Tongtong Zou
University of Maryland, Baltimore
Network
Latest external collaboration on country level. Dive into details by clicking on the dots.
Publication
Featured researches published by Tongtong Zou.
Oncogene | 2000
Takashi Tsuchiya; Gen Tamura; Kiyoshi Sato; Yasushi Endoh; Ken Sakata; Zhe Jin; Teiichi Motoyama; Osamu Usuba; Wataru Kimura; Satoshi Nishizuka; Keith T. Wilson; Stephen P. James; Jing Yin; A. Steven Fleisher; Tongtong Zou; Steven G. Silverberg; Dehe Kong; Stephen J. Meltzer
The adenomatous polyposis coli (APC) tumor suppressor gene is mutationally inactivated in both familial and sporadic forms of colorectal cancers. In addition, hypermethylation of CpG islands in the upstream portion of APC, a potential alternative mechanism of tumor suppressor gene inactivation, has been described in colorectal cancer. Because a subset of both gastric and colorectal cancers display the CpG island methylator phenotype, we hypothesized that epigenetic inactivation of APC was likely to occur in at least some gastric cancers. APC exhibits two forms of transcripts from exons 1A and 1B in the stomach. Therefore, we investigated CpG island methylation in the sequences upstream of exons 1A and 1B, i.e., promoters 1A and 1B, respectively. We evaluated DNAs from 10 gastric cancer cell lines, 40 primary gastric cancers, and 40 matching non-cancerous gastric mucosae. Methylated alleles of promoter 1A were present in 10 (100%) of 10 gastric cancer cell lines, 33 (82.5%) of 40 primary gastric cancers, and 39 (97.5%) of 40 non-cancerous gastric mucosae. In contrast, promoter 1B was unmethylated in all of these same samples. APC transcripts from exon 1A were not expressed in nine of the 10 methylated gastric cancer cell lines, whereas APC transcripts were expressed from exon 1B. Thus, expression from a given promoter correlated well with its methylation status. We conclude that in contrast to the colon, methylation of promoter 1A is a normal event in the stomach; moreover, promoter 1B is protected from methylation in the stomach and thus probably does not participate in this form of epigenetic APC inactivation.
Oncogene | 2002
Florin M. Selaru; Tongtong Zou; Yan Xu; Valentina Shustova; Jing Yin; Yuriko Mori; Fumiako Sato; Suna Wang; Andreea Olaru; David Shibata; Bruce D. Greenwald; Mark J. Krasna; John M. Abraham; Stephen J. Meltzer
In order to identify and contrast global gene expression profiles defining the premalignant syndrome, Barretts esophagus, as well as frank esophageal cancer, we utilized cDNA microarray technology in conjunction with bioinformatics tools. We hybridized microarrays, each containing 8000 cDNA clones, to RNAs extracted from 13 esophageal surgical or endoscopic biopsy specimens (seven Barretts metaplasias and six esophageal carcinomas). Hierarchical cluster analysis was performed on these results and displayed using a color-coded graphic representation (Treeview). The esophageal samples clustered naturally into two principal groups, each possessing unique global gene expression profiles. After retrieving histologic reports for these tissues, we found that one main cluster contained all seven Barretts samples, while the remaining principal cluster comprised the six esophageal cancers. The cancers also clustered according to histopathological subtype. Thus, squamous cell carcinomas (SCCAs) constituted one group, adenocarcinomas (ADCAs) clustered separately, and one signet-ring carcinoma was in its own cluster, distinct from the ADCA cluster. We conclude that cDNA microarrays and bioinformatics show promise in the classification of esophageal malignant and premalignant diseases, and that these methods can be applied to small biopsy samples.
Virchows Archiv | 2002
Kiyoshi Sato; Gen Tamura; Takashi Tsuchiya; Yasushi Endoh; Ken Sakata; Teiichi Motoyama; Osamu Usuba; Wataru Kimura; Masanori Terashima; Satoshi Nishizuka; Tongtong Zou; Stephen J. Meltzer
Abstract. The PTEN tumor suppressor gene on 10q23.3, responsible for the Cowden and Bannayan-Zonana syndromes, encodes a dual-specificity phosphatase able to dephosphorylate both tyrosine phosphate and serine/threonine phosphate residues. Mutational inactivation of PTEN has been reported in various malignancies, including endometrial cancers, ovarian cancers, and glioblastomas. In this study, we investigated PTEN gene mutations in 10 gastric cancer cell lines and 58 primary gastric cancers by polymerase chain reaction single strand conformation polymorphism (PCR-SSCP). Hypermethylation of promoter region CpG islands, an alternative mechanism of gene inactivation to coding region mutations, was also evaluated by methylation specific PCR (MSP). Only one (1.7%) of the 58 primary tumors carried a somatic 5-bp deletion in intron 7 of PTEN, which did not alter the mRNA sequence, and no mutations were detected in any of the cell lines. Similar levels of PTEN mRNA expression were observed in all cell lines and primary tumors studied by RT-PCR, and PTEN promoter CpG islands remained unmethylated. Therefore, we conclude that PTEN does not participate in gastric carcinogenesis as a tumor suppressor gene.
Oncogene | 1999
Jing Yin; Noam Harpaz; Rhonda F. Souza; Tongtong Zou; Dehe Kong; Suna Wang; Anatoly Leytin; Neil S Medalie; Kara N. Smolinski; John M. Abraham; A. Steven Fleisher; Stephen J. Meltzer
A germline sequence alteration at codonu20091307 of the APC gene (I1307K) has been reported in 6u2009–u20097% of the Ashkenazi Jewish population in the United States. This alteration is believed to predispose the APC gene to a secondary mutation at the same locus, resulting in an increased risk of colorectal carcinoma. There is an increased risk of colorectal carcinoma in patients with inflammatory bowel disease (IBD), a relatively large proportion of whom are Ashkenazi Jews. We therefore sought to determine whether the I1307K sequence variant occurred in the germline DNA of IBD patients. To our surprise, we found this sequence in only two of 267 patients with IBD (0.7%), occurring in only 1.5% of Jewish IBD patients. The I1307K sequence variant was not found in 67 patients with esophageal cancer, 53 patients with gastric carcinoma (13 MSI-H and 44 MSI-negative), or ten patients with sporadic MSI-H colon cancer. These findings suggest that the I1307K sequence is relatively rare in the germline of Jewish as well as non-Jewish IBD patients. It does not appear to contribute to the increased colorectal cancer risk present in these patients.
Nature Genetics | 1996
Rhonda F. Souza; Rebecca Appel; Jing Yin; Suna Wang; Kara N. Smolinski; John M. Abraham; Tongtong Zou; Ying Qiang Shi; Junyi Lei; John R. Cottrell; Karina Cymes; Kelli G. Biden; Lisa A. Simms; Barbara A. Leggett; Patrick M. Lynch; Marsha L. Frazier; Steven M. Powell; Noam Harpaz; Haruhiko Sugimura; Joanne Young; Stephen J. Meltzer
Journal of the National Cancer Institute | 2000
Gen Tamura; Jing Yin; Suna Wang; A. Steven Fleisher; Tongtong Zou; John M. Abraham; Dehe Kong; Kara N. Smolinski; Keith T. Wilson; Stephen P. James; Steven G. Silverberg; Satoshi Nishizuka; Masanori Terashima; Teiichi Motoyama; Stephen J. Meltzer
Cancer Research | 2000
A. Steven Fleisher; Manel Esteller; Noam Harpaz; Anatoly Leytin; Asma Rashid; Yan Xu; Jing Liang; O. Colin Stine; Jing Yin; Tongtong Zou; John M. Abraham; Dehe Kong; Keith T. Wilson; Stephen P. James; James G. Herman; Stephen J. Meltzer
Nature Genetics | 1996
Rhonda F. Souza; Rebecca Appel; Jing Yin; Suna Wang; Kara N. Smolinski; John M. Abraham; Tongtong Zou; Ying-Qiang Shi; Junyi Lei; John S. Cottrell; Karina Cymes; Kelli G. Biden; Lisa A. Simms; Barbara A. Leggett; Patrick M. Lynch; Marsha L. Frazier; Steven M. Powell; Noam Harpas; Hirohasi Sugimura; Joanne Young; Stephen J. Meltzer
Human Cell | 1996
Rhonda F. Souza; L. Garrigue-Antar; Junyi Lei; Jing Yin; Rebecca Appel; V. F. Vellucci; Tongtong Zou; Xiaoling Zhou; Suna Wang; Mg Rhyu; K. Cymes; O. Chan; Ws Park; M. J. Krasna; B. D. Greenwald; John R. Cottrell; John M. Abraham; L. Simms; B. Leggett; Joanne Young; N. Harpaz; M. Reiss; Stephen J. Meltzer
Cancer Research | 1998
Tongtong Zou; A. Steven Fleisher; Dehe Kong; Jing Yin; Rhonda F. Souza; Suna Wang; Kara N. Smolinski; John M. Abraham; Stephen J. Meltzer