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Your search keyword '"Kip, N. Sertac"' showing total 13 results
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13 results on '"Kip, N. Sertac"'

1. Proceedings of the fourth international molecular pathological epidemiology (MPE) meeting

Author

Campbell, Peter T., Ambrosone, Christine B., Nishihara, Reiko, Aerts, Hugo J. W. L., Bondy, Melissa, Chatterjee, Nilanjan, Garcia-Closas, Montserrat, Giannakis, Marios, Golden, Jeffrey A., Heng, Yujing J., Kip, N. Sertac, Koshiol, Jill, Liu, X. Shirley, Lopes-Ramos, Camila M., Mucci, Lorelei A., Nowak, Jonathan A., Phipps, Amanda I., Quackenbush, John, Schoen, Robert E., Sholl, Lynette M., Tamimi, Rulla M., Wang, Molin, Weijenberg, Matty P., Wu, Catherine J., Wu, Kana, Yao, Song, Yu, Kun-Hsing, Zhang, Xuehong, Rebbeck, Timothy R., and Ogino, Shuji

Published
2019

2. Molecular profiling reveals immunogenic cues in anaplastic large cell lymphomas with DUSP22 rearrangements

Author

Luchtel, Rebecca A., Dasari, Surendra, Oishi, Naoki, Pedersen, Martin Bjerregård, Hu, Guangzhen, Rech, Karen L., Ketterling, Rhett P., Sidhu, Jagmohan, Wang, Xueju, Katoh, Ryohei, Dogan, Ahmet, Kip, N. Sertac, Cunningham, Julie M., Sun, Zhifu, Baheti, Saurabh, Porcher, Julie C., Said, Jonathan W., Jiang, Liuyan, Hamilton-Dutoit, Stephen Jacques, Møller, Michael Boe, Nørgaard, Peter, Bennani, N. Nora, Chng, Wee-Joo, Huang, Gaofeng, Link, Brian K., Facchetti, Fabio, Cerhan, James R., d'Amore, Francesco, Ansell, Stephen M., and Feldman, Andrew L.

Published
2018
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3. Proceedings of the third international molecular pathological epidemiology (MPE) meeting

Author

Campbell, Peter T., Rebbeck, Timothy R., Nishihara, Reiko, Beck, Andrew H., Begg, Colin B., Bogdanov, Alexei A., Cao, Yin, Coleman, Helen G., Freeman, Gordon J., Heng, Yujing J., Huttenhower, Curtis, Irizarry, Rafael A., Kip, N. Sertac, Michor, Franziska, Nevo, Daniel, Peters, Ulrike, Phipps, Amanda I., Poole, Elizabeth M., Qian, Zhi Rong, Quackenbush, John, Robins, Harlan, Rogan, Peter K., Slattery, Martha L., Smith-Warner, Stephanie A., Song, Mingyang, VanderWeele, Tyler J., Xia, Daniel, Zabor, Emily C., Zhang, Xuehong, Wang, Molin, and Ogino, Shuji

Published
2017

4. The oncogenic transcription factor IRF4 is regulated by a novel CD30/NF-κB positive feedback loop in peripheral T-cell lymphoma

Author

Boddicker, Rebecca L., Kip, N. Sertac, Xing, Xiaoming, Zeng, Yu, Yang, Zhi-Zhang, Lee, Jeong-Heon, Almada, Luciana L., Elsawa, Sherine F., Knudson, Ryan A., Law, Mark E., Ketterling, Rhett P., Cunningham, Julie M., Wu, Yanhong, Maurer, Matthew J., O'Byrne, Megan M., Cerhan, James R., Slager, Susan L., Link, Brian K., Porcher, Julie C., Grote, Deanna M., Jelinek, Diane F., Dogan, Ahmet, Ansell, Stephen M., Fernandez-Zapico, Martin E., and Feldman, Andrew L.

Published
2015
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5. Genome-wide analysis reveals recurrent structural abnormalities of TP63 and other p53-related genes in peripheral T-cell lymphomas

Author

Vasmatzis, George, Johnson, Sarah H., Knudson, Ryan A., Ketterling, Rhett P., Braggio, Esteban, Fonseca, Rafael, Viswanatha, David S., Law, Mark E., Kip, N. Sertac, Özsan, Nazan, Grebe, Stefan K., Frederick, Lori A., Eckloff, Bruce W., Thompson, E. Aubrey, Kadin, Marshall E., Milosevic, Dragana, Porcher, Julie C., Asmann, Yan W., Smith, David I., Kovtun, Irina V., Ansell, Stephen M., Dogan, Ahmet, and Feldman, Andrew L.

Published
2012
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7. Molecular profiling reveals immunogenic cues in anaplastic large cell lymphomas with DUSP22 rearrangements

Author

Luchtel, Rebecca A, Dasari, Surendra, Oishi, Naoki, Pedersen, Martin Bjerregård, Hu, Guangzhen, Rech, Karen L, Ketterling, Rhett P, Sidhu, Jagmohan, Wang, Xueju, Katoh, Ryohei, Dogan, Ahmet, Kip, N Sertac, Cunningham, Julie M, Sun, Zhifu, Baheti, Saurabh, Porcher, Julie C, Said, Jonathan W, Jiang, Liuyan, Hamilton-Dutoit, Stephen Jacques, Møller, Michael Boe, Nørgaard, Peter, Bennani, N Nora, Chng, Wee-Joo, Huang, Gaofeng, Link, Brian K, Facchetti, Fabio, Cerhan, James R, d'Amore, Francesco, Ansell, Stephen M, Feldman, Andrew L, Luchtel, Rebecca A, Dasari, Surendra, Oishi, Naoki, Pedersen, Martin Bjerregård, Hu, Guangzhen, Rech, Karen L, Ketterling, Rhett P, Sidhu, Jagmohan, Wang, Xueju, Katoh, Ryohei, Dogan, Ahmet, Kip, N Sertac, Cunningham, Julie M, Sun, Zhifu, Baheti, Saurabh, Porcher, Julie C, Said, Jonathan W, Jiang, Liuyan, Hamilton-Dutoit, Stephen Jacques, Møller, Michael Boe, Nørgaard, Peter, Bennani, N Nora, Chng, Wee-Joo, Huang, Gaofeng, Link, Brian K, Facchetti, Fabio, Cerhan, James R, d'Amore, Francesco, Ansell, Stephen M, and Feldman, Andrew L

Abstract

Anaplastic large cell lymphomas (ALCLs) are CD30-positive T-cell non-Hodgkin lymphomas broadly segregated into ALK-positive and ALK-negative types. Although ALK-positive ALCLs consistently bear rearrangements of the ALK tyrosine kinase gene, ALK-negative ALCLs are clinically and genetically heterogeneous. About 30% of ALK-negative ALCLs have rearrangements of DUSP22 and have excellent long-term outcomes with standard therapy. To better understand this group of tumors, we evaluated their molecular signature using gene expression profiling. DUSP22-rearranged ALCLs belonged to a distinct subset of ALCLs that lacked expression of genes associated with JAK-STAT3 signaling, a pathway contributing to growth in the majority of ALCLs. Reverse-phase protein array and immunohistochemical studies confirmed the lack of activated STAT3 in DUSP22-rearranged ALCLs. DUSP22-rearranged ALCLs also overexpressed immunogenic cancer-testis antigen (CTA) genes and showed marked DNA hypomethylation by reduced representation bisulfate sequencing and DNA methylation arrays. Pharmacologic DNA demethylation in ALCL cells recapitulated the overexpression of CTAs and other DUSP22 signature genes. In addition, DUSP22-rearranged ALCLs minimally expressed PD-L1 compared with other ALCLs, but showed high expression of the costimulatory gene CD58 and HLA class II. Taken together, these findings indicate that DUSP22 rearrangements define a molecularly distinct subgroup of ALCLs, and that immunogenic cues related to antigenicity, costimulatory molecule expression, and inactivity of the PD-1/PD-L1 immune checkpoint likely contribute to their favorable prognosis. More aggressive ALCLs might be pharmacologically reprogrammed to a DUSP22-like immunogenic molecular signature through the use of demethylating agents and/or immune checkpoint inhibitors.

Published
2018

12. Genome-wide analysis reveals recurrent structural abnormalities of TP63and other p53-related genes in peripheral T-cell lymphomas

Author

Vasmatzis, George, Johnson, Sarah H., Knudson, Ryan A., Ketterling, Rhett P., Braggio, Esteban, Fonseca, Rafael, Viswanatha, David S., Law, Mark E., Kip, N. Sertac, Özsan, Nazan, Grebe, Stefan K., Frederick, Lori A., Eckloff, Bruce W., Thompson, E. Aubrey, Kadin, Marshall E., Milosevic, Dragana, Porcher, Julie C., Asmann, Yan W., Smith, David I., Kovtun, Irina V., Ansell, Stephen M., Dogan, Ahmet, and Feldman, Andrew L.

Abstract

Peripheral T-cell lymphomas (PTCLs) are aggressive malignancies of mature T lymphocytes with 5-year overall survival rates of only ∼ 35%. Improvement in outcomes has been stymied by poor understanding of the genetics and molecular pathogenesis of PTCL, with a resulting paucity of molecular targets for therapy. We developed bioinformatic tools to identify chromosomal rearrangements using genome-wide, next-generation sequencing analysis of mate-pair DNA libraries and applied these tools to 16 PTCL patient tissue samples and 6 PTCL cell lines. Thirteen recurrent abnormalities were identified, of which 5 involved p53-related genes (TP53, TP63, CDKN2A, WWOX, and ANKRD11). Among these abnormalities were novel TP63rearrangements encoding fusion proteins homologous to ΔNp63, a dominant-negative p63 isoform that inhibits the p53 pathway. TP63rearrangements were seen in 11 (5.8%) of 190 PTCLs and were associated with inferior overall survival; they also were detected in 2 (1.2%) of 164 diffuse large B-cell lymphomas. As TP53mutations are rare in PTCL compared with other malignancies, our findings suggest that a constellation of alternate genetic abnormalities may contribute to disruption of p53-associated tumor suppressor function in PTCL.

Published
2012
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13. HMGA2gene expression analysis performed on cytologic smears to distinguish benign from malignant thyroid nodules

Author

Lappinga, Paul J., Kip, N. Sertac, Jin, Long, Lloyd, Ricardo V., Henry, Michael R., Zhang, Jun, and Nassar, Aziza

Abstract

The results of the current study demonstrated that analysis of high mobility group AT‐hook 2 (HMGA2) gene expression with real‐time quantitative reverse transcriptase–polymerase chain reaction can distinguish benign from malignant thyroid aspirate smears with a sensitivity of 71% and a specificity of 97%.

Published
2010
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