Cancer Genome Biology
- Other groups
- Regulatory Genomics
- Chromatin and Cell Fate
- Disease Genomics
- Epigenetic Mechanisms of Cancer and Cell Differentiation
- Cancer Genetics and Epigenetics
- Cancer and Iron
- ICO-IDIBELL-IGTP* Joint Program - Genetic Diagnostics
- Genetic Variation and Cancer
- Genomics and Bioinformatics
- ABO Histo-Blood Groups and Cancer
- Cancer Genome Biology
The Cancer Genome Biology Group is now the Genetic Epidemiology of Lung Cancer Group at the Institute Germans Trias i Pujol (IGTP).
Lung cancer is the leading cause of cancer death worldwide. To improve the outcome of patients with lung cancer, it is indispensable to understand the molecular pathways of lung cancer development and its progression. In particular, small cell lung cancer (SCLC) is the most aggressive type of lung cancer and, to date, no targetable genetic alterations have been identified except for the MYC family genes. The leader of this group has a great deal of experience in studying the molecular genetics of lung cancer. Therefore, the purpose of this group's work is to identify molecular targets for new therapies for SCLC among genes that are genetically altered in SCLC cells and to develop new therapies by targeting those gene products in vivo.
Identification of targetable genetic alterations for therapy in small cell lung cancer
To identify novel genes targetable as therapy of SCLC, several kinds of genome-wide analyses, including exome sequencing, DNA methylation microarrays and splicing microarrays, are ongoing using a number of fresh SCLC tumors and SCLC cell lines. These studies are in progress with collaborations with several other research groups in Japan, Spain, Germany, and the U.S.
MYC suppression as a therapy for patients with small cell lung cancer
Three MYC family genes, MYCL1, MYCN and MYC, are known to be amplified in 20% of SCLCs. Therefore, we have selected these MYC family genes as strong candidates of targets for therapy for SCLC, and are investigating the biological significance of MYC family gene amplification for SCLC cells by either down-regulation of MYC family genes or suppression of their activities with several inhibitors.
Tel: (+34) 93 554 3050
Office 2-13, Lab 2-18 (Second Floor)
Ryan BM, Robles AI, McClary AC, Haznadar M, Bowman ED, Pine SR, Brown D, Khan M, Shiraishi K, Kohno T, Okayama H, Modali R, Yokota J, Harris CC. Identification of a functional SNP in the 3'UTR of CXCR2 that is associated with reduced risk of lung cancer. Cancer Res. 2015 Feb; 75(3): 566-75
Kurioka D, Takeshita F, Tsuta K, Sakamoto H, Watanabe S, Matsumoto K, Watanabe M, Nakagama H, Ochiya T, Yokota J, Kohno T, Tsuchiya N. NEK9-dependent proliferation of cancer cells lacking functional p53. Sci Rep 2014 Aug; 4: 6111
Umemura S, Mimaki S, Makinoshima H, Tada S, Ishii G, Ohmatsu H, Niho S, Yoh K, Matsumoto S, Takahashi A, Morise M, Nakamura Y, Ochiai A, Nagai K, Iwakawa R, Kohno T, Yokota J, Ohe Y, Esumi H, Tsuchihara K, Goto K. Therapeutic priority of the PI3K/AKT/mTOR pathway in small cell lung cancers as revealed by a comprehensive genomic analysis. J Thorac Oncol 2014 Sep; 9(9): 1324-31
Nakaoku T, Tsuta K, Ichikawa H, Shiraishi K, Sakamoto H, Enari M, Furuta K, Shimada Y, Ogiwara H, Watanabe SI, Watanabe S, Nokihara H, Yasuda K, Hiramoto M, Nammo T, Ishigame T, Schetter AJ, Okayama H, Harris CC, Kim YH, Mishima M, Yokota J, Yoshida T, Kohno T. Druggable oncogene fusions in invasive mucinous lung adenocarcinoma. Clin. Cancer Res. 2014 Jun; 20(12): 3087-93
Otsubo C, Otomo R, Miyazaki M, Matsushima-Hibiya Y, Kohno T, Iwakawa R, Takeshita F, Okayama H, Ichikawa H, Saya H, Kiyono T, Ochiya T, Tashiro F, Nakagama H, Yokota J, Enari M. TSPAN2 is involved in cell invasion and motility during lung cancer progression. Cell Rep 2014 Apr; 7(2): 527-38
Romero OA, Torres-Diz M, Pros E, Savola S, Gomez A, Moran S, Saez C, Iwakawa R, Villanueva A, Montuenga LM, Kohno T, Yokota J, Sanchez-Cespedes M. MAX inactivation in small cell lung cancer disrupts MYC-SWI/SNF programs and is synthetic lethal with BRG1. Cancer Discov 2014 Mar; 4(3): 292-303