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3. Growth dynamics in naturally progressing chronic lymphocytic leukaemia

Author

Gruber, Michaela, Bozic, Ivana, Leshchiner, Ignaty, Livitz, Dimitri, Stevenson, Kristen, Rassenti, Laura, Rosebrock, Daniel, Taylor-Weiner, Amaro, Olive, Oriol, Goyetche, Reaha, Fernandes, Stacey M, Sun, Jing, Stewart, Chip, Wong, Alicia, Cibulskis, Carrie, Zhang, Wandi, Reiter, Johannes G, Gerold, Jeffrey M, Gribben, John G, Rai, Kanti R, Keating, Michael J, Brown, Jennifer R, Neuberg, Donna, Kipps, Thomas J, Nowak, Martin A, Getz, Gad, and Wu, Catherine J

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Oncology and Carcinogenesis, Cancer, Cancer Genomics, Biotechnology, Lymphoma, Human Genome, Lymphatic Research, Rare Diseases, Hematology, Clinical Research, Genetics, 2.1 Biological and endogenous factors, Cell Proliferation, Clone Cells, Cohort Studies, Disease Progression, Evolution, Molecular, Female, High-Throughput Nucleotide Sequencing, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Male, Neoplasm Recurrence, Local, Recurrence, Reproducibility of Results, General Science & Technology
Abstract

How the genomic features of a patient's cancer relate to individual disease kinetics remains poorly understood. Here we used the indolent growth dynamics of chronic lymphocytic leukaemia (CLL) to analyse the growth rates and corresponding genomic patterns of leukaemia cells from 107 patients with CLL, spanning decades-long disease courses. We found that CLL commonly demonstrates not only exponential expansion but also logistic growth, which is sigmoidal and reaches a certain steady-state level. Each growth pattern was associated with marked differences in genetic composition, the pace of disease progression and the extent of clonal evolution. In a subset of patients, whose serial samples underwent next-generation sequencing, we found that dynamic changes in the disease course of CLL were shaped by the genetic events that were already present in the early slow-growing stages. Finally, by analysing the growth rates of subclones compared with their parental clones, we quantified the growth advantage conferred by putative CLL drivers in vivo.

Published
2019

5. Correction to: Intraclonal Complexity in Chronic Lymphocytic Leukemia: Fractions Enriched in Recently Born/Divided and Older/Quiescent Cells

Author

Calissano, Carlo, Damle, Rajendra N., Marsilio, Sonia, Yan, Xiao-Jie, Yancopoulos, Sophia, Hayes, Gregory, Emson, Claire, Murphy, Elizabeth J., Hellerstein, Marc K., Sison, Cristina, Kaufman, Matthew S., Kolitz, Jonathan E., Allen, Steven L., Rai, Kanti R., Ivanovic, Ivana, Dozmorov, Igor M., Roa, Sergio, Scharff, Matthew D., Li, Wentian, and Chiorazzi, Nicholas

Published
2022
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6. AID overexpression leads to aggressive murine CLL and nonimmunoglobulin mutations that mirror human neoplasms

Author

Morande, Pablo Elías, Yan, Xiao-Jie, Sepulveda, Julieta, Seija, Noé, Marquez, María Elena, Sotelo, Natalia, Abreu, Cecilia, Crispo, Martina, Fernández-Graña, Gabriel, Rego, Natalia, Bois, Therence, Methot, Stephen P., Palacios, Florencia, Remedi, Victoria, Rai, Kanti R., Buschiazzo, Alejandro, Di Noia, Javier M., Navarrete, Marcelo A., Chiorazzi, Nicholas, and Oppezzo, Pablo

Published
2021
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7. Myeloid-derived suppressor cell subtypes differentially influence T-cell function, T-helper subset differentiation, and clinical course in CLL

Author

Ferrer, Gerardo, Jung, Byeongho, Chiu, Pui Yan, Aslam, Rukhsana, Palacios, Florencia, Mazzarello, Andrea Nicola, Vergani, Stefano, Bagnara, Davide, Chen, Shih-Shih, Yancopoulos, Sophia, Xochelli, Aliki, Yan, Xiao-Jie, Burger, Jan A., Barrientos, Jacqueline C., Kolitz, Jonathan E., Allen, Steven L., Stamatopoulos, Kostas, Rai, Kanti R., Sherry, Barbara, and Chiorazzi, Nicholas

Published
2021
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8. Phase 2 study of the safety and efficacy of umbralisib in patients with CLL who are intolerant to BTK or PI3Kδ inhibitor therapy

Author

Mato, Anthony R., Ghosh, Nilanjan, Schuster, Stephen J., Lamanna, Nicole, Pagel, John M., Flinn, Ian W., Barrientos, Jacqueline C., Rai, Kanti R., Reeves, James A., Cheson, Bruce D., Barr, Paul M., Kambhampati, Suman, Lansigan, Frederick, Pu, Jeffrey J., Skarbnik, Alan P., Roeker, Lindsey, Fonseca, Gustavo A., Sitlinger, Andrea, Hamadeh, Issam S., Dorsey, Colleen, LaRatta, Nicole, Weissbrot, Hanna, Luning Prak, Eline T., Tsao, Patricia, Paskalis, Dana, Sportelli, Peter, Miskin, Hari P., Weiss, Michael S., Svoboda, Jakub, and Brander, Danielle M.

Published
2021
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9. Chronic lymphocytic leukemia–like monoclonal B-cell lymphocytosis exhibits an increased inflammatory signature that is reduced in early-stage chronic lymphocytic leukemia

Author

Blanco, Gonzalo, Puiggros, Anna, Sherry, Barbara, Nonell, Lara, Calvo, Xavier, Puigdecanet, Eulàlia, Chiu, Pui Yan, Kieso, Yasmine, Ferrer, Gerardo, Palacios, Florencia, Arnal, Magdalena, Rodríguez-Rivera, María, Gimeno, Eva, Abella, Eugènia, Rai, Kanti R., Abrisqueta, Pau, Bosch, Francesc, Calon, Alexandre, Ferrer, Ana, Chiorazzi, Nicholas, and Espinet, Blanca

Published
2021
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12. Developmental subtypes assessed by DNA methylation-iPLEX forecast the natural history of chronic lymphocytic leukemia

Author

Giacopelli, Brian, Zhao, Qiuhong, Ruppert, Amy S., Agyeman, Akwasi, Weigel, Christoph, Wu, Yue-Zhong, Gerber, Madelyn M., Rabe, Kari G., Larson, Melissa C., Lu, Junyan, Blachly, James S., Rogers, Kerry A., Wierda, William G., Brown, Jennifer R., Rai, Kanti R., Keating, Michael, Rassenti, Laura Z., Kipps, Thomas J., Zenz, Thorsten, Shanafelt, Tait D., Kay, Neil E., Abruzzo, Lynne V., Coombes, Kevin R., Woyach, Jennifer A., Byrd, John C., and Oakes, Christopher C.

Published
2019
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13. Lenalidomide and Rituximab for the Initial Treatment of Patients With Chronic Lymphocytic Leukemia: A Multicenter Clinical-Translational Study From the Chronic Lymphocytic Leukemia Research Consortium

Author

James, Danelle F, Werner, Lillian, Brown, Jennifer R, Wierda, William G, Barrientos, Jacqueline C, Castro, Januario E, Greaves, Andrew, Johnson, Amy J, Rassenti, Laura Z, Rai, Kanti R, Neuberg, Donna, and Kipps, Thomas J

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Oncology and Carcinogenesis, Clinical Trials and Supportive Activities, Clinical Research, Hematology, Rare Diseases, Lymphatic Research, Lymphoma, Patient Safety, Cancer, 6.1 Pharmaceuticals, 6.2 Cellular and gene therapies, Aged, Aged, 80 and over, Antibodies, Monoclonal, Murine-Derived, Antineoplastic Combined Chemotherapy Protocols, Disease-Free Survival, Drug Administration Schedule, Female, Humans, Immunophenotyping, Kaplan-Meier Estimate, Lenalidomide, Leukemia, Lymphocytic, Chronic, B-Cell, Male, Middle Aged, Polymorphism, Single Nucleotide, Prognosis, Receptors, Fc, Risk Factors, Rituximab, Thalidomide, Treatment Outcome, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

PurposeLenalidomide is an immunomodulatory agent with therapeutic activity in chronic lymphocytic leukemia (CLL). In preclinical models, lenalidomide acted synergistically with rituximab. The CLL Research Consortium initiated a phase II study to evaluate this combination in treatment-naive patients.Patients and methodsLenalidomide was initiated at 2.5 mg/day and was escalated based on treatment tolerability to a maximum of 10 mg/day, for 21 days/cycle, for a maximum of seven cycles. Rituximab was administered at the end of cycle 1 and was continued for seven cycles. Patients received allopurinol and aspirin for prophylaxis.ResultsSixty-nine patients enrolled onto one of two age-specific strata; patients' median age was 56 and 70 years for arms A and B, respectively. Patients in the older-patient stratum more frequently had elevated serum beta-2 microglobulin levels, high-risk Rai stage, and were less likely to complete the maximum planned therapy. Adverse events were similar in the two arms. Nonhematologic toxicity was predominantly at grade 1/2, and neutropenia was the most common hematologic adverse event. The response rate for arm A was 95%, with 20% complete responses (CRs) and 20% nodular partial responses. Of arm B patients, 78% achieved a response, of which 11% were CRs. Median progression-free survival (PFS) was 19 months for the younger cohort and 20 months for the older cohort.ConclusionIntrapatient dose-escalation was safe. The majority of patients reached the maximum lenalidomide dose and experienced a response to a defined seven-cycle course of lenalidomide and rituximab therapy. Despite differences in baseline characteristics and the response rate between the two strata, the PFS did not differ.

Published
2014

14. iwCLL guidelines for diagnosis, indications for treatment, response assessment, and supportive management of CLL

Author

Hallek, Michael, Cheson, Bruce D., Catovsky, Daniel, Caligaris-Cappio, Federico, Dighiero, Guillermo, Döhner, Hartmut, Hillmen, Peter, Keating, Michael, Montserrat, Emili, Chiorazzi, Nicholas, Stilgenbauer, Stephan, Rai, Kanti R., Byrd, John C., Eichhorst, Barbara, O'Brien, Susan, Robak, Tadeusz, Seymour, John F., and Kipps, Thomas J.

Published
2018
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15. Characterization of the Intraclonal Complexity of Chronic Lymphocytic Leukemia B Cells: Potential Influences of B-Cell Receptor Crosstalk with Other Stimuli

Author

Mazzarello, Andrea N., primary, Fitch, Mark, additional, Cardillo, Martina, additional, Ng, Anita, additional, Bhuiya, Sabreen, additional, Sharma, Esha, additional, Bagnara, Davide, additional, Kolitz, Jonathan E., additional, Barrientos, Jacqueline C., additional, Allen, Steven L., additional, Rai, Kanti R., additional, Rhodes, Joanna, additional, Hellerstein, Marc K., additional, and Chiorazzi, Nicholas, additional

Published
2023
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16. B cell receptor isotypes differentially associate with cell signaling, kinetics, and outcome in chronic lymphocytic leukemia

Author

Mazzarello, Andrea N., Gentner-Gobel, Eva, Minden, Marcus Duhren-von, Tarasenko, Tatyana N., Nicolo, Antonella, Ferrer, Gerardo, Vergani, Stefano, Liu, Yun, Bagnara, Davide, Rai, Kanti R., Burger, Jan A., McGuire, Peter J., Maity, Palash C., Jumaa, Hassan, and Chiorazzi, Nicholas

Subjects
Development and progression, Genetic aspects, Patient outcomes, Health aspects, B cells -- Genetic aspects -- Health aspects, Cellular signal transduction -- Genetic aspects -- Health aspects, Chronic lymphocytic leukemia -- Genetic aspects -- Development and progression -- Patient outcomes, Immunoglobulins -- Genetic aspects -- Health aspects
Abstract

Introduction Chronic lymphocytic leukemia (CLL), the most prevalent leukemia among individuals of European descent, is a clonal disease of human B lymphocytes expressing membrane CD5 (1, 2). The disease is [...], In chronic lymphocytic leukemia (CLL), the B cell receptor (BCR) plays a critical role in disease development and progression, as indicated by the therapeutic efficacy of drugs blocking BCR signaling. However, the mechanism(s) underlying BCR responsiveness are not completely defined. Selective engagement of membrane IgM or IgD on CLL cells, each coexpressed by more than 90% of cases, leads to distinct signaling events. Since both IgM and IgD carry the same antigen-binding domains, the divergent actions of the receptors are attributed to differences in immunoglobulin (Ig) structure or the outcome of signal transduction. We showed that IgM, not IgD, level and organization associated with CLL-cell birth rate and the type and consequences of BCR signaling in humans and mice. The latter IgM-driven effects were abrogated when BCR signaling was inhibited. Collectively, these studies demonstrated a critical, selective role for IgM in BCR signaling and B cell fate decisions, possibly opening new avenues for CLL therapy.

Published
2022
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17. Consensus guidelines for the diagnosis and management of patients with classic hairy cell leukemia

Author

Grever, Michael R., Abdel-Wahab, Omar, Andritsos, Leslie A., Banerji, Versha, Barrientos, Jacqueline, Blachly, James S., Call, Timothy G., Catovsky, Daniel, Dearden, Claire, Demeter, Judit, Else, Monica, Forconi, Francesco, Gozzetti, Alessandro, Ho, Anthony D., Johnston, James B., Jones, Jeffrey, Juliusson, Gunnar, Kraut, Eric, Kreitman, Robert J., Larratt, Loree, Lauria, Francesco, Lozanski, Gerard, Montserrat, Emili, Parikh, Sameer A., Park, Jae H., Polliack, Aaron, Quest, Graeme R., Rai, Kanti R., Ravandi, Farhad, Robak, Tadeusz, Saven, Alan, Seymour, John F., Tadmor, Tamar, Tallman, Martin S., Tam, Constantine, Tiacci, Enrico, Troussard, Xavier, Zent, Clive S., Zenz, Thorsten, Zinzani, Pier Luigi, and Falini, Brunangelo

Published
2017
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18. Chronic lymphocytic leukemia B cells can undergo somatic hypermutation and intraclonal immunoglobulin V(H)DJ(H) gene diversification.

Author

Gurrieri, Carmela, McGuire, Peter, Zan, Hong, Yan, Xiao-Jie, Cerutti, Andrea, Albesiano, Emilia, Allen, Steven L, Vinciguerra, Vincent, Rai, Kanti R, Ferrarini, Manlio, Casali, Paolo, and Chiorazzi, Nicholas

Subjects
Humans, DNA, Neoplasm, DNA, Complementary, Evolution, Molecular, Antibody Diversity, Gene Rearrangement, B-Lymphocyte, Heavy Chain, Point Mutation, Polymorphism, Single-Stranded Conformational, Molecular Sequence Data, Female, Male, Leukemia, Lymphocytic, Chronic, B-Cell, In Vitro Techniques, B lymphocyte, chronic lymphocytic leukemia, somatic hypermutation, Ig gene, V gene diversification, DNA, Complementary, Neoplasm, Evolution, Molecular, Gene Rearrangement, B-Lymphocyte, Heavy Chain, Leukemia, Lymphocytic, Chronic, B-Cell, Polymorphism, Single-Stranded Conformational, Medical and Health Sciences, Immunology
Abstract

Chronic lymphocytic leukemia (CLL) arises from the clonal expansion of a CD5(+) B lymphocyte that is thought not to undergo intraclonal diversification. Using V(H)DJ(H) cDNA single strand conformation polymorphism analyses, we detected intraclonal mobility variants in 11 of 18 CLL cases. cDNA sequence analyses indicated that these variants represented unique point-mutations (1-35/patient). In nine cases, these mutations were unique to individual submembers of the CLL clone, although in two cases they occurred in a large percentage of the clonal submembers and genealogical trees could be identified. The diversification process responsible for these changes led to single nucleotide changes that favored transitions over transversions, but did not target A nucleotides and did not have the replacement/silent nucleotide change characteristics of antigen-selected B cells. Intraclonal diversification did not correlate with the original mutational load of an individual CLL case in that diversification was as frequent in CLL cells with little or no somatic mutations as in those with considerable mutations. Finally, CLL B cells that did not exhibit intraclonal diversification in vivo could be induced to mutate their V(H)DJ(H) genes in vitro after stimulation. These data indicate that a somatic mutation mechanism remains functional in CLL cells and could play a role in the evolution of the clone.

Published
2002

22. Supplementary Figure S2 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model

Author

Chen, Shih-Shih, primary, Barrientos, Jacqueline C., primary, Ferrer, Gerardo, primary, King-Richards, Morgan, primary, Chen, Yu-Ju, primary, Ravichandran, Priyadarshini, primary, Ibrahim, Michael, primary, Kieso, Yasmine, primary, Waters, Sheila, primary, Kutok, Jeffery L., primary, Peluso, Marisa, primary, Sharma, Sujata, primary, Weaver, David T., primary, Pachter, Jonathan A., primary, Rai, Kanti R., primary, and Chiorazzi, Nicholas, primary

Published
2023
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23. Data from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model

Author

Chen, Shih-Shih, primary, Barrientos, Jacqueline C., primary, Ferrer, Gerardo, primary, King-Richards, Morgan, primary, Chen, Yu-Ju, primary, Ravichandran, Priyadarshini, primary, Ibrahim, Michael, primary, Kieso, Yasmine, primary, Waters, Sheila, primary, Kutok, Jeffery L., primary, Peluso, Marisa, primary, Sharma, Sujata, primary, Weaver, David T., primary, Pachter, Jonathan A., primary, Rai, Kanti R., primary, and Chiorazzi, Nicholas, primary

Published
2023
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24. Supplementary Table S1 from Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model

Author

Chen, Shih-Shih, primary, Barrientos, Jacqueline C., primary, Ferrer, Gerardo, primary, King-Richards, Morgan, primary, Chen, Yu-Ju, primary, Ravichandran, Priyadarshini, primary, Ibrahim, Michael, primary, Kieso, Yasmine, primary, Waters, Sheila, primary, Kutok, Jeffery L., primary, Peluso, Marisa, primary, Sharma, Sujata, primary, Weaver, David T., primary, Pachter, Jonathan A., primary, Rai, Kanti R., primary, and Chiorazzi, Nicholas, primary

Published
2023
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25. Duvelisib Eliminates CLL B Cells, Impairs CLL-Supporting Cells, and Overcomes Ibrutinib Resistance in a Xenograft Model

Author

Chen, Shih-Shih, primary, Barrientos, Jacqueline C., additional, Ferrer, Gerardo, additional, King-Richards, Morgan, additional, Chen, Yu-Ju, additional, Ravichandran, Priyadarshini, additional, Ibrahim, Michael, additional, Kieso, Yasmine, additional, Waters, Sheila, additional, Kutok, Jeffery L., additional, Peluso, Marisa, additional, Sharma, Sujata, additional, Weaver, David T., additional, Pachter, Jonathan A., additional, Rai, Kanti R., additional, and Chiorazzi, Nicholas, additional

Published
2023
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26. Abstract 4933: Duvelisib eliminates CLL B Cells, impairs CLL-supporting cells, and overcomes ibrutinib resistance in a patient-derived xenograft model

Author

Chen, Shih-Shih, primary, Barrientos, Jacqueline C., additional, Ferrer, Gerardo, additional, Ravichandran, Priyadarshini, additional, Ibrahim, Michael, additional, Kieso, Yasmine, additional, Kutok, Jeffery L., additional, Peluso, Marisa, additional, Sharma, Sujata, additional, Weaver, David T., additional, Pachter, Jonathan A., additional, Rai, Kanti R., additional, and Chiorazzi, Nicholas, additional

Published
2023
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27. CLL stereotyped B-cell receptor immunoglobulin sequences are recurrent in the B-cell repertoire of healthy individuals: Apparent lack of central and early peripheral tolerance censoring

Author

Vergani, Stefano, primary, Bagnara, Davide, additional, Agathangelidis, Andreas, additional, Ng, Anita Kar Yun, additional, Ferrer, Gerardo, additional, Mazzarello, Andrea N., additional, Palacios, Florencia, additional, Yancopoulos, Sophia, additional, Yan, Xiao-Jie, additional, Barrientos, Jaqueline C., additional, Rai, Kanti R., additional, Stamatopoulos, Kostas, additional, and Chiorazzi, Nicholas, additional

Published
2023
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29. Validation of ZAP-70 methylation and its relative significance in predicting outcome in chronic lymphocytic leukemia

Author

Claus, Rainer, Lucas, David M., Ruppert, Amy S., Williams, Katie E., Weng, Daniel, Patterson, Kara, Zucknick, Manuela, Oakes, Christopher C., Rassenti, Laura Z., Greaves, Andrew W., Geyer, Susan, Wierda, William G., Brown, Jennifer R., Gribben, John G., Barrientos, Jacqueline C., Rai, Kanti R., Kay, Neil E., Kipps, Thomas J., Shields, Peter, Zhao, Weiqiang, Grever, Michael R., Plass, Christoph, and Byrd, John C.

Published
2014
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31. Integrin Signaling Pathway Is Crucial for the Recently Divided Fraction of CLL Cells and Facilitates Cell Migration in a Disease Progressive Manner

Author

Yan, Xiao J., primary, Palacios, Florencia, additional, Chen, Shih-Shih, additional, Li, Wentian, additional, Rhodes, Joanna M., additional, Barrientos, Jacqueline C., additional, Allen, Steven L, additional, Kolitz, Jonathan E., additional, Rai, Kanti R, additional, and Chiorazzi, Nicholas, additional

Published
2022
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32. CLECL1+ CLL Cells: A Key Subset That Drives CLL Survival and Proliferation and Shapes a Th2-Biased Tumor Microenvironment

Author

Chen, Shih-Shih, primary, Yan, Xiao-Jie, additional, Cardillo, Martina, additional, Ng, Anita, additional, Shih, Andrew, additional, Blanco, Gonzalo, additional, King-Richards, Morgan, additional, Chen, Yu-Ju, additional, Kieso, Yasmine, additional, Rhodes, Joanna M., additional, Rai, Kanti R, additional, and Chiorazzi, Nicholas, additional

Published
2022
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33. CD8+ T Cells from Patients with CLL Show Evidence of Granzyme B and Perforin Cytotoxic Capacity, Which Is Enhanced upon Exposure to Exogenous IL2 and/or IL21

Author

Paraschivescu, Cristina, primary, Chhabra, Shivani, additional, Aslam, Rukhsana, additional, Jung, Byeongho, additional, Ferrer, Gerardo, additional, Barrientos, Jacqueline C., additional, Rhodes, Joanna M., additional, Kolitz, Jonathan E., additional, Allen, Steven L, additional, Rai, Kanti R, additional, Sherry, Barbara, additional, and Chiorazzi, Nicholas, additional

Published
2022
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34. Identification of Three Unique Clusters of Serum Proteins with Distinctive Functionalities in IGHV-Mutated MBL

Author

Blanco, Gonzalo, primary, Palacios, Florencia, additional, Vanarsa, Kamala, additional, Dugyala, Poojitha, additional, Chiu, Pui Yan, additional, Allen, Steven L, additional, Kieso, Yasmine, additional, Puiggros, Anna, additional, Barrientos, Jacqueline C., additional, Calvo, Xavier, additional, Kolitz, Jonathan E., additional, Gimeno, Eva, additional, Rhodes, Joanna M., additional, Ferrer, Ana, additional, Rai, Kanti R, additional, Sherry, Barbara, additional, Espinet, Blanca, additional, Mohan, Chandra, additional, and Chiorazzi, Nicholas, additional

Published
2022
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38. IGHV-unmutated and IGHV-mutated chronic lymphocytic leukemia cells produce activation-induced deaminase protein with a full range of biologic functions

Author

Patten, Piers E.M., Chu, Charles C., Albesiano, Emilia, Damle, Rajendra N., Yan, Xiao-Jie, Kim, Dorothy, Zhang, Lu, Magli, Amanda R., Barrientos, Jacqueline, Kolitz, Jonathan E., Allen, Steven L., Rai, Kanti R., Roa, Sergio, Mongini, Patricia K., MacCarthy, Thomas, Scharff, Matthew D., and Chiorazzi, Nicholas

Published
2012
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40. A seven-gene expression panel distinguishing clonal expansions of pre-leukemic and chronic lymphocytic leukemia B cells from normal B lymphocytes

Author

McCarthy, Brian A., Yancopoulos, Sophia, Tipping, Mike, Yan, Xiao-jie, Wang, Xue Ping, Bennett, Fiona, Li, Wentian, Lesser, Martin, Paul, Santanu, Boyle, Erin, Moreno, Carolina, Catera, Rosa, Messmer, Bradley T., Cutrona, Giovanna, Ferrarini, Manlio, Kolitz, Jonathan E., Allen, Steven L., Rai, Kanti R., Rawstron, Andrew C., and Chiorazzi, Nicholas

Published
2015
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42. Impact of the Types and Relative Quantities of IGHV Gene Mutations in Predicting Prognosis of Patients With Chronic Lymphocytic Leukemia

Author

Kaufman, Matthew, primary, Yan, Xiao-Jie, additional, Li, Wentian, additional, Ghia, Emanuela M., additional, Langerak, Anton W., additional, Rassenti, Laura Z., additional, Belessi, Chrysoula, additional, Kay, Neil E., additional, Davi, Frederic, additional, Byrd, John C., additional, Pospisilova, Sarka, additional, Brown, Jennifer R., additional, Catherwood, Mark, additional, Davis, Zadie, additional, Oscier, David, additional, Montillo, Marco, additional, Trentin, Livio, additional, Rosenquist, Richard, additional, Ghia, Paolo, additional, Barrientos, Jacqueline C., additional, Kolitz, Jonathan E., additional, Allen, Steven L., additional, Rai, Kanti R., additional, Stamatopoulos, Kostas, additional, Kipps, Thomas J., additional, Neuberg, Donna, additional, and Chiorazzi, Nicholas, additional

Published
2022
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43. Activated CLL cells regulate IL-17F–producing Th17 cells in miR155-dependent and outcome-specific manners

Author

Jung, Byeongho, primary, Ferrer, Gerardo, additional, Chiu, Pui Yan, additional, Aslam, Rukhsana, additional, Ng, Anita, additional, Palacios, Florencia, additional, Wysota, Michael, additional, Cardillo, Martina, additional, Kolitz, Jonathan E., additional, Allen, Steven L., additional, Barrientos, Jacqueline C., additional, Rai, Kanti R., additional, Chiorazzi, Nicholas, additional, and Sherry, Barbara, additional

Published
2022
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44. Impact of the Types and Relative Quantities of IGHV Gene Mutations in Predicting Prognosis of Patients With Chronic Lymphocytic Leukemia.

Author

Kaufman, Matthew, Kaufman, Matthew, Yan, Xiao-Jie, Li, Wentian, Ghia, Emanuela M, Langerak, Anton W, Rassenti, Laura Z, Belessi, Chrysoula, Kay, Neil E, Davi, Frederic, Byrd, John C, Pospisilova, Sarka, Brown, Jennifer R, Catherwood, Mark, Davis, Zadie, Oscier, David, Montillo, Marco, Trentin, Livio, Rosenquist, Richard, Ghia, Paolo, Barrientos, Jacqueline C, Kolitz, Jonathan E, Allen, Steven L, Rai, Kanti R, Stamatopoulos, Kostas, Kipps, Thomas J, Neuberg, Donna, Chiorazzi, Nicholas, Kaufman, Matthew, Kaufman, Matthew, Yan, Xiao-Jie, Li, Wentian, Ghia, Emanuela M, Langerak, Anton W, Rassenti, Laura Z, Belessi, Chrysoula, Kay, Neil E, Davi, Frederic, Byrd, John C, Pospisilova, Sarka, Brown, Jennifer R, Catherwood, Mark, Davis, Zadie, Oscier, David, Montillo, Marco, Trentin, Livio, Rosenquist, Richard, Ghia, Paolo, Barrientos, Jacqueline C, Kolitz, Jonathan E, Allen, Steven L, Rai, Kanti R, Stamatopoulos, Kostas, Kipps, Thomas J, Neuberg, Donna, and Chiorazzi, Nicholas

Abstract

Patients with CLL with mutated IGHV genes (M-CLL) have better outcomes than patients with unmutated IGHVs (U-CLL). Since U-CLL usually express immunoglobulins (IGs) that are more autoreactive and more effectively transduce signals to leukemic B cells, B-cell receptor (BCR) signaling is likely at the heart of the worse outcomes of CLL cases without/few IGHV mutations. A corollary of this conclusion is that M-CLL follow less aggressive clinical courses because somatic IGHV mutations have altered BCR structures and no longer bind stimulatory (auto)antigens and so cannot deliver trophic signals to leukemic B cells. However, the latter assumption has not been confirmed in a large patient cohort. We tried to address the latter by measuring the relative numbers of replacement (R) mutations that lead to non-conservative amino acid changes (Rnc) to the combined numbers of conservative (Rc) and silent (S) amino acid R mutations that likely do not or cannot change amino acids, "(S+Rc) to Rnc IGHV mutation ratio". When comparing time-to-first-treatment (TTFT) of patients with (S+Rc)/Rnc ≤ 1 and >1, TTFTs were similar, even after matching groups for equal numbers of samples and identical numbers of mutations per sample. Thus, BCR structural change might not be the main reason for better outcomes for M-CLL. Since the total number of IGHV mutations associated better with longer TTFT, better clinical courses appear due to the biologic state of a B cell having undergone many stimulatory events leading to IGHV mutations. Analyses of larger patient cohorts will be needed to definitively answer this question.

Published
2022

47. A novel adoptive transfer model of chronic lymphocytic leukemia suggests a key role for T lymphocytes in the disease

Author

Bagnara, Davide, Kaufman, Matthew S., Calissano, Carlo, Marsilio, Sonia, Patten, Piers E.M., Simone, Rita, Chum, Philip, Yan, Xiao-Jie, Allen, Steven L., Kolitz, Jonathan E., Baskar, Sivasubramanian, Rader, Christoph, Mellstedt, Hakan, Rabbani, Hodjattallah, Lee, Annette, Gregersen, Peter K., Rai, Kanti R., and Chiorazzi, Nicholas

Published
2011
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