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Artificial intelligence and omics in cancer

Artificial Intelligence in cancer 2020年第1期1卷 1-7页

作者： cédric coulouarn Institut National de la Sante et de la Recherche Medicale(Inserm) Universitéde Rennes 1Rennes F-35000France

cancer is a major public health problem *** predictions suggest that 13 million people will die each year from cancer by ***,new ideas are urgently needed to change paradigms in the global fight against *** the last decades,artificial intelligence(AI)emerged in the field of cancer research as a new and promising *** emerging,a great potential is appreciated in AI to improve cancer diagnosis and prognosis,as well as to identify relevant therapeutics in the current era of personalized *** pipelines connecting patient-generated health data easily translatable into clinical practice to assist clinicians in decision making represents a challenging but fascinating *** algorithms are mainly fueled by multi omics data which,in the case of cancer research,have been largely derived from international cancer programs,including The cancer Genome Atlas(TcGA).Here,I briefly review some examples of supervised and unsupervised big data derived from TcGA programs and comment on how AI algorithms have been applied to improve the management of patients with *** this context,Artificial Intelligence in cancer journal was specifically launched to promote the development of this discipline,by serving as a forum to publish high-quality basic and clinical research articles in various fields of AI in oncology.

关键词： Omics Big data Artificial intelligence Deep learning Precision medicine

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Genome-wide differences in hepatitis c-vs alcoholism-associated hepatocellular carcinoma

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World Journal of Gastroenterology 2008年第11期14卷 1749-1758页

作者： céline Derambure cédric coulouarn Frédérique caillot Romain Daveau Martine Hiron Michel Scotte Arnaud Franois celia Duclos Odile Goria Marie Gueudin catherine cavard Benoit Terris Maryvonne Daveau Jean-Philippe Salier Inserm Unité519 and Institut Fédératif de Recherches Multidisciplinaires sur les Peptides Facultéde Médecine-PharmacieRouenFrance Inserm Unité519 and Institut Fédératif de Recherches Multidisciplinaires sur les Peptides Facultéde Médecine-PharmacieRouenFrance Service de Chirurgie Générale et DigestiveCentre Hospitalier UniversitaireRouenFrance Département de Pathologie Centre Hospitalier UniversitaireRouenFrance Inserm Unité519 and Institut Fédératif de Recherches Multidisciplinaires sur les Peptides Facultéde Médecine-PharmacieRouenFrance Service d'Hépato-gastro-enterologieCentre Hospitalier UniversitaireRouenFrance Laboratoire de Virologie and UPRES EA 2646 Centre Hospitalier UniversitaireRouenFrance Inserm Unité567 CNRS UMR 8104 UniversitéParis 5Département GDPMInstitut CochinParis France

AIM:To look at a comprehensive picture of etiology- dependent gene abnormalities in hepatocellular carcinoma in Western Europe. METHODS:With a liver-oriented microarray,transcript levels were compared in nodules and cirrhosis from a training set of patients with hepatocellular carcinoma (alcoholism,12;hepatitis c,10)and 5 *** or tight selection of informative transcripts with an abnormal abundance was statistically valid and the tightly selected transcripts were next quantified by qRTPcR in the nodules from our training set(12+10) and a test set(6+7). RESULTS:A selection of 475 transcripts pointed to significant gene over-representation on chromosome 8 (alcoholism)or-2(hepatitis c)and ontology indicated a predominant inflammatory response(alcoholism)or changes in cell cycle regulation,transcription factors and interferon responsiveness(hepatitis c).A stringent selection of 23 transcripts whose differences betweenetiologies were significant in nodules but not in cirrhotic tissue indicated that the above dysregulations take place in tumor but not in the surrounding *** 23 transcripts separated our test set according to etiologies. The inflammation-associated transcripts pointed to limited alterations of free iron metabolism in alcoholic vs hepatitis c tumors. cONcLUSION:Etiology-specific abnormalities(chromo- some preference;differences in transcriptomes and related functions)have been identified in hepatocellular carcinoma driven by alcoholism or hepatitis *** may open novel avenues for differential therapies in this disease.

关键词： Alcoholism chromosome cirrhosis Hepatitis c Transcriptomes Protein function

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肝细胞癌与胎儿肝脏中对表达抑制的基因的全面研究,dudulin-2mRNA的表达抑制可作为肝硬化发展至肿瘤过程中的一种可能标记

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世界核心医学期刊文摘（胃肠病学分册） 2005年第9期1卷 58-58页

作者： coulouarn c. Derambure c. Lefebvre G. J.-P. Salier 陈云茹 Inserm Unité519 Inst. Federatif Rech. M. Fac. de Médecine-Pharmacie 22 Bvd Gambetta 76183 Rouen Cedex France

Background/Aims: Whether the transcriptional reprogramming process induced by hepatocellular carcinoma recapitulates that of the developing liver is at present unclear. Methods: With a complete coverage of the liver transcriptome by microarray using adult livers as controls, we searched for similarities and differences in mRNA abundances between hepatocellular carcinoma nodules and fetal livers taken before (early) or after (late) the 22-24th week of gestation. changes in some mRNA levels were studied in further liver samples by quantitative RT-PcR. Results: Altered gene expression in hepatocellular carcinoma mostly results in down-regulated mRNAs which largely overlap with those repressed in the late fetal liver. Different frequencies of transcription factor binding sites in the down-regulated genes vs control genes as well as changes in abundance of mRNAs for relevant transcription factors point to a transcriptional repression. The down-regulated mRNAs code for proteins involved in (i) transcription and translation, (ii) specific functions of the differentiated hepatocyte or (iii) activation of proliferation and apoptosis. conclusions: Apoptosis limitation is likely to predominate over active proliferation during liver development and hepatocellular carcinoma. Repression of the apoptosis-associated dudulin-2 mRNA points to a potential marker for the transition from a carcinoma-free to carcinoma-associated cirrhosis.

关键词：肝细胞癌 dudulin-2mRNA 基因表达抑制人肝细胞下调基因癌性基因转录本癌结节用成微阵列技术

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