Faculty Profile

Dr. B. Hilda Ye, Ph.D.

B. Hilda Ye, Ph.D.

Associate Professor, Department of Cell Biology

Areas of Research: We are studying how transcription regulation and cell signaling events govern lymphocyte differentiation and lymphoma development. The current focus is on diffuse large B-cell lymphoma and adult T-cell leukemia/lymphoma

Professional Interests

Transcription Regulation and Cell Signaling Control in Normal B/T Cells and Germinal Center Derived Lymphomas

Molecular pathogenesis of lymphomas situates at the crossroad of B cell differentiation, cancer genetics, transcription regulation, and cell signaling. Thus, we constantly draw upon the most recent advances in these perspective fields to address the mechanisms responsible for lymphoma initiation and development. As each lymphoma entity often corresponds to a specific lymphocyte activation/differentiation state that is phenotypically “frozen” by the malignant transformation process, our lymphoma-related studies also provide valuable insights to the regulatory mechanisms that govern the normal immune system. Our research has three major goals: to better understand mature B and T cell development in molecular terms, to decipher how this process is perturbed during lymphomagenesis, and to help develop better lymphoma therapy.

The germinal center (GC) response is a T-cell dependent B cell activation, expansion, and maturation process that has the unique property of generating high affinity antibodies and B cell memory. Because dysregulated GC responses contribute to the development of B cell lymphomas and autoimmune diseases, in-depth understanding of the control mechanisms governing the GC response has both immunological and clinical implications. GCs are dynamic and specialized structures in the secondary lymphoid organs where the B cell genome is subject to two types of genetic alterations catalyzed by AID (activation induced cytidine deaminase), e.g. Ig class switch recombination (CSR) and somatic hypermutation (SHM). Prior to their GC exit, B cells bearing mutated surface Ig molecules undergo positive and negative selections through interaction with two other types of cells in the GC, e.g. follicular dendritic cells and follicular T helper cells. As a result, only those B cells with the proper Ig specificity and affinity are allowed to escape the fate of apoptosis or anergy, gaining license to terminally differentiate into memory or plasma cells. At the single cell level, the acquisition and termination of GC phenotype is the coordinated transcriptional response to various extracellular and intracellular stimuli; yet the precise sequence and nature of events that orchestrate this process is incompletely understood. Two types of CD4 T cells are also critically important for proper GC development and function, namely follicular T helper (Tfh) cells and T follicular regulatory (Tfr) cells. We are particularly interested in two transcriptional factors, BCL6 and STAT3, both are known to play pivotal roles in the 3 types of GC cells described above. Within GC B cells, BCL6 coordinates the initiation of GC response and maintains the GC phenotype by regulating an extensive gene expression program which restricts B cell responsiveness to activation signals, genotoxic stress, and terminal differentiation potential. In the late phase of GC response, BCL6 downregulation triggers the rise of STAT3 expression and activity, which then collaborate with IRF4 to control the commitment step to the plasma cell fate. Functional studies of BCL6 within the Tfh and Tfr lineages are still at a relatively early stage with many unanswered questions.

Non-Hodgkin’s lymphoma (NHL) is the 5th most common type of cancer in the U.S. Many NHLs have a B cell phenotype and are transformed from normal GC B cells. A hallmark of the GC-associated lymphomagenesis is driver mutations generated by AID, an enzyme responsible for normal Ig CSR and SHM. In fact, BCL6 was initially cloned through its involvement in lymphoma-associated chromosomal translocations and is the most frequently targeted proto-oncogene in NHL. In past 25 years, our work has focused on the molecular pathogenesis and translational studies of diffuse large B cell lymphoma (DLBCL), the most common form of aggressive NHL. Recently, we have started to investigate the pathogenesis and immunologic features of adult T-cell leukemia/lymphoma (ATLL). ATLL is a rare CD4 T cell neoplasm, endemic in the Japanese, Caribbean and Latin American populations. It arises in HTLV-1 carriers and is an extremely aggressive cancer with a dismal outcome and lack of effective therapies. In a new study published in Blood, we demonstrate that ATLL patients diagnosed in North American have a distinct genomic landscape compared to the Japanese cohort. In particular, North American ATLL is characterized by a much higher frequency of prognostic epigenetic mutations and is targetable preclinically with DNA de-methylation drugs.

We are currently pursuing the following lines of studies:

1. Can the therapeutic outcome of the ABC subtype of DLBCLs be improved by manipulating the endogenous redox homeostasis of the lymphoma cells?

2. Novel mechanisms and novel physiological roles of BCL6 function.  

3. Molecular mechanism(s) underlying the extreme chemo-resistance of ATLL.

4. Role of dysregulated epigenome in the pathogenesis of ATLL.

5. The cell-of-original of ATLL.

Selected Publications

Shah UA, Chung EY, Giricz O, Pradhan K, Kataoka K, Gordon-Mitchell S, Bhagat TD, Mai Y, Wei Y, Ishida E, Choudhary GS, Joseph A, Rice R, Gitego N, Parrish C, Bartenstein M, Goel S, Mantzaris I, Shastri A, Derman O, Binder A, Gritsman K, Kornblum N, Braunschweig I, Bhagat C, Hall J, Graber A, Ratner L, Wang Y, Ogawa S, Verma A*, Ye BH*, Janakiram M*. North American ATLL has a Distinct Mutational and Transcriptional Profile and responds to epigenetic therapies. Blood. 2018 Aug 13. pii: blood-2018-01-824607. doi: 10.1182/blood-2018-01-824607. PMID: 30104217. * communication authors

Kuo PY, Jatiani SS, Rahman AH, Edwards D, Jiang Z, Ahr K, Perumal D, Leshchenko VV, Brody J, Shaknovich R, Ye BH, Parekh S.  SOX11 augments BCR signaling to drive MCL-like tumor development.  Blood. 2018 Apr 3. pii: blood-2018-02-832535. doi: 10.1182/blood-2018-02-832535. PMID: 29615403

Mai Y, Yu JJ, Bartholdy B, Xu-Monette ZY, Knapp EE, Yuan F, Chen H, Ding BB, Yao Z, Das B, Zou Y, Young KH, Parekh S, Ye BH. Subtype-specific mechanism for Doxorubicin-triggered cytotoxicity in diffuse large B cell lymphomas. Blood. 128(24):2797-2807, 2016. PMID: 27737889. [PDF FULL Text]

Alvarez, M. J., Shen, Y., Giorgi, F.M., Lachmann, A., Ding, B.B., Ye, B.H., Califano, A. Network-based inference of protein activity helps functionalize the genetic landscape of cancer. Nature Genet, 48(8):838-4, 2016. PMID: 27322546. [PDF Full Text]

Zell, M., Assal, A., Derman, O., Kornblum, N., Battini, R., Wang, Y., Mantzaris, I., Shastri, A., Verma, A., Ye, B.H., Braunschweig, I., and Janakiram, M. Adult T-Cell Leukemia/Lymphoma in the Caribbean cohort is a distinct clinical entity with dismal response to conventional chemotherapy. Oncotarget, 2016 Jun 22. doi: 10.18632/oncotarget.10223. PMID: 27341021. [PDF Full Text]

Geng H, Hurtz C, Lenz KB, Chen Z, Baumjohann D, Thompson S, Goloviznina NA, Chen WY, Huan J, LaTocha D, Ballabio E, Xiao G, Lee JW, Deucher A, Qi Z, Park E, Huang C, Nahar R, Kweon SM, Shojaee S, Chan LN, Yu J, Kornblau SM, Bijl JJ, Ye BH, Ansel KM, Paietta E, Melnick A, Hunger SP, Kurre P, Tyner JW, Loh ML, Roeder RG, Druker BJ, Burger JA, Milne TA, Chang BH, Müschen M. Self-Enforcing Feedback Activation between BCL6 and Pre-B Cell Receptor Signaling Defines a Distinct Subtype of Acute Lymphoblastic Leukemia. Cancer Cell. 27(3):409-25, 2015. PMID: 25759025. [PDF Full Text]

Zhao, H., Bauzon, F., Bi, E., Yu, J.J., Fu, H., Lu, Z., Cui, J., Jeon, H., Zang, X., Ye, B.H. and Zhu, L. Mutating Threonine 187 of p27 To An Alanine Prevents Pituitary Tumorigenesis By Two-Hit Loss Of Rb1 And Enhances Humoral Immunity In Old Age. J Biol Chem. 290(9):5787-809. 2015. PMID: 25583987, PMCID: PMC4342489.[PDF Full Text]

Kuo P.Y., Leshchenko V.V., Fazzari M.J., Perumal D., Gellen T., He T., Iqbal J., Baumgartner-Wennerholm S., Nygren L., Zhang F., Zhang W., Suh K.S., Goy A., Yang D.T., Chan W.C., Kahl B.S., Verma A.K., Gascoyne R.D., Kimby. E., Sander. B., Ye B.H., Melnick A.M., Parekh S. High resolution Chromatin Immunoprecipitation (ChIP) sequencing reveals novel bindings targets and prognostic role for SOX11 in Mantle cell lymphoma. Oncogene. 34(10):1231-4, 2015. PMID: 24681958, PMCID: PMC4511176. [PDF Full Text]

Wei, X., Xu, M., Wei, Y., Huang, F., Zhao, T., Li, X., Feng, R.*, and Ye, B.H.* The addition of rituximab to CHOP therapy altered the prognostic significance of CD44 expression. (*Communication authors). J Hematol Oncol. 7(1):34-36, 2014. PMID: 24739401, PMCID: PMC4022142. [PDF Full Text]

Huang, X., Meng, B., Iqbal, J., Ding, B.B., Perry, A.M., Cao, W., Smith, L.M., Bi, C., Jiang, C., Greiner, T.C., Weisenburger, D., Rimsza, L., Rosenwald, A., Ott, G., Delabie, J., Campo, E., Braziel, R., Gascoyne, R., Cook, J., Tubbs, R., Jaffe, E., Armitage, J., Vose, J., Staudt, L., McKeithan, T.W., Chan, W., Ye, B.H.*, Fu, K*. Activation of the STAT3 signaling pathway is associated with poor survival in diffuse large B-cell lymphoma patients treated with R-CHOP. J Clin Oncol., 31:4520-8, 2013 (*communication authors). [PDF Full Text]

Ye, B.H., Mai, Y. A Bach2 Link between Pre-B Cell Receptor Checkpoint and Pre-B Cell ALL. Cancer Cell. 2013 24(3):282-4. [PDF Full Text]

Ding, B.B., Bi, E., Chen, H., Yu, J.J. and Ye, B.H. IL-21/STAT3 and CD40L/NF-kappaB synergistically promote plasma cell differentiation through upregulation of Blimp-1. J Immunol. 190(4):1827-36, 2013. [PDF Full Text]

Will, B., Zhou, L., Vogler, T.O., Ben-Neriah, S., Schinke, C.,Tamari, R., Yu, Y., Bhagat, T., Bhattacharya, S., Barreyro, L., Heuck, C., Mo, Y., Parekh, S., McMahon, C., Pellagatti, A., Boultwood, J., Montagna, C., Silverman, L., Maciejewski, J., Greally, J.M., Ye, B.H., List, A.F., Steidl, C., Steidl, U., Verma, A, Stem and progenitor cells in myelodysplastic syndromes show aberrant stage specific expansion and harbor genetic and epigenetic alterations. Blood, 120:2076-86, 2012. [PDF Full Text]

Petrich, A., Leshchenko, V., Kuo, P.-Y., Xia, B., Thirukonda, V.K., Ulahannan, N., Gordon, S., Fazzari, M.J., Ye, B.H., Sparano, J., Parekh, S. Akt Inhibitors MK-2206 and Nelfinavir overcome mTOR inhibitor resistance in DLBCL. Clin Cancer Res. 18:2534-44, 2012. [PDF Full Text]

Nahar R, Ramezani-Rad P, Mossner M, Duy C, Cerchietti L, Geng H, Dovat S, Jumaa H, Ye BH, Melnick A, Müschen M. Pre-B cell receptor-mediated activation of BCL6 induces pre-B cell quiescence through transcriptional repression of MYC. Blood. 118:4174-8, 2011. [PDF Full Text]

Hurtz, C., Hatzi, K., Cerchietti, L., Braig, M., Park, E., Kim, Y-M., Herzog, S., Ramezani-Rad, P., Jumaa, H., Müller, M. C., Hofmann, W-K., Hochhaus, A., Ye, B. H., Agarwal, A., Druker, B. J., Shah, N. P., Melnick A. M. and Müschen, M. BCL6-mediated repression of p53 is critical for leukemia stem cell survival in chronic myeloid leukemia. J Exp Med. 208:2163-74, 2011. [PDF Full Text]

Duy, C., Hurtz, C., Shojaee, S., Cerchietti, L., Geng, H., Swaminathan, S., Klemm, L., Kweon, S-M., Nahar, R., Braig, M., Park, E., Kim, Y-M., Hofmann, W-K., Herzog, S., Jumaa, H., Koeffler, H. P., Yu, J.J., Heisterkamp, N., Graeber, T. G., Wu, H., Ye, B. H., Melnick, A., & Müschen, M. BCL6 enables survival of Ph+ acute lymphoblastic leukemia cells upon BCR-ABL1 kinase inhibition. Nature, 473:384-388, 2011. [PDF Full Text]

Peled, J.U., Yu, J.J., Venkatesh, J., Bi, E., Ding, B.B., Krupski-Downs, M., Shaknovich, R., Sicinski, P., Diamond, B., Scharff, M.D., Ye, B.H. Requirement for cyclin D3 in germinal center formation and function. Cell Research 20:631-646, 2010.

Duy, C., Yu, J.J., Nahar, R., Swaminathan, S., Kweon, S.-M., Polo, J.M., Valls, E., Klemm, L., Shojaee, S., Cerchietti, L., Schuh, W., Jack, H.-M., Hurtz, C., Ramezani-Rad, P., Herzog, S., Jumaa, H., Koeffler, H.P., de Alborán, I.M., Melnick, A.M., Ye, B.H. and Müschen, M. BCL6 is critical for the development of a diverse primary B cell repertoire. J Exp Med., 207:1209-21, 2010.

Mendez, L.M., Polo, J., Krupski, M., Yu, J.J., Melnick, A., Ye, B.H. CtBP1 is an essential corepressor for BCL6 autoregulation. Mol. Cell. Biol., 28:2175-2186, 2008.

Ding, B.B., Yu, J.J., Yu, Y.-L.R., Mendez, L.M., Shaknovich, R., Zhang, Y, Cattoretti, G., and Ye, B.H. Constitutively activated STAT3 promotes cell proliferation and survival in the activated B cell subtype of diffuse large B-cell lymphoma. Blood 111:1515-1523, 2008.

Wang, X., Ding, B.B., Mendez, L.M., Papetti, M., and Ye, B.H. Re: Torlakovic et al. PU.1 protein expression has a positive linear association with protein expression of germinal centre B cell genes including BCL-6, CD10, CD20 and CD22: identification of PU.1 putative binding sites in the BCL-6 promotor. J Pathol210: 130-131, 2006.

Pixley, F.J., Xiong, Y., Yu, Y.-L.R., Sahai, E., Stanley, E.R., and Ye, B.H. BCL-6 suppresses RhoA activity to alter macrophage morphology and motility. J. Cell Science. 118:1873-1883, 2005.

Li, Z.P., Wang, X., Yu, Y.-L. R., Ding, B.B., Yu, J.J., Dai, X.-M., Naganuma, A., Stanley, E.R., and Ye, B.H. BCL-6 negatively regulates expression of the NF-kB1 p105/p50 subunit. J. Immunol. 174: 205-214, 2005.

Yu, Y.-L.R., Wang, X., Pixley, F.J., Yu, J.J., Dent, A.L., Broxmeyer, H.E., Stanley, E.R., and Ye, B.H. BCL-6 negatively regulates macrophage proliferation by suppressing autocrine IL-6 production. Blood. 105:1111-1784, 2005.

Pasqualucci, L., Migliazza, A., Ye, B. H., Dalla-Favera, R. Transcriptional Deregulation of Mutated BCL6 Alleles by Loss of Negative Autoregulation in Diffuse Large B Cell Lymphoma.Ann NY Acad Sci, 987: 314-315, 2003.

Wang, X., Li, Z.-P., Naganuma, A., Ye, B.H. Negative autoregulation of BCL - 6 is bypassed by genetic alterations in diffuse large B cell lymphoma. Proc Natl Acad Sci U S A. 99:15018-23, 2002.

Ye, B.H. The Role of BCL-6 in normal lymphoid system and non-Hodgkin’s lymphomas. In: Normal and malignant development of blood cells. Ravid, K. and Licht J. (eds) Wiley-Liss, Inc. 2001.

Toney, L.M., Cattoretti, G., Merghoub, T., Pandolfi, P.-P., Dalla-Favera, R., Ye, B.H., Dent, A.L. BCL-6 regulates chemokine gene transcription in macrophages. Nature Imm. 1:214-220, 2000.

Qi, C., Hori. M., Coleman, A.E., Torrey, T.A., Taddesse-Heath, L., Ye, B.H., Chattopadhyay, S.K., Hartley, J.W., Morse, H.C. 3rd. Genomic organisation and expression of BCL6 in murine B-cell lymphomas. Leuk Res. 24:719-732, 2000. [MEDLINE]

Ye, B.H. Role of BCL-6 in the pathogenesis of non-Hodgkin’s lymphoma. Cancer Invest. 18:356-365, 2000. [MEDLINE]

Harris, M.B., Chang, C.C., Berton, M.T., Danial, N.N., Zhang, J., Kuehner, D., Ye, B.H., Kvatyuk, M., Pandolfi, P.P., Cattoretti, G., Dalla-Favera, R., Rothman, P.B. Transcriptional Repression of Stat6-Dependent Interleukin-4-Induced Genes by BCL-6: Specific Regulation of Iε Transcription and Immunoglobulin E Switching. Mol. Cell. Biol.19:7264-7275, 1999.

Niu H., Ye B. H., Dalla-Favera R. Antigen receptor signaling induces MAP kinase-mediated phosphorylation and degradation of the BCL-6 transcription factor. Genes Dev. 12:1953-1961, 1998.

Ye, B. H., Cattoretti, G., Zhang, J., Hawe, N., Shen, Q., de Waard, R., Orazi, A., Nouri-Shirazi, M., Chaganti, R.S.K., Rothman, P., Stall, A. M., Pandolfi P.-P., and Dalla-Favera, R. The BCL-6 proto-oncogene controls germinal-center formation and Th2-type inflammation. Nature Genet. 16:611-620, 1997.

Flenghi, L, Bigerna, B., Fizzotti, M., Venturi, S., Pasqualucci, L., Pileri, S., Ye, B. H., Gambacorta, M., Pacini, R., Baroni, C. D., Pescarmona, E., Anagnostopoulos, I., Stein, H., Asdrubali, G., Martelli, M. F., Pelicci, P. G., Dalla-Favera, R., and Falini, B. Monoclonal antibodies PG-B6a and PG-B6p recognize, respectively, a highly conserved and a formol-resistant epitope on the human BCL-6 protein amino-terminal region. Am. J. Pathol. 148:1543-55, 1996.

Chang C.-C., Ye, B. H., Chaganti, RSK., and Dalla-Favera, R. BCL-6, a POZ/Zinc-finger protein, is a sequence specific transcription repressor. Proc. Natl. Acad. Sci. USA. 93:6947-6952, 1996.

Dalla-Favera, R., Ye, B. H., Cattoretti, G., Lo Coco, F., Chang, C.-C., Zhang, J., Migliazza, A., Cechova, K., Niu, H., Chaganti, S., Chen, W., Louie, D. C., Offit, K., and Chaganti, RSK. BCL-6 in diffuse large-cell lymphomas. In: Important Advances in Oncology 1996. DeVita, V. T., Hellman, S., and Rosenberg, S. A. (eds) Lippincott-Raven Publishers, Philadelphia, pp. 139-148, 1996.

Ye, B. H., Chaganti, S., Chang, C.-C., Niu, H., Corradini, P., Chaganti, RSK., and Dalla-Favera, R. Chromosomal translocations cause deregulated BCL6 expression by promoter substitution in B cell lymphoma. EMBO J. 14:6209-6217, 1995.

Ye, B. H., Lo Coco, F., Chang, C.-C., Zhang, J., Migliazza, A., Cechova, K., Knowles, D. M., Offit, K., Chaganti, R.S., and Dalla-Favera, R. Alterations of the BCL-6 gene in diffuse large-cell lymphoma. In: Current Topics in Microbiology & Immunology. M, Potter (ed), 194:101-8, 1995.

Cechova, K., Gu, W., Ye, B. H., Lo Coco, F., Chang, C-C., Zhang, J., Migliazza, A., Mellado, W., Niu, H., and Dalla-Favera, R. Advances in the understanding of the molecular pathogenesis of aggressive B cell lymphomas. In: Normal and Malignant Hematopoiesis: New Advances, Mihichm, E., Metcalf, D. (eds) Plenum Press, pp. 131-154, 1995.

Migliazza, A., Martinotti, S., Chen, W., Fusco, C., Ye, B. H., Knowles, D. M., Offit, K., Chaganti, R.S.K., and Dalla-Favera, R. Frequent somatic hypermutation of the 5' non-coding region of the BCL-6 gene in B-cell lymphoma. Proc. Natl. Acad. Sci. USA. 92:12520-12524, 1995.

Flenghi, L., Ye, B. H., Fizzotti, M., Bigerna, B., Cattoretti, G., Venturi, S., Pacini, R., Pileri, S., Lo Coco, F., Pescarmona, E., Pelicci, P-G., Dalla-Favera, R., and Falini, B. A specific monoclonal antibody (PG-B6) detects expression of the BCL-6 Protein in germinal center B cells. Am. J. Pathol. 147:405-411, 1995.

Cattoretti, G., Chang, C-C., Cechova, K., Zhang, J., Ye, B. H., Falini, B., Louie, C. C., Offit, K., Chaganti, R.S.K., and Dalla-Favera, R. The BCL-6 protein is expressed in germinal center B-cells. Blood86:45-53, 1995.

Offit, K., Lo Coco, F., Louie, D. C., Parsa, N. Z., Leong, D., Portlock, C., Ye, B. H., Lista, F., Filippa, D. A., Rosenbaum, A., Ladanyi, M., Dalla-Favera, R., and Chaganti, R.S.K. Rearrangement of the BCL-6 gene as a prognostic marker in diffuse large cell lymphoma. N.Engl. J. Med. 331:74-80, 1994. [MEDLINE]

Gaidano, G., Lo Coco, F., Ye, B. H., Shibata, D., Levine, A. M., Knowles, D. M., and Dalla-Favera, R. Rearrangements of the BCL-6 gene in acquired immunodeficiency syndrome- associated non-Hodgkin's lymphoma: association with diffuse large-cell subtype. Blood 84:397-402, 1994.

Lo Coco, F., Ye, B. H., Lista, F., Corradini, P., Offit, K., Knowles, D. M., Chaganti, R.S.K., and Dalla-Favera, R. Rearrangements of the BCL-6 gene in diffuse large-cell non Hodgkin's lymphoma. Blood 83:1757-1759, 1994.

Dalla-Favera, R., Ye, B. H., Lo Coco, F., Chang, C-C.,Cechova, K., Zhang, J., Migliazza, A., Mellado, W., Niu, H., Chaganti, S., Chen, W., Offit, K., and Chaganti, R.S.K. BCL-6 and the molecular pathogenesis of B Cell lymphoma. In: Molecular Genetics of Cancer, CSH Symposia on Quantitative Biology, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, NY, Vol. 59, pp. 117-123, 1994.

Dalla-Favera, R., Ye, B. H., Lo Coco, F., Gaidano, G., Lista, F., Knowles, D. M., Louie, D. C., Offit, K., and Chaganti, R.S.K. Identification of genetic lesions associated with diffuse large-cell lymphoma. In: Annals of Oncology 5 (Suppl. 1):S55-60, 1994.

Ye, B. H., Lista, F., Lo Coco, F., Knowles, D. M., Offit, O., Chaganti, R.S.K., and Dalla-Favera, R. Alterations of a zinc-finger encoding gene, BCL-6, in diffuse large-cell lymphoma. Science 262:747-750, 1993.

Ye, B. H., Rao, P. H., Chaganti, R.S.K., and Dalla-Favera, R. Cloning of BCL-6, the locus involved in chromosomal translocations affecting Band 3q27 in B-cell lymphoma. Cancer Res. 53:2732-35, 1993.  

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