ENG  Vol.5 No.10 B , October 2013
Integrative Self-Organizing Map—A Mean Pattern Model

We propose an integrative self-organizing map (iSOM) for exploring differential expression patterns across multiple microarray experiments. The algorithm is based on the assumption that observed differential expressions are random samples of a mean pattern model which is unknowna priori. The learning mechanism of iSOM is similar to the conventional SOM. The mean pattern model which underlies the proposed iSOM models mean differential expressions using a one-dimension of mean differential expressions for the mean differential expressions. The feature map of an iSOM model can be used to reveal correlation between multiple medically/biologically related disease types or multiple platform experiments for one disease. We illustrate applications of iSOM using simulated data and real data.

Cite this paper: Yang, Z. and Yang, Z. (2013) Integrative Self-Organizing Map—A Mean Pattern Model. Engineering, 5, 244-249. doi: 10.4236/eng.2013.510B050.

[1]   T. Kohonen, “Self-Organizing Maps,” Springer, Berlin, 2001.

[2]   J. Yao, Q. Zhao, Y. Yuan, L. Zhang, X. Liu, W. K. Yung and J. N. Weinstein, “Identification of Common Prognostic Gene Expression Signatures with Biological Meanings From Microarray Gene Expression Datasets,” PLoS One, Vol. 7, 2012, Article ID: e45894.

[3]   Y. Park, E. S. Park, S. B. Kim, S. C. Kim, B. H. Sohn, I. S. Chu, W. Jeong, G. B. Mills, L. A. Byers and J. S. Lee, “Development and Validation of a Prognostic Gene-Expression Signature for Lung Adenocarcinoma,” PLoS One, Vol. 7, 2012, Article ID: e44225.

[4]   A. Zaravinos, G. I. Lambrou, D. Volanis, D. Delakas and D. A. Spandidos, “Spotlight on Differentially Expressed Genes in Urinary Bladder Cancer,” PLoS One, No. 6, 2011, Article ID: e18255.

[5]   M. LaBonte, P. M Wilson, W. Fazzone, S. Groshen, H. J. Lenz and R. D. Ladner, “DNA Microarray Profiling of Genes Differentially Regulated by the Histone Deacetylase Inhibitors Vorinostat and LBH589 in Colon Cancer Cell Lines,” BMC Med Genomics, Vol. 2, 2009, p. 67.

[6]   M. Howlett, A. S. Giraud, H. Lescesen, C. B. Jackson, A. Kalantzis, I. R. Van Driel, L. Robb, M. Van der Hoek, M. Ernst, T. Minamoto, A. Boussioutas, H. Oshima, M. Oshima and L. M. Judd, “The Interleukin-6 Family Cytokine Interleukin-11 Regulates Homeostatic Epithelial Cell Turnover and Promotes Gastric Tumor Development,” Gas-troenterology, Vol. 136, 2009, pp. 967-977.

[7]   A. Alaiya, M. Al-Mohanna, M. Aslam, Z. Shinwari, L. Al-Mansouri, M. Al-Rodayan, M. Al-Eid, I. Ahmad, K. Hanash, A. Tulbah, A. Mahfooz and C. Adra, “Proteomics-Based Signature for Human Benign Prostate Hyperplasia and Prostate Adenocarcinoma,” International Journal of Oncology, Vol. 38, 2011, pp. 1047-1057.

[8]   L. Cheng, W. Lu, B. Kulkarni, T. Pejovic, X. Yan, J. H. Chiang, L. Hood, K. Odunsi and B. Lin, “Analysis of Chemotherapy Response Programs in Ovarian Cancers by the Next-Generation Sequencing Technologies,” Gyneco-logic Oncology, Vol. 117, 2010, pp. 159-169.

[9]   A. Planche, M. Bacac, P. Provero, C. Fusco, M. Delorenzi, J. C Stehle and I. Stamenkovic, “Identification of Prognostic Molecular Features in the Reactive Stroma of Human Breast and Prostate Cancer,” PLoS One, Vol. 6, 2011, Article ID: e18640.

[10]   A. Collura, L. Marisa, D. Trojan, O. Buhard, A. Lagrange, A. Saget, M. Bombled, P. Méchighel, M. Ayadi, M. Muleris, A. de Reynies, M. Svrcek, J. F. Fléjou, J. C. Florent, F. Mahuteau-Betzer, A. M. Faussat and A. Duval, “Extensive Characterization of Sphere Models Es-tablished From Colorectal Cancer Cell Lines,” Cellular and Molecular Life Sciences, 2012, in Press.

[11]   M. Stevenson, W. Mostertz, C. Acharya, W. Kim, K. Walters, W. Barry, K. Higgins, S. A. Tuchman, J. Crawford, G. Vlahovic, N. Ready, M. Onaitis and A. Potti, “Characterizing the Clinical Relevance of an Embryonic Stem Cell Phenotype in Lung Adenocarcinoma,” Clinical Cancer Research, Vol. 15, 2009, pp. 7553-7561.

[12]   E. Markert, A. J. Levine and A. Vazquez, “Proliferation and Tissue Remodeling in Cancer: The Hallmarks Revisited,” Cell Death & Disease, Vol. 3, 2012, p. 3397.

[13]   N. Fankhauser, I. Cima, P. Wild and W. Krek, “Identification of a Gene Expression Signature Common to Distinct Cancer Pathways,” Cancer Information, Vol. 11, 2012, pp. 139-146.

[14]   M. Daves, S. G. Hilsenbeck, C. C. Lau and T. K. Man, “Meta-Analysis of Multiple Microarray Datasets Reveals a Common Gene Signature of Metastasis in Solid Tu-mors,” BMC Med Genomics, Vol. 4, 2011, p. 56.

[15]   S. De and F. Michor, “DNA Secondary Structures and Epigenetic Determinants of Cancer Genome Evolution,” Nature Structural & Molecular Biology, Vol. 18, 2011, pp. 950-955.

[16]   F. Buffa, A. L. Harris, C. M. West and C. J. Miller, “Large Meta-Analysis of Multiple Cancers Reveals a Common, Compact and Highly Prognostic Hypoxia Metagene,” British Journal of Cancer, Vol. 102, 2010, pp. 428-435.

[17]   N. Slavov and K. A. Dawson, “Correlation Signature of the Macro-scopic States of the Gene Regulatory Network in Cancer,” Proceedings of the National Academy of Sciences, Vol. 106, 2009, pp. 4079-4084.

[18]   I. Wang, B. Zhang, X. Yang, J. Zhu, S. Stepaniants, C. Zhang, Q. Meng, M. Peters, Y. He, C. Ni, D. Slipetz, M. A. Crackower, H. Houshyar, C. M. Tan, E. Asante-Appiah, G. O’Neill, M. J. Luo, R. Thieringer, J. Yuan, C. S. Chiu, P. Y. Lum, J. Lamb, Y. Boie, H. A. Wilkinson, E. E. Schadt, H. Dai and C. Roberts, “Systems Analysis of Eleven Rodent Disease Models Reveals an Inflammatome Signature and Key Drivers,” Molecular Systems Biology, Vol. 8, 2012, p. 594.

[19]   S. Michiels, S. Koscielny and C. Hill, “Prediction of cancer Outcome with Microarrays: A Multiple Random Validation Strategy,” Lancet, Vol. 365, 2005, pp. 488-492, 2005.

[20]   E. Segal, N. Friedman, D. Koller and A. Regev, “A Module Map Showing Conditional Activity of Expression Modules in Cancer,” Nature Genetics, Vol. 36, 2004, pp. 1090-1098.

[21]   P. Ta-mayo, D. Scanfeld, B. L. Ebert, M. A. Gillette, C. W. Roberts and J. P. Mesirov, “Metagene Projection for Cross-Platform, Cross-Species Characterization of Global Transcriptional States,” Proceedings of the National Academy of Sciences, Vol. 104, 2007, pp. 5959-5964.

[22]   K. Devarajan, “Nonnegative Matrix Factorization: An Analytic and Interpretive Tool in Computational Biology,” PLOS Computational Biology, Vol. 4, 2008, Article ID: e1000029.

[23]   B. Efron, R. Tibshirani, J. D. Storey and V. Tusher, “Empirical Bayes Analysis of a Microarray Experiment,” Journal of American Statistical Association, Vol. 96, 2001, pp. 1151-1160.

[24]   H. Gautrey and A. J. Tyson-Capper, “Regulation of Mcl-1 by SRSF1 and SRSF5 in Cancer Cells,” PLoS One, Vol. 7, 2012, Article ID: e51497.

[25]   ú. Muñoz, J. E. Puche, R. Hannivoort, U. E. Lang, M. Cohen-Naftaly and S. L. Friedman, “Hepatocyte Growth Factor Enhances Alternative Splicing of the Kruppel-Like Factor 6 (KLF6) Tumor Suppressor to Promote Growth through SRSF1,” Molecular Cancer Research, Vol. 10, 2012, pp. 1216-1227.

[26]   M. Kulak, A. R. Cyr, G. W. Woodfield, M. Bogachek, P. M. Spanheimer, T. Li, D. H. Price, F. E. Domann and R. J. Weigel, “Transcriptional Regulation of the GPX1 Gene by TFAP2C and Aberrant CpG Methylation in Human Breast Cancer,” Oncogene, 2013, in Press.

[27]   N. Blum, K. Mueller, D. Lippmann, C. C. Metges, T. Linn, J. Pallauf and A. S. Mueller, “Feeding of Selenium Alone or in Combination with Glucoraphanin Differentially Affects Intestinal and Hepatic Antioxidant and Phase II Enzymes in Growing rats,” Biological Trace Element Research, Vol. 151, 2013, pp. 384-399.

[28]   T. Reddy, C. Li, X. Guo, H. K. Myrvang, P. M. Fischer and L. V. Dekker, “Design, Synthesis, and Structure-Activity Relationship Exploration of 1-Substituted 4-Aroyl-3-hydroxy-5-phenyl-1H-pyrrol-2(5H)-One Analogues as Inhibitors of the Annexin A2-S100A10 Protein Interaction,” Journal of Medicinal Chemistry, Vol. 54, 2011, pp. 2080-2094.

[29]   Y. Tan, S. Y. Ma, F. Q. Wang, H. P. Meng, C. Mei, A. Liu and H. R. Wu, “Proteomic-Based Analysis for Identification of Potential Serum Biomarkers in Gallbladder Cancer,” Oncology Reports, Vol. 26, 2011, pp. 853-859.

[30]   V. Perissi, C. Scafoglio, J. Zhang, K. A. Ohgi, D. W. Rose, C. K. Glass and M. G. Rosenfeld, “TBL1 and TBLR1 Phosphorylation on Regulated Gene Promoters Overcomes Dual CtBP and NCoR/SMRT Transcriptional Repression Checkpoints,” Molecular Cell, Vol. 29, 2008, pp. 755-766.

[31]   A. Qattan, M. Radulovic, M. Crawford and J. Godovac-Zimmermann, “Spatial Distribution of Cellular Function: The Partitioning of Proteins between Mito-chondria and the Nucleus in MCF7 Breast Cancer Cells,” Journal of Proteome Research, Vol. 11, 2012, pp. 6080-6101.

[32]   T. Neill, H. Painter, S. Buraschi, R. T. Owens, M. P. Lisanti, L. Schaefer and R. V. Iozzo, “Decorin Antagonizes the Angiogenic Network: Con-current Inhibition of Met, Hypoxia Inducible Factor 1α, Vascular Endothelial Growth Factor A, and Induction of Thrombospondin-1 and TIMP3,” The Journal of Biological Chemistry, Vol. 287, 2012, pp. 5492-5506.

[33]   S. Turner, D. Mangnall, N. C. Bird, R. A. Bunning and M. E. Blair-Zajdel, “Expression of ADAMTS-1, ADAMTS-4, ADAMTS-5 and TIMP3 by Hepatocellular Carcinoma Cell Lines,” International Journal of Oncology, Vol. 41, 2012, pp. 1043-1049.

[34]   W. Cui, S. Y. Li, J. F. Du, Z. M. Zhu and P. An, “Silencing Phospholipid Scramblase 1 Expression by RNA Interference in Colorectal Cancer and Metastatic Liver Cancer,” Hepatobiliary & Pancreatic Diseases International, Vol. 11, 2012, pp. 393-400.