chemotherapy and an independent negative prognostic factor in untreated patients (p for interaction = 0.003). After siRNA suppression of RBM3 in vitro, pancreatic cancer cells displayed reduced migration and invasion compared to control, as well as a significantly increased resistance to chemotherapy. In conclusion, the strong indication of a positive response predictive effect of RBM3 expression in pancreatic cancer may be highly relevant in the clinical setting and merits further validation.

Place, publisher, year, edition, pages
Impact Journals LLC, 2018
Keywords
Pancreatic cancer, Periampullary cancer, Prediction, Prognosis, RBM3, antineoplastic agent, cyclooxygenase 2, gemcitabine, interleukin 8, messenger RNA, RNA binding motif protein 3, RNA binding protein, small interfering RNA, unclassified drug, adult, aged, Article, cancer adjuvant therapy, cancer prognosis, cell migration, cell motility, cell viability, cohort analysis, controlled study, drug resistance, drug sensitivity, female, fetus, human, human cell, human tissue, in vitro study, lymph node metastasis, major clinical study, male, overall survival, pancreas cancer, pancreatic cancer cell line, pancreaticoduodenectomy, periampullary adenocarcinoma, predictive value, protein expression, protein function, recurrence free survival, retrospective study, translational research, tumor invasion
National Category
Clinical Medicine
Identifiers
urn:nbn:se:kth:diva-223186 (URN)10.18632/oncotarget.23486 (DOI)2-s2.0-85040697313 (Scopus ID)
Note

Export Date: 13 February 2018; Article; Correspondence Address: Jirström, K.; Division of Oncology and Pathology, Department of Clinical Sciences, Lund University, Skåne University HospitalSweden; email: karin.jirstrom@med.lu.se. QC 20180228

Available from: 2018-02-28 Created: 2018-02-28 Last updated: 2018-02-28Bibliographically approved
Fasterius, E., Raso, C., Kennedy, S., Rauch, N., Lundin, P., Kolch, W., . . . Al-Khalili Szigyarto, C. (2017). A novel RNA sequencing data analysis method for cell line authentication. PLoS ONE, 12(2), Article ID e0171435.
Open this publication in new window or tab >>A novel RNA sequencing data analysis method for cell line authentication
Show others...
2017 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 12, no 2, article id e0171435Article in journal (Refereed) Published
Abstract [en]

We have developed a novel analysis method that can interrogate the authenticity of biological samples used for generation of transcriptome profiles in public data repositories. The method uses RNA sequencing information to reveal mutations in expressed transcripts and subsequently confirms the identity of analysed cells by comparison with publicly available cell-specific mutational profiles. Cell lines constitute key model systems widely used within cancer research, but their identity needs to be confirmed in order to minimise the influence of cell contaminations and genetic drift on the analysis. Using both public and novel data, we demonstrate the use of RNA-sequencing data analysis for cell line authentication by examining the validity of COLO205, DLD1, HCT15, HCT116, HKE3, HT29 and RKO colorectal cancer cell lines. We successfully authenticate the studied cell lines and validate previous reports indicating that DLD1 and HCT15 are synonymous. We also show that the analysed HKE3 cells harbour an unexpected KRAS-G13D mutation and confirm that this cell line is a genuine KRAS dosage mutant, rather than a true isogenic derivative of HCT116 expressing only the wild type KRAS. This authentication method could be used to revisit the numerous cell line based RNA sequencing experiments available in public data repositories, analyse new experiments where whole genome sequencing is not available, as well as facilitate comparisons of data from different experiments, platforms and laboratories.

Place, publisher, year, edition, pages
PUBLIC LIBRARY SCIENCE, 2017
National Category
Biological Sciences
Identifiers
urn:nbn:se:kth:diva-204084 (URN)10.1371/journal.pone.0171435 (DOI)000394423800024 ()28192450 (PubMedID)2-s2.0-85012231859 (Scopus ID)
Note

QC 20170329

Available from: 2017-03-29 Created: 2017-03-29 Last updated: 2017-11-29Bibliographically approved
Organisations
Identifiers
ORCID iD: ORCID iD iconorcid.org/0000-0001-8993-048X

Search in DiVA

Show all publications