Search

Your search keyword '"Risinger, John I."' showing total 16 results
Start Over Author "Risinger, John I." Journal cancer research
16 results on '"Risinger, John I."'

3. Abstract 1570: ARID1A regulation of ATAD2 in gynecologic cancer

Author

Shoji, Yutaka, primary, Conrads, Kelly A., additional, Challa, Rusheeswar, additional, Hood, Brian L., additional, Wang, Guisong, additional, Darcy, Kathleen M., additional, Hamilton, Chad A., additional, Maxwell, George Larry, additional, Conrads, Thomas P., additional, and Risinger, John I., additional

Published
2014
Full Text
View/download PDF

6. Abstract 3375: Normal viability of Kai1/CD82 deficient mice

Author

Risinger, John I., primary, Custer, Mary, additional, Feigenbaum, Lionel, additional, Simpson, R Mark, additional, Hoover, Shelley, additional, Webster, Josh, additional, Chandramouli, Gadisetti VR, additional, Tessarollo, Lino, additional, and Barrett, J Carl, additional

Published
2010
Full Text
View/download PDF

12. Reciprocal Binding of CTCF and BORIS to the NY-ESO-1 Promoter Coincides with Derepression of this Cancer-Testis Gene in Lung Cancer Cells

Author

Hong, Julie A., primary, Kang, Yang, additional, Abdullaev, Ziedulla, additional, Flanagan, Patrick T., additional, Pack, Svetlana D., additional, Fischette, Maria R., additional, Adnani, Mina T., additional, Loukinov, Dmitri I., additional, Vatolin, Sergei, additional, Risinger, John I., additional, Custer, Mary, additional, Chen, G. Aaron, additional, Zhao, Ming, additional, Nguyen, Dao M., additional, Barrett, J. Carl, additional, Lobanenkov, Victor V., additional, and Schrump, David S., additional

Published
2005
Full Text
View/download PDF

13. Conditional Expression of the CTCF-Paralogous Transcriptional Factor BORIS in Normal Cells Results in Demethylation and Derepression of MAGE-A1 and Reactivation of Other Cancer-Testis Genes

Author

Vatolin, Sergei, primary, Abdullaev, Ziedulla, additional, Pack, Svetlana D., additional, Flanagan, Patrick T., additional, Custer, Mary, additional, Loukinov, Dmitri I., additional, Pugacheva, Elena, additional, Hong, Julie A., additional, Morse, Herbert, additional, Schrump, David S., additional, Risinger, John I., additional, Barrett, J. Carl, additional, and Lobanenkov, Victor V., additional

Published
2005
Full Text
View/download PDF

15. Microarray analysis reveals distinct gene expression profiles among different histologic types of endometrial cancer.

Author

Risinger JI, Maxwell GL, Chandramouli GV, Jazaeri A, Aprelikova O, Patterson T, Berchuck A, and Barrett JC

Subjects
Endometrial Neoplasms classification, Endometrium cytology, Endometrium physiology, Female, Humans, Reference Values, Endometrial Neoplasms genetics, Endometrial Neoplasms pathology, Gene Expression Profiling, Gene Expression Regulation, Neoplastic
Abstract

Previous studies of oncogene and tumor suppressor gene alterations have suggested that differences exist in the molecular pathogenesis of the various histological types of endometrial cancer. To elucidate further the molecular events involved in endometrial carcinogenesis, we examined global expression patterns of 16 nonendometrioid cancers (13 serous papillary and 3 clear cell), 19 endometrioid cancers, and 7 age-matched normal endometria using cDNA microarrays. Unsupervised analysis of gene expression identified 191 genes that exhibited >2-fold differences (P < 0.001) between the histological groups. Many genes were similarly dysregulated in both nonendometrioid and endometrioid cancers relative to normal endometria. Gene expression differences in only 24 transcripts could distinguish serous from endometrioid cancers, the two most common subgroups. These data provide the basis for investigation of previously unrecognized novel pathways involved in the development of endometrial cancers.

Published
2003

16. Splice variants but not mutations of DNA polymerase beta are common in bladder cancer.

Author

Thompson TE, Rogan PK, Risinger JI, and Taylor JA

Subjects
Alternative Splicing, DNA, Complementary genetics, DNA, Neoplasm genetics, Exons, Gene Deletion, Humans, Point Mutation, Polymorphism, Genetic, Tumor Cells, Cultured, Carcinoma, Transitional Cell enzymology, Carcinoma, Transitional Cell genetics, DNA Polymerase beta genetics, Urinary Bladder Neoplasms enzymology, Urinary Bladder Neoplasms genetics
Abstract

DNA polymerase beta (POLbeta) is a highly conserved protein that functions in base excision repair. Loss of the POLbeta locus on chromosome 8p is a frequent event in bladder cancer, and loss of POLbeta function could hinder DNA repair leading to a mutator phenotype. Both point mutations and large intragenic deletions of POLbeta have been reported from analysis of various tumor cDNAs but not from genomic DNA. We noticed that the breakpoints of the presumed rearrangements were delineated by exon-exon junctions, which could instead be consistent with alternative splicing of POLbeta mRNA. We tested the hypothesis that the reported intragenic deletion were splice variants by screening genomic DNA of human bladder tumors, bladder cancer cell lines, and normal bladder tissues for mutations or deletions in exons 1-14, exon alpha, and the promoter region of POLbeta. We found no evidence of somatic mutations or deletions in our sample set, although two polymorphisms were identified. Examination of cDNA from a subset of the original sample set revealed that truncated forms of POLbeta were surprisingly common. Forty-eight of 89 (54%) sequenced cDNA clones had large deletions, each beginning and/or ending exactly at exon-exon junctions. Because these deletions occur at exon-exon junctions and are seen in cDNA but not genomic DNA, they are consistent with alternative mRNA splicing. We describe 12 different splicing events occurring in 18 different combinations. Loss of exon 2 was the most frequent, being found in 42 of 49 (86%) of the variant sequenced clones. The splice variants appear to be somewhat more common and variable in bladder cancer cell lines and tumor tissues but occur at a high frequency in normal bladder tissues as well. We examine alternative splicing in terms of the information content of splice donor and acceptor site sequences, and discuss possible explanations for the predominant splicing event, the loss of exon 2.

Published
2002

Catalog

Books, media, physical & digital resources
See catalog results