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Article: Analytical and Clinical Significance of Rare Hemoglobin Variants during HbA1c Monitoring in Patients with Diabetes Mellitus: Two Cases of Hemoglobin G-Ferrara and Hemoglobin G-Copenhagen in Diabetic Patients with Sickle Cell Trait.

Karimi, Saman S / Jin, Ming / Murga-Zamalloa, Carlos

The journal of applied laboratory medicine

2023 Volume 8, Issue 2, Page(s) 407–412

MeSH term(s)	Humans ; Glycated Hemoglobin ; Sickle Cell Trait/complications ; Sickle Cell Trait/diagnosis ; Clinical Relevance ; Hematologic Tests ; Diabetes Mellitus/diagnosis
Chemical Substances	hemoglobin G Ferrara (54577-93-4) ; Glycated Hemoglobin
Language	English
Publishing date	2023-02-04
Publishing country	England
Document type	Case Reports ; Journal Article
ISSN	2576-9456
ISSN	2576-9456
DOI	10.1093/jalm/jfac135
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Article ; Online: SOHO State of the Art Updates and Next Questions | New Pathways and New Targets in PTCL: Staying on Target.

Carty, Shannon A / Murga-Zamalloa, Carlos A / Wilcox, Ryan A

Clinical lymphoma, myeloma & leukemia

2023 Volume 23, Issue 8, Page(s) 561–574

Abstract: While the peripheral T-cell lymphomas (PTCL) remain a therapeutic challenge, and increasingly account for a disproportionate number of lymphoma-related deaths, improved understanding of disease pathogenesis and classification, and the development of ... ...

Abstract	While the peripheral T-cell lymphomas (PTCL) remain a therapeutic challenge, and increasingly account for a disproportionate number of lymphoma-related deaths, improved understanding of disease pathogenesis and classification, and the development of novel therapeutic agents over the past decade, all provide reasons for a more optimistic outlook in the next. Despite their genetic and molecular heterogeneity, many PTCL are dependent upon signaling input provided by antigen, costimulatory, and cytokine receptors. While gain-of-function alterations effecting these pathways are recurrently observed in many PTCL, more often than not, signaling remains ligand-and tumor microenvironment (TME)-dependent. Consequently, the TME and its constituents are increasingly recognized as "on target". Utilizing a "3 signal" model, we will review new-and old-therapeutic targets that are relevant for the more common nodal PTCL subtypes.
MeSH term(s)	Humans ; Lymphoma, T-Cell, Peripheral/pathology ; Tumor Microenvironment
Language	English
Publishing date	2023-04-19
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2540992-X
ISSN	2152-2669 ; 2152-2650
ISSN (online)	2152-2669
ISSN	2152-2650
DOI	10.1016/j.clml.2023.04.007
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Article ; Online: Binding sites in the epidermal growth factor receptor are responsible for bisphenol S effects on trophoblast cell invasion

Ticiani, Elvis / Villegas, José A. / Murga-Zamalloa, Carlos / Veiga-Lopez, Almudena

Chemosphere. 2023 Mar., v. 318 p.137960-

2023

Abstract: Bisphenol S (BPS) is an endocrine disrupting chemical and the second most abundant bisphenol detected in humans. We have recently demonstrated that in utero exposure to BPS reduces human placenta cell fusion by interfering with epidermal growth factor ( ... ...

Abstract	Bisphenol S (BPS) is an endocrine disrupting chemical and the second most abundant bisphenol detected in humans. We have recently demonstrated that in utero exposure to BPS reduces human placenta cell fusion by interfering with epidermal growth factor (EGF)-dependent EGF receptor (EGFR) activation. Our previous work suggests that this occurs via binding of BPS to the extracellular domain of EGFR. However, whether BPS directly binds to EGFR has not been confirmed. We evaluated the binding ability of BPA, BPF and BPS to EGFR to determine whether EGFR binding is a unique attribute of BPS. To test these hypotheses, we first exposed HTR-8/SVneo cells to BPS, BPA, or BPF, with or without EGF. When co-exposed to EGF, BPS, but not BPA nor BPF, reduced EGFR phosphorylation by ∼60%, demonstrating that only BPS can interfere with EGF-dependent EGFR activation. As this indicates that BPS binding to the extracellular domain is responsible for its effect, we performed a computational search for putative binding sites on the EGFR extracellular domain, and performed ligand docking of BPS, BPA, and BPF at these sites. We identified three sites where polar interactions between positively charged residues and the sulfonyl group of BPS could lead binding selectivity over BPA and BPF. To test whether EGFR mutations at the predicted BPS binding sites (Arg255, Lys454, and Arg297) could prevent BPS's interference on EGFR activation, mutations for each EGFR target amino acids (R255A, R297A, and K454A) were introduced. For variants with R297A or K454A mutations, BPS did not affect EGF-mediated EGFR phosphorylation or EGFR-mediated cell invasion, suggesting that these residues are needed for the BPS antagonism effect on EGFR. In conclusion, BPS, but not BPA or BPF, interferes with EGFR-mediated trophoblast cell functions through binding at Arg297 and Lys454 amino acid residues in the extracellular domain of EGFR.
Keywords	amino acids ; antagonism ; bisphenol S ; cell fusion ; epidermal growth factor ; epidermal growth factor receptors ; humans ; ligands ; maternal exposure ; phosphorylation ; trophoblast ; Bisphenols ; Membrane receptor ; Molecular docking ; Mutagenesis
Language	English
Dates of publication	2023-03
Publishing place	Elsevier Ltd
Document type	Article ; Online
ZDB-ID	120089-6
ISSN	1879-1298 ; 0045-6535 ; 0366-7111
ISSN (online)	1879-1298
ISSN	0045-6535 ; 0366-7111
DOI	10.1016/j.chemosphere.2023.137960
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Article ; Online: Binding sites in the epidermal growth factor receptor are responsible for bisphenol S effects on trophoblast cell invasion.

Ticiani, Elvis / Villegas, José A / Murga-Zamalloa, Carlos / Veiga-Lopez, Almudena

Chemosphere

2023 Volume 318, Page(s) 137960

Abstract	Bisphenol S (BPS) is an endocrine disrupting chemical and the second most abundant bisphenol detected in humans. We have recently demonstrated that in utero exposure to BPS reduces human placenta cell fusion by interfering with epidermal growth factor (EGF)-dependent EGF receptor (EGFR) activation. Our previous work suggests that this occurs via binding of BPS to the extracellular domain of EGFR. However, whether BPS directly binds to EGFR has not been confirmed. We evaluated the binding ability of BPA, BPF and BPS to EGFR to determine whether EGFR binding is a unique attribute of BPS. To test these hypotheses, we first exposed HTR-8/SVneo cells to BPS, BPA, or BPF, with or without EGF. When co-exposed to EGF, BPS, but not BPA nor BPF, reduced EGFR phosphorylation by ∼60%, demonstrating that only BPS can interfere with EGF-dependent EGFR activation. As this indicates that BPS binding to the extracellular domain is responsible for its effect, we performed a computational search for putative binding sites on the EGFR extracellular domain, and performed ligand docking of BPS, BPA, and BPF at these sites. We identified three sites where polar interactions between positively charged residues and the sulfonyl group of BPS could lead binding selectivity over BPA and BPF. To test whether EGFR mutations at the predicted BPS binding sites (Arg255, Lys454, and Arg297) could prevent BPS's interference on EGFR activation, mutations for each EGFR target amino acids (R255A, R297A, and K454A) were introduced. For variants with R297A or K454A mutations, BPS did not affect EGF-mediated EGFR phosphorylation or EGFR-mediated cell invasion, suggesting that these residues are needed for the BPS antagonism effect on EGFR. In conclusion, BPS, but not BPA or BPF, interferes with EGFR-mediated trophoblast cell functions through binding at Arg297 and Lys454 amino acid residues in the extracellular domain of EGFR.
MeSH term(s)	Female ; Pregnancy ; Humans ; Trophoblasts ; Epidermal Growth Factor/pharmacology ; ErbB Receptors/metabolism ; Binding Sites ; Benzhydryl Compounds/metabolism
Chemical Substances	Epidermal Growth Factor (62229-50-9) ; ErbB Receptors (EC 2.7.10.1) ; bis(4-hydroxyphenyl)sulfone (80-09-1) ; Benzhydryl Compounds
Language	English
Publishing date	2023-01-27
Publishing country	England
Document type	Journal Article
ZDB-ID	120089-6
ISSN	1879-1298 ; 0045-6535 ; 0366-7111
ISSN (online)	1879-1298
ISSN	0045-6535 ; 0366-7111
DOI	10.1016/j.chemosphere.2023.137960
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Article ; Online: T-Cell Prolymphocytic Leukemia: Diagnosis, Pathogenesis, and Treatment.

Gutierrez, Marc / Bladek, Patrick / Goksu, Busra / Murga-Zamalloa, Carlos / Bixby, Dale / Wilcox, Ryan

International journal of molecular sciences

2023 Volume 24, Issue 15

Abstract: T-cell prolymphocytic leukemia (T-PLL) is a rare and aggressive neoplasm of mature T-cells. Most patients with T-PLL present with lymphocytosis, anemia, thrombocytopenia, and hepatosplenomegaly. Correct identification of T-PLL is essential because ... ...

Abstract	T-cell prolymphocytic leukemia (T-PLL) is a rare and aggressive neoplasm of mature T-cells. Most patients with T-PLL present with lymphocytosis, anemia, thrombocytopenia, and hepatosplenomegaly. Correct identification of T-PLL is essential because treatment for this disease is distinct from that of other T-cell neoplasms. In 2019, the T-PLL International Study Group (TPLL-ISG) established criteria for the diagnosis, staging, and assessment of response to treatment of T-PLL with the goal of harmonizing research efforts and supporting clinical decision-making. T-PLL pathogenesis is commonly driven by T-cell leukemia 1 (
MeSH term(s)	Humans ; Leukemia, Prolymphocytic, T-Cell/etiology ; Leukemia, Prolymphocytic, T-Cell/genetics ; Alemtuzumab/therapeutic use ; Hematopoietic Stem Cell Transplantation ; Mutation
Chemical Substances	Alemtuzumab (3A189DH42V)
Language	English
Publishing date	2023-07-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241512106
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Article ; Online: The role of aurora A and polo-like kinases in high-risk lymphomas.

Murga-Zamalloa, Carlos / Inamdar, Kedar V / Wilcox, Ryan A

Blood advances

2019 Volume 3, Issue 11, Page(s) 1778–1787

Abstract: High-risk lymphomas (HRLs) are associated with dismal outcomes and remain a therapeutic challenge. Recurrent genetic and molecular alterations, including c-myc expression and aurora A kinase (AAK) and polo-like kinase-1 (PLK1) activation, promote cell ... ...

Abstract	High-risk lymphomas (HRLs) are associated with dismal outcomes and remain a therapeutic challenge. Recurrent genetic and molecular alterations, including c-myc expression and aurora A kinase (AAK) and polo-like kinase-1 (PLK1) activation, promote cell proliferation and contribute to the highly aggressive natural history associated with these lymphoproliferative disorders. In addition to its canonical targets regulating mitosis, the AAK/PLK1 axis directly regulates noncanonical targets, including c-myc. Recent studies demonstrate that HRLs, including T-cell lymphomas and many highly aggressive B-cell lymphomas, are dependent upon the AAK/PLK1 axis. Therefore, the AAK/PLK1 axis has emerged as an attractive therapeutic target in these lymphomas. In addition to reviewing these recent findings, we summarize the rationale for targeting AAK/PLK1 in high-risk and c-myc-driven lymphoproliferative disorders.
MeSH term(s)	Animals ; Aurora Kinase A/metabolism ; Cell Cycle Proteins/metabolism ; Humans ; Lymphoma, B-Cell/enzymology ; Lymphoma, B-Cell/pathology ; Lymphoma, B-Cell/therapy ; Lymphoma, T-Cell/enzymology ; Lymphoma, T-Cell/pathology ; Lymphoma, T-Cell/therapy ; Protein Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; Risk Factors ; Signal Transduction ; Polo-Like Kinase 1
Chemical Substances	Cell Cycle Proteins ; MYC protein, human ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-myc ; AURKA protein, human (EC 2.7.11.1) ; Aurora Kinase A (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2019-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2019000232
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Zs.A 7153: Show issues

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Article ; Online: GATA-3 in T-cell lymphoproliferative disorders.

Murga-Zamalloa, Carlos / Wilcox, Ryan A

IUBMB life

2019 Volume 72, Issue 1, Page(s) 170–177

Abstract: GATA-3 regulates the differentiation, proliferation, survival, and function of peripheral T cells and their thymic progenitors. Recent findings, reviewed here, not only implicate GATA-3 in the pathogenesis of molecularly, genetically, and clinically ... ...

Abstract	GATA-3 regulates the differentiation, proliferation, survival, and function of peripheral T cells and their thymic progenitors. Recent findings, reviewed here, not only implicate GATA-3 in the pathogenesis of molecularly, genetically, and clinically distinct T-cell lymphoproliferative disorders, but also have significant diagnostic, prognostic, and therapeutic implications.
MeSH term(s)	Cell Differentiation ; GATA3 Transcription Factor/genetics ; Humans ; Lymphoproliferative Disorders/genetics ; Lymphoproliferative Disorders/pathology ; Mutation ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology
Chemical Substances	GATA3 Transcription Factor
Language	English
Publishing date	2019-07-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1492141-8
ISSN	1521-6551 ; 1521-6543
ISSN (online)	1521-6551
ISSN	1521-6543
DOI	10.1002/iub.2130
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Article ; Online: Characterization of T-/natural killer cell lymphoproliferative neoplasms associated with systemic, chronic, active Epstein-Barr virus in adults: A report of 5 cases in a Western population.

Murga-Zamalloa, Carlos / Stone, Michael Brandon / Gutierrez, Marc G / Hippalgaonkar, Neha Rajendra / Tariq, Hamza / Sadeh, Morteza / Mehta, Ankit / Khan, Irum / Alkan, Serhan / Inamdar, Kedar V / Wilcox, Ryan / Behdad, Amir

American journal of clinical pathology

2024

Abstract: Objectives: Because of its low frequency in adult populations and clinical and laboratory overlap with hemophagocytic lymphohistiocytosis and other T-cell lymphomas, T-cell/natural killer (NK) cell systemic, chronic, active Epstein-Barr virus (EBV) (T/ ... ...

Abstract	Objectives: Because of its low frequency in adult populations and clinical and laboratory overlap with hemophagocytic lymphohistiocytosis and other T-cell lymphomas, T-cell/natural killer (NK) cell systemic, chronic, active Epstein-Barr virus (EBV) (T/NK sCAEBV) infection remains underdiagnosed, preventing critical, prompt therapeutic interventions. Methods: We report a 5-case series that included 2 adult patients with T/NK sCAEBV and 3 additional adult patients with T/NK lymphomas with concomitant systemic EBV infection to review these entities' overlapping diagnostic and clinical features. Results: Approximately 95% of the world population has been infected with EBV during their lifetime, and infection is usually asymptomatic, with symptomatic cases eventually resolving spontaneously. A small subset of immunocompetent patients develops CAEBV, a life-threatening complication resulting from EBV-infected T-cell or NK cell neoplastic lymphocytes. The sites of end-organ damage in T/NK sCAEBV demonstrate pathologic findings such as reactive lymphoid proliferations, making the diagnosis difficult to establish, with the only curative option being an allogeneic hematopoietic stem cell transplant. Conclusions: This diagnosis is most prevalent in Asia, with few cases reported in Western countries. Adult age is an independent risk factor for poor outcomes, and most cases are diagnosed in pediatric populations.
Language	English
Publishing date	2024-02-12
Publishing country	England
Document type	Journal Article
ZDB-ID	2944-0
ISSN	1943-7722 ; 0002-9173
ISSN (online)	1943-7722
ISSN	0002-9173
DOI	10.1093/ajcp/aqad184
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Article ; Online: GATA-3-dependent Gene Transcription is Impaired upon HDAC Inhibition.

Geng, Xiangrong / Wang, Chenguang / Abdelrahman, Suhaib / Perera, Thilini / Saed, Badeia / Hu, Ying S / Wolfe, Ashley / Reneau, John / Murga-Zamalloa, Carlos / Wilcox, Ryan A

Clinical cancer research : an official journal of the American Association for Cancer Research

2024 Volume 30, Issue 5, Page(s) 1054–1066

Abstract: Purpose: Many peripheral and cutaneous T-cell lymphoma (CTCL) subtypes are poorly responsive to conventional chemotherapeutic agents and associated with dismal outcomes. The zinc finger transcription factor GATA-3 and the transcriptional program it ... ...

Abstract	Purpose: Many peripheral and cutaneous T-cell lymphoma (CTCL) subtypes are poorly responsive to conventional chemotherapeutic agents and associated with dismal outcomes. The zinc finger transcription factor GATA-3 and the transcriptional program it instigates are oncogenic and highly expressed in various T-cell neoplasms. Posttranslational acetylation regulates GATA-3 DNA binding and target gene expression. Given the widespread use of histone deacetylase inhibitors (HDACi) in relapsed/refractory CTCL, we sought to examine the extent to which these agents attenuate the transcriptional landscape in these lymphomas. Experimental design: Integrated GATA-3 chromatin immunoprecipitation sequencing and RNA sequencing analyses were performed in complementary cell line models and primary CTCL specimens treated with clinically available HDACi. Results: We observed that exposure to clinically available HDACi led to significant transcriptional reprogramming and increased GATA-3 acetylation. HDACi-dependent GATA-3 acetylation significantly impaired both its ability to bind DNA and transcriptionally regulate its target genes, thus leading to significant transcriptional reprogramming in HDACi-treated CTCL. Conclusions: Beyond shedding new light on the mechanism of action associated with HDACi in CTCL, these findings have significant implications for their use, both as single agents and in combination with other novel agents, in GATA-3-driven lymphoproliferative neoplasms.
MeSH term(s)	Humans ; Lymphoma, T-Cell, Cutaneous/drug therapy ; Lymphoma, T-Cell, Cutaneous/genetics ; Acetylation ; Histone Deacetylase Inhibitors/pharmacology ; Skin Neoplasms ; DNA ; Transcription, Genetic
Chemical Substances	Histone Deacetylase Inhibitors ; DNA (9007-49-2)
Language	English
Publishing date	2024-01-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-23-1699
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Article ; Online: Richter Syndrome Presenting as Subcutaneous Nodules and a Dermal Plaque.

Nickles, Melissa / Hunt, Samantha / Turcios-Escobar, Saul / Babwah, Amaara / Mobayed, Nisreen / Murga-Zamalloa, Carlos / Bain, Michelle / Quigley, John / Rubinstein, Paul / Galvez, Carlos

The American Journal of dermatopathology

2024

Abstract: Abstract: Richter syndrome (RS) describes a phenomenon in which a patient with chronic lymphocytic leukemia (CLL) develops an aggressive lymphoma, most commonly diffuse large B-cell lymphoma (DLBCL). Reports of cutaneous RS remain exceedingly rare. We ... ...

Abstract	Abstract: Richter syndrome (RS) describes a phenomenon in which a patient with chronic lymphocytic leukemia (CLL) develops an aggressive lymphoma, most commonly diffuse large B-cell lymphoma (DLBCL). Reports of cutaneous RS remain exceedingly rare. We report a 61-year-old woman with relapsed/refractory CLL presenting with several subcutaneous nodules on her arms and legs and a single dermal plaque on her abdomen. Skin biopsy revealed a diagnosis of DLBCL, ABC-type, and her clinical status rapidly deteriorated following diagnosis. We review the variety of clinical presentations of cutaneous RS, its association with CLL, risk factors for RS development in CLL patients, and the distinctive histopathologic and immunophenotypic features of DLBCL. We hope to highlight the importance of prompt skin biopsy in patients with CLL presenting with progressive skin lesions and increase awareness of this aggressive clinical syndrome.
Language	English
Publishing date	2024-04-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	448469-1
ISSN	1533-0311 ; 0193-1091
ISSN (online)	1533-0311
ISSN	0193-1091
DOI	10.1097/DAD.0000000000002720
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