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Article ; Online: Emerging new cell therapies/immune therapies in B-cell non-Hodgkin's lymphoma.

Banerjee, Titas / Vallurupalli, Anusha

2021 Volume 46, Issue 1, Page(s) 100825

Abstract: Non-Hodgkin's lymphomas (NHL) are a heterogeneous group of lymphoproliferative disorders originating in B-lymphocytes, T-lymphocytes, or natural killer (NK) lymphocytes. First line therapy is well established and generally a combination of steroids and ... ...

Abstract	Non-Hodgkin's lymphomas (NHL) are a heterogeneous group of lymphoproliferative disorders originating in B-lymphocytes, T-lymphocytes, or natural killer (NK) lymphocytes. First line therapy is well established and generally a combination of steroids and chemotherapy. Treatment of relapsed/refractory (R/R) NHL however remains a challenge with rapidly evolving new therapies. Many of these new therapies focus on manipulating the body's natural immune mechanisms to identify and eradicate tumor cells. There has been much success with using checkpoint inhibitors in Hodgkin's Lymphoma (HL). However, results have been modest in NHL, prompting further studies of immunomodulatory strategies to target NHL. In this article, we review the emerging immune and cell therapies for R/R B-NHL including checkpoint inhibitors, bispecific antibodies, chimeric antigen receptor (CAR) T-cell therapy, and small molecule inhibitors both alone and in combination.
MeSH term(s)	Antibodies, Bispecific/therapeutic use ; Cell- and Tissue-Based Therapy ; Humans ; Immunotherapy, Adoptive/methods ; Lymphoma, Non-Hodgkin/drug therapy ; Neoplasm Recurrence, Local/drug therapy
Chemical Substances	Antibodies, Bispecific
Language	English
Publishing date	2021-12-26
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	441816-5
ISSN	1535-6345 ; 0147-0272
ISSN (online)	1535-6345
ISSN	0147-0272
DOI	10.1016/j.currproblcancer.2021.100825
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Article ; Online: A retrospective single-center analysis of CD-19 directed CAR T-cell therapy in relapsed/refractory mantle cell lymphoma.

Banerjee, Titas / Newman, Matthew / Chen, Andy / Maziarz, Richard T / Schachter, Levanto / Spurgeon, Stephen E / Vallurupalli, Anusha

Leukemia & lymphoma

2023 Volume 64, Issue 8, Page(s) 1472–1475

MeSH term(s)	Adult ; Humans ; Lymphoma, Mantle-Cell/diagnosis ; Lymphoma, Mantle-Cell/therapy ; Lymphoma, Mantle-Cell/pathology ; Immunotherapy, Adoptive/adverse effects ; Retrospective Studies ; Antigens, CD19 ; Neoplasm Recurrence, Local/therapy ; Neoplasm Recurrence, Local/pathology
Chemical Substances	Antigens, CD19
Language	English
Publishing date	2023-06-07
Publishing country	United States
Document type	Research Support, Non-U.S. Gov't ; Letter
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2023.2212098
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Article ; Online: Functional cooperativity of p97 and histone deacetylase 6 in mediating DNA repair in mantle cell lymphoma cells.

Vekaria, Pratikkumar H / Kumar, Amar / Subramaniam, Dharmalingam / Dunavin, Neil / Vallurupalli, Anusha / Schoenen, Frank / Ganguly, Siddhartha / Anant, Shrikant / McGuirk, Joseph P / Jensen, Roy A / Rao, Rekha

Leukemia

2019 Volume 33, Issue 7, Page(s) 1675–1686

Abstract: p97 is an ATPase that works in concert with histone deacetylase 6 (HDAC6), to facilitate the degradation of misfolded proteins by autophagosomes. p97 has also been implicated in DNA repair and maintaining genomic stability. In this study, we determined ... ...

Abstract	p97 is an ATPase that works in concert with histone deacetylase 6 (HDAC6), to facilitate the degradation of misfolded proteins by autophagosomes. p97 has also been implicated in DNA repair and maintaining genomic stability. In this study, we determined the effect of combined inhibition of p97 and HDAC6 activities in mantle cell lymphoma (MCL) cells. We report that treatment with p97 inhibitors induces dose-dependent apoptosis in MCL cells. The p97 inhibitor CB-5083 induces ER stress markers GRP78 and CHOP and results in the accumulation of polyubiquitylated proteins. Co-treatment with CB-5083 and the HDAC6 inhibitor ACY-1215 result in marked downregulation of CDK4, Cyclin D1, and BRCA1 levels without inhibiting autophagic flux. Consequently, treatment with CB-5083 accentuates DNA damage in response to treatment with ACY-1215 resulting in enhanced accumulation of H2AX-γ and synergistic apoptosis. Furthermore, ATM loss severely impairs phosphorylation of 53BP1 following co-treatment with CB-5083 and ACY-1215 in response to gamma irradiation. Finally, co-treatment CB-5083 and ACY-1215 results in reduced tumor volumes and improves survival in Z138C and Jeko-1 xenografts in NSG mice. These observations suggest that combined inhibition of p97 and HDAC6 abrogates resolution of proteotoxic stress and impairs DNA repair mechanisms in MCL cells.
MeSH term(s)	Adenosine Triphosphatases/antagonists & inhibitors ; Animals ; Apoptosis ; Autophagy ; Cell Proliferation ; DNA Damage/drug effects ; DNA Repair/drug effects ; Drug Synergism ; Drug Therapy, Combination ; Gene Expression Regulation, Neoplastic ; Histone Deacetylase 6/antagonists & inhibitors ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Hydroxamic Acids/pharmacology ; Indoles/pharmacology ; Lymphoma, Mantle-Cell/drug therapy ; Lymphoma, Mantle-Cell/genetics ; Lymphoma, Mantle-Cell/pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Nuclear Proteins/antagonists & inhibitors ; Pyrimidines/pharmacology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	CB-5083 ; Histone Deacetylase Inhibitors ; Hydroxamic Acids ; Indoles ; Nuclear Proteins ; Pyrimidines ; HDAC6 protein, human (EC 3.5.1.98) ; Histone Deacetylase 6 (EC 3.5.1.98) ; Adenosine Triphosphatases (EC 3.6.1.-) ; p97 ATPase (EC 3.6.1.-) ; ricolinostat (WKT909C62B)
Language	English
Publishing date	2019-01-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-018-0355-y
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Article ; Online: A New Zealand Black-derived locus suppresses chronic graft-versus-host disease and autoantibody production through nonlymphoid bone marrow-derived cells.

Xu, Zhiwei / Vallurupalli, Anusha / Fuhrman, Christopher / Ostrov, David / Morel, Laurence

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 186, Issue 7, Page(s) 4130–4139

Abstract: The development of lupus pathogenesis results from the integration of susceptibility and resistance genes. We have used a chronic graft-versus-host disease (cGVHD) model to characterize a suppressive locus at the telomeric end of the NZM2410-derived Sle2 ...

Abstract	The development of lupus pathogenesis results from the integration of susceptibility and resistance genes. We have used a chronic graft-versus-host disease (cGVHD) model to characterize a suppressive locus at the telomeric end of the NZM2410-derived Sle2 susceptibility locus, which we named Sle2c2. cGVHD is induced normally in Sle2c2-expressing mice, but it is not sustained. The analysis of mixed bone marrow chimeras revealed that cGVHD resistance was eliminated by non-B non-T hematopoietic cells expressing the B6 allele, suggesting that resistance is mediated by this same cell type. Furthermore, Sle2c2 expression was associated with an increased number and activation of the CD11b(+) GR-1(+) subset of granulocytes before and in the early stage of cGVHD induction. We have mapped the Sle2c2 critical interval to a 6-Mb region that contains the Cfs3r gene, which encodes for the G-CSFR, and its NZM2410 allele carries a nonsynonymous mutation. The G-CSFR-G-CSF pathway has been previously implicated in the regulation of GVHD, and our functional data on Sle2c2 suppression suggest a novel regulation of T cell-induced systemic autoimmunity through myeloid-derived suppressor cells. The validation of Csf3r as the causative gene for Sle2c2 and the further characterization of the Sle2c2 MDSCs promise to unveil new mechanisms by which lupus pathogenesis is regulated.
MeSH term(s)	Animals ; Antibodies, Antinuclear/biosynthesis ; Antibodies, Antinuclear/metabolism ; Bone Marrow Cells/immunology ; Bone Marrow Cells/metabolism ; Bone Marrow Cells/pathology ; Chronic Disease ; Disease Models, Animal ; Genes, Suppressor ; Genetic Loci/immunology ; Genetic Predisposition to Disease ; Graft vs Host Disease/genetics ; Graft vs Host Disease/immunology ; Graft vs Host Disease/prevention & control ; Immune Tolerance/genetics ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/pathology ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NZB ; Mice, Knockout ; Myeloid Cells/immunology ; Myeloid Cells/metabolism ; Myeloid Cells/pathology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology
Chemical Substances	Antibodies, Antinuclear
Language	English
Publishing date	2011-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1003512
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Article ; Online: A Diverse Spectrum of Immune Complex- and Complement-Mediated Kidney Diseases Is Associated With Mantle Cell Lymphoma.

Kidney international reports

2021 Volume 7, Issue 3, Page(s) 568–579

Abstract: Introduction: There are limited reports on kidney biopsy findings in patients with mantle cell lymphoma (MCL).: Methods: We initiated a multi-institutional, retrospective review of kidney biopsy findings in patients with active and treated MCL.: ... ...

Abstract	Introduction: There are limited reports on kidney biopsy findings in patients with mantle cell lymphoma (MCL). Methods: We initiated a multi-institutional, retrospective review of kidney biopsy findings in patients with active and treated MCL. Results: A total of 30 patients with MCL and kidney biopsies were identified, with a median age of 67 (range 48-87) years, 73% of whom were men. A total of 20 patients had active MCL at the time of biopsy, of whom 14 (70%) presented with acute kidney injury (AKI), proteinuria and/or hematuria, and biopsy findings potentially attributable to lymphoma. Of the 14, 11 had immune complex (IC) or complement-mediated (C3) disease including proliferative glomerulonephritis (GN) with monotypic Ig deposits (PGNMID [2]), C3GN, (2), secondary membranous nephropathy (MN [3]), tubular basement membrane (TBM) deposits (2), and modest lupus-like GN (2). Lymphomatous infiltration was present in 8 of the 20 patients, 5 with coincident IC or C3 lesions. A total of 6 patients with available follow-up were treated for MCL, all with clinical remission of GN (2 PGNMID, 2 C3GN, and 2 MN). Conclusion: MCL is associated with diverse monoclonal and polyclonal glomerular and extra-glomerular IC and C3 disease. For patients with active MCL and kidney dysfunction requiring biopsy, 70% had findings due or potentially due to lymphoma, including 55% with IC or C3 disease and 40% had lymphomatous kidney infiltration. IC and C3GN in the setting of active MCL was responsive to lymphoma-directed therapy.
Language	English
Publishing date	2021-12-27
Publishing country	United States
Document type	Journal Article
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2021.12.020
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Article ; Online: A phase 1/2 study of the combination of acalabrutinib and vistusertib in patients with relapsed/refractory B-cell malignancies.

Collins, Graham P / Clevenger, Tracy N / Burke, Kathleen A / Yang, Buyue / MacDonald, Alex / Cunningham, David / Fox, Christopher P / Goy, Andre / Gribben, John / Nowakowski, Grzegorz S / Roschewski, Mark / Vose, Julie M / Vallurupalli, Anusha / Cheung, Jean / Raymond, Amelia / Nuttall, Barrett / Stetson, Dan / Dougherty, Brian A / Schalkwijk, Stein /

Carnevalli, Larissa S / Willis, Brandon / Tao, Lin / Harrington, Elizabeth A / Hamdy, Ahmed / Izumi, Raquel / Pease, J Elizabeth / Frigault, Melanie M / Flinn, Ian

Leukemia & lymphoma

2021 Volume 62, Issue 11, Page(s) 2625–2636

Abstract: In a phase 1b study of acalabrutinib (a covalent Bruton tyrosine kinase (BTK) inhibitor) in combination with vistusertib (a dual mTORC1/2 inhibitor) in patients with relapsed/refractory diffuse large B-cell lymphoma (DLBCL), multiple ascending doses of ... ...

Abstract	In a phase 1b study of acalabrutinib (a covalent Bruton tyrosine kinase (BTK) inhibitor) in combination with vistusertib (a dual mTORC1/2 inhibitor) in patients with relapsed/refractory diffuse large B-cell lymphoma (DLBCL), multiple ascending doses of the combination as intermittent or continuous schedules of vistusertib were evaluated. The overall response rate was 12% (3/25). The pharmacodynamic (PD) profile for acalabrutinib showed that BTK occupancy in all patients was >95%. In contrast, PD analysis for vistusertib showed variable inhibition of phosphorylated 4EBP1 (p4EBP1) without modulation of AKT phosphorylation (pAKT). The pharmacokinetic (PK)/PD relationship of vistusertib was direct for TORC1 inhibition (p4EBP1) but did not correlate with TORC2 inhibition (pAKT). Cell-of-origin subtyping or next-generation sequencing did not identify a subset of DLBCL patients with clinical benefit; however, circulating tumor DNA dynamics correlated with radiographic response. These data suggest that vistusertib does not modulate targets sufficiently to add to the clinical activity of acalabrutinib monotherapy.
MeSH term(s)	B-Lymphocytes ; Benzamides ; Humans ; Morpholines ; Neoplasm Recurrence, Local ; Protein Kinase Inhibitors/therapeutic use ; Pyrazines ; Pyrimidines
Chemical Substances	Benzamides ; Morpholines ; Protein Kinase Inhibitors ; Pyrazines ; Pyrimidines ; vistusertib (0BSC3P4H5X) ; acalabrutinib (I42748ELQW)
Language	English
Publishing date	2021-07-16
Publishing country	United States
Document type	Clinical Trial, Phase I ; Clinical Trial, Phase II ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1042374-6
ISSN	1029-2403 ; 1042-8194
ISSN (online)	1029-2403
ISSN	1042-8194
DOI	10.1080/10428194.2021.1938027
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Article ; Online: Cyclin-dependent kinase inhibitor Cdkn2c regulates B cell homeostasis and function in the NZM2410-derived murine lupus susceptibility locus Sle2c1.

Xu, Zhiwei / Potula, Hari-Hara S K / Vallurupalli, Anusha / Perry, Daniel / Baker, Henry / Croker, Byron P / Dozmorov, Igor / Morel, Laurence

Journal of immunology (Baltimore, Md. : 1950)

2011 Volume 186, Issue 12, Page(s) 6673–6682

Abstract: Sle2c1 is an NZM2410- and NZB-derived lupus susceptibility locus that induces an expansion of the B1a cell compartment. B1a cells have a repertoire enriched for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of ... ...

Abstract	Sle2c1 is an NZM2410- and NZB-derived lupus susceptibility locus that induces an expansion of the B1a cell compartment. B1a cells have a repertoire enriched for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus. A combination of genetic mapping and candidate gene analysis presents Cdkn2c, a gene encoding for cyclin-dependent kinase inhibitor p18(INK4c) (p18), as the top candidate gene for inducing the Slec2c1-associated expansion of B1a cells. A novel single nucleotide polymorphism in the NZB allele of the Cdkn2c promoter is associated with a significantly reduced Cdkn2c expression in the splenic B cells and peritoneal cavity B1a cells from Sle2c1-carrying mice, which leads to a defective G1 cell cycle arrest in splenic B cells and increased proliferation of peritoneal cavity B1a cells. As the cell cycle is differentially regulated in B1a and B2 cells, these results suggest that Cdkn2c plays a critical role in B1a cell self-renewal and that its impaired expression leads to an accumulation of these cells with high autoreactive potential.
MeSH term(s)	Animals ; Autoimmunity/genetics ; B-Lymphocyte Subsets/pathology ; B-Lymphocytes/cytology ; B-Lymphocytes/pathology ; B-Lymphocytes/physiology ; Cell Cycle ; Cell Proliferation ; Chromosome Mapping ; Cyclin-Dependent Kinase Inhibitor p18/genetics ; Cyclin-Dependent Kinase Inhibitor p18/physiology ; Disease Models, Animal ; Genetic Loci/genetics ; Genetic Predisposition to Disease/genetics ; Homeostasis ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/pathology ; Lymphocyte Count ; Mice ; Polymorphism, Single Nucleotide
Chemical Substances	Cdkn2c protein, mouse ; Cyclin-Dependent Kinase Inhibitor p18
Language	English
Publishing date	2011-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1002544
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Article ; Online: Emerging new cell therapies/immune therapies in B-cell non-Hodgkin's lymphoma.

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Article ; Online: A retrospective single-center analysis of CD-19 directed CAR T-cell therapy in relapsed/refractory mantle cell lymphoma.

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Article ; Online: Functional cooperativity of p97 and histone deacetylase 6 in mediating DNA repair in mantle cell lymphoma cells.

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Article ; Online: A New Zealand Black-derived locus suppresses chronic graft-versus-host disease and autoantibody production through nonlymphoid bone marrow-derived cells.

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Article ; Online: A Diverse Spectrum of Immune Complex- and Complement-Mediated Kidney Diseases Is Associated With Mantle Cell Lymphoma.

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Article ; Online: A phase 1/2 study of the combination of acalabrutinib and vistusertib in patients with relapsed/refractory B-cell malignancies.

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Article ; Online: Cyclin-dependent kinase inhibitor Cdkn2c regulates B cell homeostasis and function in the NZM2410-derived murine lupus susceptibility locus Sle2c1.

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