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151. Relative frequency and clinicopathologic characteristics of MYC-rearranged follicular lymphoma

Author

Chaudhary, Shweta, primary, Brown, Noah, additional, Song, Joo Y., additional, Yang, Lin, additional, Skrabek, Pamela, additional, Nasr, Michel R., additional, Wong, Jerry T., additional, Bedell, Victoria, additional, Murata-Collins, Joyce, additional, Kochan, Lindsay, additional, Li, Jie, additional, Zhang, Weiwei, additional, Chan, Wing C., additional, Weisenburger, Dennis D., additional, and Perry, Anamarija M., additional

Published
2021
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152. Integrative Genomic and Transcriptomic Analysis Reveals Targetable Vulnerabilities in Angioimmunoblastic T-Cell Lymphoma

Author

Bouska, Alyssa, Zhang, Weiwei, Sharma, Sunandini, Holte, Harald, Shah, Ab Rauf, Lone, Waseem Gul, Cappelli, Luca Vincenzo, Fiore, Danilo, Gong, Qiang, Heavican-Foral, Tayla, Cannatella, Jeffrey, Amador, Catalina, Arif, Aiza, Smith, Lynette, Lim, Soon Thye, Ong, Choon Kiat, Feldman, Andrew L., Du, Ming-Qing, de Leval, Laurence, Greiner, Timothy C., Fu, Kai, Trøen, Gunhild, Vodak, Daniel, Nakken, Sigve, Delabie, Jan, Weinstock, David M., Pileri, Stefano A., Laginestra, Antonella, Kim, Kyeongjin, Pajvani, Utpal, Vose, Julie M., Weisenburger, Dennis D, Dave, Sandeep, Inghirami, Giorgio, Chan, Wing C., and Iqbal, Javeed

Published
2023
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158. Province-Wide Analysis of Patient-Reported Outcomes for Stage IV Non-Small Cell Lung Cancer

Author

Tjong, Michael C., primary, Doherty, Mark, additional, Tan, Hendrick, additional, Chan, Wing C., additional, Zhao, Haoyu, additional, Hallet, Julie, additional, Darling, Gail, additional, Kidane, Biniam, additional, Wright, Frances C., additional, Mahar, Alyson, additional, Davis, Laura E., additional, Delibasic, Victoria, additional, Parmar, Ambika, additional, Mittmann, Nicole, additional, Coburn, Natalie G., additional, and Louie, Alexander V., additional

Published
2021
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159. EBV‐positive HIV‐associated diffuse large B cell lymphomas are characterized by JAK/STAT (STAT3) pathway mutations and unique clinicopathologic features

Author

Chapman, Jennifer R., primary, Bouska, Alyssa C., additional, Zhang, Weiwei, additional, Alderuccio, Juan Pablo, additional, Lossos, Izidore S., additional, Rimsza, Lisa M., additional, Maguire, Alanna, additional, Yi, Shuhua, additional, Chan, Wing C., additional, Vega, Francisco, additional, and Song, Joo Y., additional

Published
2021
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160. MAPK and JAK-STAT pathways dysregulation in plasmablastic lymphoma

Author

Ramis-Zaldivar, Joan Enric, primary, Gonzalez-Farre, Blanca, additional, Nicolae, Alina, additional, Pack, Svetlana, additional, Clot, Guillem, additional, Nadeu, Ferran, additional, Mottok, Anja, additional, Horn, Heike, additional, Song, Joo Y, additional, Fu, Kai, additional, Wright, George, additional, Gascoyne, Randy D., additional, Chan, Wing C., additional, Scott, David W., additional, Feldman, Andrew L., additional, Valera, Alexandra, additional, Enjuanes, Anna, additional, Braziel, Rita M., additional, Smeland, Erlend B., additional, Staudt, Louis M., additional, Rosenwald, Andreas, additional, Rimsza, Lisa M., additional, Ott, German, additional, Jaffe, Elaine S, additional, Salaverria, Itziar, additional, and Campo, Elias, additional

Published
2021
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161. Validation of the Double-Hit Gene Expression Signature (DLBCL90) in an Independent Cohort of Patients with Diffuse Large B-Cell Lymphoma of Germinal Center Origin

Author

Nguyen, Ha, primary, Perry, Anamarija, additional, Skrabek, Pamela, additional, Nasr, Michel, additional, Herrera, Alex F., additional, Bedell, Victoria, additional, Murata-Collins, Joyce, additional, Pillai, Raju, additional, Xu, Minlin, additional, Chen, Lu, additional, Chan, Wing C., additional, Weisenburger, Dennis D., additional, Scott, David W., additional, and Song, Joo Y., additional

Published
2021
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162. Loss of Dnmt3b function upregulates the tumor modifier Ment and accelerates mouse lymphomagenesis

Author

Hlady, Ryan A., Novakova, Slavomira, Opavska, Jana, Klinkebiel, David, Peters, Staci L., Bies, Juraj, Hannah, Jay, Iqbal, Javeed, Anderson, Kristi M., Siebler, Hollie M., Smith, Lynette M., Greiner, Timothy C., Bastola, Dhundy, Joshi, Shantaram, Lockridge, Oksana, Simpson, Melanie A., Felsher, Dean W., Wagner, Kay-Uwe, Chan, Wing C., Christman, Judith K., and Opavsky, Rene

Subjects
T cells -- Physiological aspects -- Research, Methylation -- Research, Lymphomas -- Diagnosis -- Genetic aspects -- Research -- Care and treatment, Methyltransferases -- Physiological aspects -- Research, Health care industry
Abstract

DNA methyltransferase 3B (Dnmt3b) belongs to a family of enzymes responsible for methylation of cytosine residues in mammals. DNA methylation contributes to the epigenetic control of gene transcription and is deregulated in virtually all human tumors. To better understand the generation of cancer-specific methylation patterns, we genetically inactivated Dnmt3b in a mouse model of MYC-induced lymphomagenesis. Ablation of Dnmt3b function using a conditional knockout in T cells accelerated lymphomagenesis by increasing cellular proliferation, which suggests that Dnmt3b functions as a tumor suppressor. Global methylation profiling revealed numerous gene promoters as potential targets of Dnmt3b activity, the majority of which were demethylated in Dnmt[3b.sup.-/-] lymphomas, but not in Dnmt[3b.sup.-/-] pretumor thymocytes, implicating Dnmt3b in maintenance of cytosine methylation in cancer. Functional analysis identified the gene Gm128 (which we termed herein methylated in normal thymocytes [Ment]) as a target of Dnmt3b activity. We found that Ment was gradually demethylated and overexpressed during tumor progression in Dnmt[3b.sup.-/-] lymphomas. Similarly, MENT was overexpressed in 67% of human lymphomas, and its transcription inversely correlated with methylation and levels of DNMT3B. Importantly, knockdown of Ment inhibited growth of mouse and human cells, whereas overexpression of Ment provided Dnmt[3b.sup.+/+] cells with a proliferative advantage. Our findings identify Ment as an enhancer of lymphomagenesis that contributes to the tumor suppressor function of Dnmt3b and suggest it could be a potential target for anticancer therapies., Introduction Cytosine methylation represents a heritable epigenetic modification affecting gene transcription and the integrity of the genome. The DNA methyltransferases (DNMTs) DNMT1, DNMT3A, and DNMT3B are the enzymes primarily responsible [...]

Published
2012
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163. Structural profiles of TP53 gene mutations predict clinical outcome in diffuse large B-cell lymphoma: an international collaborative study

Author

Young, Ken H., Leroy, Karen, Møller, Michael B., Colleoni, Gisele W.B., Sánchez-Beato, Margarita, Kerbauy, Fábio R., Haioun, Corinne, Eickhoff, Jens C., Young, Allen H., Gaulard, Philippe, Piris, Miguel A., Oberley, Terry D., Rehrauer, William M., Kahl, Brad S., Malter, James S., Campo, Elias, Delabie, Jan, Gascoyne, Randy D., Rosenwald, Andreas, Rimsza, Lisa, Huang, James, Braziel, Rita M., Jaffe, Elaine S., Wilson, Wyndham H., Staudt, Louis M., Vose, Julie M., Chan, Wing C., Weisenburger, Dennis D., and Greiner, Timothy C.

Published
2008
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169. Oncogenic CARD11 mutations in human diffuse large B cell lymphoma

Author

Lenz, Georg, Davis, R. Eric, Ngo, Vu N., Lam, Lloyd, George, Thaddeus C., Wright, George W., Dave, Sandeep S., Zhao, Hong, Xu, Weihong, Rosenwald, Andreas, Ott, German, Muller-Hermelink, Hans Konrad, Gascoyne, Randy D., Connors, Joseph M., Rimsza, Lisa M., Campo, Elias, Jaffe, Elaine S., Delabie, Jan, Smeland, Erlend B., Fisher, Richard I., Chan, Wing C., and Staudt, Louis M.

Subjects
Lymphomas -- Genetic aspects, Oncogenes -- Research, Gene mutations -- Health aspects
Published
2008

171. Myeloproliferative and lymphoproliferative malignancies occurring in the same patient:A nationwide discovery cohort

Author

Holst, Johanne M., Plesner, Trine L., Pedersen, Martin B., Frederiksen, Henrik, Møller, Michael B., Clausen, Michael R., Hansen, Marcus C., Hamilton-Dutoit, Stephen Jacques, Nørgaard, Peter, Johansen, Preben, Eberlein, Tobias Ramm, Mortensen, Bo K., Mathiasen, Gustav, Øvlisen, Andreas, Wang, Rui, Wang, Chao, Zhang, Weiwei, Ommen, Hans Beier, Stentoft, Jesper, Ludvigsen, Maja, Tam, Wayne, Chan, Wing C., Inghirami, Giorgio, d'Amore, Francesco, Holst, Johanne M., Plesner, Trine L., Pedersen, Martin B., Frederiksen, Henrik, Møller, Michael B., Clausen, Michael R., Hansen, Marcus C., Hamilton-Dutoit, Stephen Jacques, Nørgaard, Peter, Johansen, Preben, Eberlein, Tobias Ramm, Mortensen, Bo K., Mathiasen, Gustav, Øvlisen, Andreas, Wang, Rui, Wang, Chao, Zhang, Weiwei, Ommen, Hans Beier, Stentoft, Jesper, Ludvigsen, Maja, Tam, Wayne, Chan, Wing C., Inghirami, Giorgio, and d'Amore, Francesco

Abstract

Myeloid and lymphoid malignancies are postulated to have distinct pathogenic mechanisms. The recent observation that patients with a myeloproliferative neoplasm have an increased risk of developing lymphoproliferative malignancies has challenged this assumption. We collected a nationwide cohort of patients with both malignancies. Patients diagnosed between 1990 and 2015 were identified through the national Danish Pathology Registry. We identified 599 patients with a myeloproliferative neoplasm and a concomitant or subsequent diagnosis of lymphoma. Histopathological review of the diagnostic samples from each patient led to a final cohort of 97 individuals with confirmed dual diagnoses of myeloproliferative neoplasm and lymphoma. The age range at diagnosis of these individuals was 19-94 years (median: 71 years). To avoid the inclusion of cases of therapy-induced myeloproliferative neoplasm occurring in patients previously treated for lymphoma, only patients with myeloproliferative neoplasm diagnosed unequivocally before the development of lymphoma were included. The average time interval between the diagnoses of the two malignancies was 1.5 years. In the majority of patients (90%) both diagnoses were established within 5 years of each other. Among the lymphoma entities, the frequency of peripheral T-cell lymphomas was markedly increased. Interestingly, all but one of the T-cell lymphomas were of angioimmunoblastic type. These findings suggest that a myeloproliferative neoplasm and lymphoproliferative malignancy developing in the same patient may have common pathogenic events, possibly already at the progenitor level. We believe that the molecular characterization of the newly developed biorepository will help to highlight the mechanisms driving the genesis and clonal evolution of these hematopoietic malignancies.

Published
2020

172. Double-hit Signature with TP53 Abnormalities Predicts Poor Survival in Patients with Germinal Center Type Diffuse Large B-cell Lymphoma Treated with R-CHOP

Author

Song, Joo Y., primary, Perry, Anamarija M., additional, Herrera, Alex F., additional, Chen, Lu, additional, Skrabek, Pamela, additional, Nasr, Michel R., additional, Ottesen, Rebecca A., additional, Nikowitz, Janet, additional, Bedell, Victoria, additional, Murata-Collins, Joyce, additional, Li, Yuping, additional, McCarthy, Christine, additional, Pillai, Raju, additional, Wang, Jinhui, additional, Wu, Xiwei, additional, Zain, Jasmine, additional, Popplewell, Leslie, additional, Kwak, Larry W., additional, Nademanee, Auayporn P., additional, Niland, Joyce C., additional, Scott, David W., additional, Gong, Qiang, additional, Chan, Wing C., additional, and Weisenburger, Dennis D., additional

Published
2021
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179. Prediction of survival in follicular lymphoma based on molecular features of tumor-infiltrating immune cells

Author

Dave, Sandeep S., Chan, Wing C., Miller, Thomas P., Vose, Julie, Delabie, Jan, Davies, Andrew J., Montserrat, Emilio, Powell, John, Wright, George, Fisher, Richard I., LeBlanc, Michael, Armitage, James O., Connors, Joseph M., Norton, Andrew J., Wilson, Wyndham H., Hong Zhao, Tan, Bruce., Braziel, Rita M., Greiner, Timothy C., Smeland, Erlend B., Lansdorp, Peter M., Muller-Hermelink, H. Konrad, Jaffe, Elaine S., Goldschmidt, Neta, Rosenwald, Andreas, Rimsza, Lisa M., Weisenburger, Dennis D., Kvaloy, Stein, Qin Ouyang, Ott, German, Simon, Richard, French biblical critic, Chiorazzi, Michael, Gascoyne, Randy D., Grogan, Thomas M., Lynch, James C., Holte, Harald, Lister, T. Andrew, Campo, Elias, Liming Yang, and Staudt, Louis M.

Subjects
Patients -- Research, Lymphomas -- Diagnosis, Lymphomas -- Patient outcomes
Abstract

The patients with follicular lymphoma survival are determined to be for periods less than 1 year to more than 20 years after diagnosis. The gene-expression profiles of tumor-biopsy specimens obtained at diagnosis are used to develop a molecular predictor of the length of survival. It is found that the length of survival among patients with follicular lymphoma correlates with the molecular features of nonmalignant immune cells present in the tumor at diagnosis.

Published
2004

184. Contributors

Author

Abati, Andrea, primary, Arber, Daniel A., additional, Atayar, Çiğdem, additional, Bagg, Adam, additional, Bain, Barbara J., additional, Barry, Todd S., additional, Borowitz, Michael J., additional, Brousset, Pierre, additional, Brynes, Russell K., additional, Camacho, Francisca I., additional, Campo, Elias, additional, Chacón, Ignacio, additional, Chaganti, R.S.K., additional, Chan, Alexander C.L., additional, Chan, John K.C., additional, Chan, Wing C. (John), additional, Chang, Karen L., additional, Cheuk, Wah, additional, Connors, Joseph M., additional, Craig, Fiona E., additional, de la Cruz Mora, Miguel Ángel, additional, Delsol, Georges, additional, Djokic, Miroslav, additional, Duncan, Lyn McDivitt, additional, Elenitoba-Johnson, Kojo S.J., additional, Facchetti, Fabio, additional, Fend, Falko, additional, Ferry, Judith A., additional, Filie, Armando C., additional, Foucar, Kathryn, additional, García, Juan F., additional, Gascoyne, Randy D., additional, Gaulard, Philippe, additional, Greiner, Timothy C., additional, Hamilton, Katherine S., additional, Harris, Nancy Lee, additional, Hasserjian, Robert P., additional, Head, David R., additional, Heerema-McKenney, Amy, additional, Horny, Hans-Peter, additional, Houldsworth, Jane, additional, Hsi, Eric D., additional, Hutchison, Robert E., additional, Hyjek, Elizabeth, additional, Isaacson, Peter G., additional, Jaffe, Elaine S., additional, Jaffe, Ronald, additional, Jares, Pedro, additional, Jones, Dan, additional, Kadin, Marshall E., additional, Ko, Young Hyeh, additional, Kroft, Steven H., additional, Kumar, Shimareet, additional, Lamant-Rochaix, Laurence, additional, LeBoit, Philip E., additional, de Leval, Laurence, additional, Lim, Megan S., additional, McKenna, Robert W., additional, Medeiros, L. Jeffrey, additional, Mollejo, Manuela, additional, Montgomery, Karen Dyer, additional, Nanjangud, Gouri, additional, Natkunam, Yasodha, additional, Nelson, Beverly P., additional, Nguyen, Phuong L., additional, O’Malley, Dennis P., additional, Orazi, Attilio, additional, Ott, German, additional, Palanisamy, Nallasivam, additional, Peterson, LoAnn C., additional, Piris, Miguel A., additional, Pittaluga, Stefania, additional, Poppema, Sibrand, additional, Porwit, Anna, additional, Quintanilla-Martinez,, Priv.Doz.Dr. Leticia, additional, Racke, Frederick Karl, additional, Raffeld, Mark, additional, Ralfkiaer, Elisabeth, additional, Rezk, Sherif A., additional, Rosenthal, Nancy S., additional, Said, Jonathan, additional, Schnitzer, Bertram, additional, Siebert, Reiner, additional, Sotlar, Karl, additional, Stetler-Stevenson, Maryalice, additional, Sullivan, John L., additional, Swerdlow, Steven H., additional, Valent, Peter, additional, Vardiman, James W., additional, Viswanatha, David S., additional, Warnke, Roger A., additional, Weir, Edward G., additional, Weiss, Lawrence M., additional, Wilson, Carla S., additional, Woda, Bruce A., additional, Yuan, Constance M., additional, and Zhou, Fan, additional

Published
2011
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185. The International Consensus Classification of Mature Lymphoid Neoplasms: a report from the Clinical Advisory Committee

Author

Campo, Elias, Jaffe, Elaine S., Cook, James R., Quintanilla-Martinez, Leticia, Swerdlow, Steven H., Anderson, Kenneth C., Brousset, Pierre, Cerroni, Lorenzo, de Leval, Laurence, Dirnhofer, Stefan, Dogan, Ahmet, Feldman, Andrew L., Fend, Falko, Friedberg, Jonathan W., Gaulard, Philippe, Ghia, Paolo, Horwitz, Steven M., King, Rebecca L., Salles, Gilles, San-Miguel, Jesus, Seymour, John F., Treon, Steven P., Vose, Julie M., Zucca, Emanuele, Advani, Ranjana, Ansell, Stephen, Au, Wing-Yan, Barrionuevo, Carlos, Bergsagel, Leif, Chan, Wing C., Cohen, Jeffrey I., d’Amore, Francesco, Davies, Andrew, Falini, Brunangelo, Ghobrial, Irene M., Goodlad, John R., Gribben, John G., Hsi, Eric D., Kahl, Brad S., Kim, Won-Seog, Kumar, Shaji, LaCasce, Ann S., Laurent, Camille, Lenz, Georg, Leonard, John P., Link, Michael P., Lopez-Guillermo, Armando, Mateos, Maria Victoria, Macintyre, Elizabeth, Melnick, Ari M., Morschhauser, Franck, Nakamura, Shigeo, Narbaitz, Marina, Pavlovsky, Astrid, Pileri, Stefano A., Piris, Miguel, Pro, Barbara, Rajkumar, Vincent, Rosen, Steven T., Sander, Birgitta, Sehn, Laurie, Shipp, Margaret A., Smith, Sonali M., Staudt, Louis M., Thieblemont, Catherine, Tousseyn, Thomas, Wilson, Wyndham H., Yoshino, Tadashi, Zinzani, Pier-Luigi, Dreyling, Martin, Scott, David W., Winter, Jane N., and Zelenetz, Andrew D.

Abstract

Since the publication of the Revised European-American Classification of Lymphoid Neoplasms in 1994, subsequent updates of the classification of lymphoid neoplasms have been generated through iterative international efforts to achieve broad consensus among hematopathologists, geneticists, molecular scientists, and clinicians. Significant progress has recently been made in the characterization of malignancies of the immune system, with many new insights provided by genomic studies. They have led to this proposal. We have followed the same process that was successfully used for the third and fourth editions of the World Health Organization Classification of Hematologic Neoplasms. The definition, recommended studies, and criteria for the diagnosis of many entities have been extensively refined. Some categories considered provisional have now been upgraded to definite entities. Terminology for some diseases has been revised to adapt nomenclature to the current knowledge of their biology, but these modifications have been restricted to well-justified situations. Major findings from recent genomic studies have impacted the conceptual framework and diagnostic criteria for many disease entities. These changes will have an impact on optimal clinical management. The conclusions of this work are summarized in this report as the proposed International Consensus Classification of mature lymphoid, histiocytic, and dendritic cell tumors.

Published
2022
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186. DNMT3A mutations define a unique biological and prognostic subgroup associated with cytotoxic T cells in PTCL-NOS

Author

Herek, Tyler A., Bouska, Alyssa, Lone, Waseem, Sharma, Sunandini, Amador, Catalina, Heavican, Tayla B., Li, Yuping, Wei, Qi, Jochum, Dylan, Greiner, Timothy C., Smith, Lynette, Pileri, Stefano, Feldman, Andrew L., Rosenwald, Andreas, Ott, German, Lim, Soon Thye, Ong, Choon Kiat, Song, Joo, Jaffe, Elaine S., Wang, Gang Greg, Staudt, Louis, Rimsza, Lisa M., Vose, Julie, d’Amore, Francesco, Weisenburger, Dennis D., Chan, Wing C., and Iqbal, Javeed

Abstract

Peripheral T-cell lymphomas (PTCLs) are heterogenous T-cell neoplasms often associated with epigenetic dysregulation. We investigated de novo DNA methyltransferase 3A (DNMT3A) mutations in common PTCL entities, including angioimmunoblastic T-cell lymphoma and novel molecular subtypes identified within PTCL–not otherwise specified (PTCL-NOS) designated as PTCL-GATA3 and PTCL-TBX21. DNMT3A-mutated PTCL-TBX21 cases showed inferior overall survival (OS), with DNMT3A-mutated residues skewed toward the methyltransferase domain and dimerization motif (S881–R887). Transcriptional profiling demonstrated significant enrichment of activated CD8+ T-cell cytotoxic gene signatures in the DNMT3A-mutant PTCL-TBX21 cases, which was further validated using immunohistochemistry. Genomewide methylation analysis of DNMT3A-mutant vs wild-type (WT) PTCL-TBX21 cases demonstrated hypomethylation in target genes regulating interferon-γ (IFN-γ), T-cell receptor signaling, and EOMES (eomesodermin), a master transcriptional regulator of cytotoxic effector cells. Similar findings were observed in a murine model of PTCL with Dnmt3a loss (in vivo) and further validated in vitro by ectopic expression of DNMT3A mutants (DNMT3A-R882, -Q886, and -V716, vs WT) in CD8+ T-cell line, resulting in T-cell activation and EOMES upregulation. Furthermore, stable, ectopic expression of the DNMT3A mutants in primary CD3+ T-cell cultures resulted in the preferential outgrowth of CD8+ T cells with DNMT3AR882H mutation. Single-cell RNA sequencing(RNA-seq) analysis of CD3+ T cells revealed differential CD8+ T-cell subset polarization, mirroring findings in DNMT3A-mutated PTCL-TBX21 and validating the cytotoxic and T-cell memory transcriptional programs associated with the DNMT3AR882H mutation. Our findings indicate that DNMT3A mutations define a cytotoxic subset in PTCL-TBX21 with prognostic significance and thus may further refine pathological heterogeneity in PTCL-NOS and suggest alternative treatment strategies for this subset.

Published
2022
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187. Genomic profiling identifies distinct genetic subtypes in extra-nodal natural killer/T-cell lymphoma

Author

Dong, Gehong, Liu, Xuxiang, Wang, Lifu, Yin, Wenjuan, Bouska, Alyssa, Gong, Qiang, Shetty, Kunal, Chen, Lu, Sharma, Sunandini, Zhang, Jibin, Lome-Maldonado, Carmen, Quintanilla-Martinez, Leticia, Li, Yuping, Song, Joo Y., Zhang, Wenyan, Shi, Yunfei, Wang, Jinhui, Kong, Lingbo, Wu, Xiwei, Wang, Jingwen, Liu, Hong-gang, Kong, Lingfei, Sun, Wenyong, Liu, Weiping, Wang, Lili, McKeithan, Timothy W., Iqbal, Javeed, and Chan, Wing C.

Abstract

Extra-nodal NK/T-cell lymphoma, nasal type (ENKTCL) is a highly aggressive Epstein-Barr virus associated lymphoma, typically presenting in the nasal and paranasal areas. We assembled a large series of ENKTCL (n= 209) for comprehensive genomic analysis and correlative clinical study. The International Lymphoma Prognostic Index (IPI), site of disease, stage, lymphadenopathy, and hepatomegaly were associated with overall survival. Genetic analysis revealed frequent oncogenic activation of the JAK/STAT3 pathway and alterations in tumor suppressor genes (TSGs) and genes associated with epigenomic regulation. Integrated genomic analysis including recurrent mutations and genomic copy number alterations using consensus clustering identified seven distinct genetic clusters that were associated with different clinical outcomes, thus constituting previously unrecognized risk groups. The genetic profiles of ENTKCLs from Asian and Hispanic ethnic groups showed striking similarity, indicating shared pathogenetic mechanism and tumor evolution. Interestingly, we discovered a novel functional cooperation between activating STAT3mutations and loss of the TSG, PRDM1, in promoting NK-cell growth and survival. This study provides a genetic roadmap for further analysis and facilitates investigation of actionable therapeutic opportunities in this aggressive lymphoma.

Published
2022
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188. Oligonucleotide microarrays demonstrate the highest frequency of ATM mutations in the mantle cell subtype of lymphoma

Author

Fang, Nicole Y., Greiner, Timothy C., Weisenburger, Dennis D., Chan, Wing C., Vose, Julie M., Smith, Lynette M., Armitage, James O., Mayer, R. Aeryn, Pike, Brian L., Collins, Francis, and Hacia, Joseph G.

Subjects
T cells -- Physiological aspects, Lymphomas -- Physiological aspects, Science and technology
Abstract

Mutations have been described in the ataxia telangiectasia mutated (ATM) gene in small numbers of cases of lymphoid neoplasia. However, surveys of the ATM mutation status in lymphoma have been limited due to the large size (62 exons) and complex mutational spectrum of this gene. We have used microarray-based assays with 250,000 oligonucleotides to screen lymphomas from 120 patients for all possible ATM coding and splice junction mutations. The subtypes included were diffuse large B cell, mantle cell, immunoblastic large B cell, follicular, posttransplant lymphoproliferative disorder, and peripheral T cell lymphoma. We found the highest percentage of ATM mutations within the mantle cell (MCL) subtype (43%, 12 of 28 cases), followed by a lower level (10% of cases) in the other subtypes. A frame-shift ATM mutation was found in one peripheral T cell lymphoma patient. In six MCL cases examined, four ATM variants were due to somatic mutation in the tumor cells whereas two others seemed to be germ-line in origin. There was no difference in p53 mutation status in the ATM mutant and wild-type groups of MCL. There was no statistically significant difference in the median overall survival of patients with wild-type vs. mutated ATM in MCL. Additional mutational and functional analyses are needed to determine whether ATM mutations contribute to the development and progression of MCL or are just the consequence of genomic instability in MCL.

Published
2003

190. Loss of major histocompatibility class II expression in non-immune-privileged site diffuse large B-cell lymphoma is highly coordinated and not due to chromosomal deletions

Author

Rimsza, Lisa M., Roberts, Robin A., Campo, Elias, Grogan, Thomas M., Bea, Silvia, Salaverria, Itziar, Zettl, Andreas, Rosenwald, Andreas, Ott, German, Muller-Hermelink, H. Konrad, Delabie, Jan, Fisher, Richard I., Unger, Joseph M., LeBlanc, Michael, Staudt, Louis M., Jaffe, Elaine S., Gascoyne, Randy D., Chan, Wing C., Weisenburger, Dennis D., Greiner, Timothy, Braziel, Rita M., and Miller, Thomas P.

Published
2006
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191. The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma

Author

Rosenwald, Andreas, Wright, George, Chan, Wing C., Connors, Joseph M., Campo, Elias, Fisher, Richard I., Gascoyne, Randy D., Muller-Hermelink, H. Konrad, Smeland, Erlend B., and Staudt, Louis M.

Subjects
Lymphomas -- Genetic aspects
Abstract

Researchers have found 17 genes that can be used to determine the prognosis of a patient with diffuse large-B-cell lymphoma. They did this by analyzing DNA from tumor biopsy samples of 240 patients with this type of cancer.

Published
2002

192. Burkitt lymphoma pathogenesis and therapeutic targets from structural and functional genomics

Author

Schmitz, Roland, Young, Ryan M., Ceribelli, Michele, Jhavar, Sameer, Xiao, Wenming, Zhang, Meili, Wright, George, Shaffer, Arthur L., Hodson, Daniel J., Buras, Eric, Liu, Xuelu, Powell, John, Yang, Yandan, Xu, Weihong, Zhao, Hong, Kohlhammer, Holger, Rosenwald, Andreas, Kluin, Philip, Müller-Hermelink, Hans Konrad, Ott, German, Gascoyne, Randy D., Connors, Joseph M., Rimsza, Lisa M., Campo, Elias, Jaffe, Elaine S., Delabie, Jan, Smeland, Erlend B., Ogwang, Martin D., Reynolds, Steven J., Fisher, Richard I., Braziel, Rita M., Tubbs, Raymond R., Cook, James R., Weisenburger, Dennis D., Chan, Wing C., Pittaluga, Stefania, Wilson, Wyndham, Waldmann, Thomas A., Rowe, Martin, Mbulaiteye, Sam M., Rickinson, Alan B., and Staudt, Louis M.

Published
2012
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197. Integrated profiling of diffuse large B-cell lymphoma with 7q gain

Author

Chigrinova, Ekaterina, Mian, Michael, Shen, Yulei, Greiner, Timothy C., Chan, Wing C., Vose, Julie M., Inghirami, Giorgio, Chiappella, Annalisa, Baldini, Luca, Ponzoni, Maurilio, Ferreri, Andrés J. M., Franceschetti, Silvia, Gaidano, Gianluca, Tucci, Alessandra, Facchetti, Fabio, Lazure, Thierry, Lambotte, Olivier, Montes-Moreno, Santiago, Piris, Miguel A., Zucca, Emanuele, Kwee, Ivo, and Bertoni, Francesco

Published
2011
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198. Oncogenically active MYD88 mutations in human lymphoma

Author

Ngo, Vu N., Young, Ryan M., Schmitz, Roland, Jhavar, Sameer, Xiao, Wenming, Lim, Kian-Huat, Kohlhammer, Holger, Xu, Weihong, Yang, Yandan, Zhao, Hong, Shaffer, Arthur L., Romesser, Paul, Wright, George, Powell, John, Rosenwald, Andreas, Muller-Hermelink, Hans Konrad, Ott, German, Gascoyne, Randy D., Connors, Joseph M., Rimsza, Lisa M., Campo, Elias, Jaffe, Elaine S., Delabie, Jan, Smeland, Erlend B., Fisher, Richard I., Braziel, Rita M., Tubbs, Raymond R., Cook, J. R., Weisenburger, Denny D., Chan, Wing C., and Staudt, Louis M.

Published
2011
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200. The novel lncRNA BlackMamba controls the neoplastic phenotype of ALK− anaplastic large cell lymphoma by regulating the DNA helicase HELLS

Author

Fragliasso, Valentina, primary, Verma, Akanksha, additional, Manzotti, Gloria, additional, Tameni, Annalisa, additional, Bareja, Rohan, additional, Heavican, Tayla B., additional, Iqbal, Javeed, additional, Wang, Rui, additional, Fiore, Danilo, additional, Mularoni, Valentina, additional, Chan, Wing C., additional, Lhoumaud, Priscillia, additional, Skok, Jane, additional, Zanetti, Eleonora, additional, Merli, Francesco, additional, Ciarrocchi, Alessia, additional, Elemento, Oliver, additional, and Inghirami, Giorgio, additional

Published
2020
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