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Article ; Online: Therapeutic targeting of isocitrate dehydrogenase mutant AML.

Boddu, Prajwal / Borthakur, Gautam

2017 Volume 26, Issue 5, Page(s) 525–530

Language	English
Publishing date	2017-05
Publishing country	England
Document type	Journal Article
ZDB-ID	1182884-5
ISSN	1744-7658 ; 0967-8298 ; 1354-3784
ISSN (online)	1744-7658
ISSN	0967-8298 ; 1354-3784
DOI	10.1080/13543784.2017.1317745
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Article ; Online: Myeloid disorders after autoimmune disease.

Boddu, Prajwal C / Zeidan, Amer M

Best practice & research. Clinical haematology

2019 Volume 32, Issue 1, Page(s) 74–88

Abstract: Autoimmune diseases (ADs) are associated with an increased risk not only of lymphoproliferative disorders but also of myeloid malignancies. The excess risk of myelodysplastic syndromes and/or acute myeloid leukemia is observed across several AD types, ... ...

Abstract	Autoimmune diseases (ADs) are associated with an increased risk not only of lymphoproliferative disorders but also of myeloid malignancies. The excess risk of myelodysplastic syndromes and/or acute myeloid leukemia is observed across several AD types, including systemic lupus erythematosus, rheumatoid arthritis, inflammatory bowel disorders, multiple sclerosis, among others. The risk of developing myeloid neoplasms (MNs) is dependent on several variables, including the specific AD type, chronicity and severity of the AD, type and duration of exposure of disease modifying anti-rheumatic drugs or cytotoxics/immunosuppressives, and genetic predisposition risk. Putative triggering factors linking AD to elevated MN risk include AD-directed medications, shared genetic susceptibilities between the two disease entities, and chronic immune stimulation or bone marrow infiltration by the AD. Molecular mechanisms underpinning leukemogenesis remain largely speculative and warrant further investigation. Leukemias arising in patients with AD are not always 'therapy-related' in that MNs may develop in certain AD subtypes even among patients with no prior therapy exposure. Only a few studies have attempted to determine factors associated with MN development in AD but failed to demonstrate consistent characteristic clinical or paraclinical features. These reports have failed to demonstrate a clear correlation between individual agent exposure and subsequent leukemia development due to the low rates of therapy exposure compounded by the rarity of MN occurrence. Notwithstanding, the leukemogenic potential is best documented with agents such as azathioprine, cyclophosphamide, and mitoxantrone; this risk of MN development does not appear to be shared by biologic approaches such as anti-tumor necrosis factors-alpha inhibitors. In this article, we discuss plausible biologic mechanisms underlying MN pathogenesis in AD and review the data available on the development of MNs in patients with AD.
MeSH term(s)	Arthritis, Rheumatoid/drug therapy ; Arthritis, Rheumatoid/genetics ; Arthritis, Rheumatoid/metabolism ; Arthritis, Rheumatoid/pathology ; Cyclophosphamide/adverse effects ; Cyclophosphamide/therapeutic use ; Genetic Predisposition to Disease ; Humans ; Immunosuppressive Agents/adverse effects ; Immunosuppressive Agents/therapeutic use ; Leukemia, Myeloid, Acute/chemically induced ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/pathology ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/pathology ; Mitoxantrone/adverse effects ; Mitoxantrone/therapeutic use ; Myelodysplastic Syndromes/chemically induced ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/metabolism ; Myelodysplastic Syndromes/pathology ; Neoplasms, Second Primary/genetics ; Neoplasms, Second Primary/metabolism ; Neoplasms, Second Primary/pathology
Chemical Substances	Immunosuppressive Agents ; Cyclophosphamide (8N3DW7272P) ; Mitoxantrone (BZ114NVM5P)
Language	English
Publishing date	2019-02-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2048027-1
ISSN	1532-1924 ; 1521-6926
ISSN (online)	1532-1924
ISSN	1521-6926
DOI	10.1016/j.beha.2019.02.002
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Article ; Online: 40008 COMBINED CRISPR/CAS9 AND AAV FOR THE GENERATION OF CONDITIONAL ISOGENIC GENE KNOCK-INS

Prajwal Boddu / Abhishek Gupta / Todd Waldman / Manoj Pillai

Journal of Clinical and Translational Science, Vol 5, Pp 22-

2021 Volume 22

Abstract: ABSTRACT IMPACT: We describe a novel methodology that combines CRISPR/Cas9-induced double stranded DNA breaks with homology dependent repair from an adeno associated virus (AAV) encoded template to generate single-allele edited isogenic cell line models ... ...

Abstract	ABSTRACT IMPACT: We describe a novel methodology that combines CRISPR/Cas9-induced double stranded DNA breaks with homology dependent repair from an adeno associated virus (AAV) encoded template to generate single-allele edited isogenic cell line models of cancer-associated mutations with high efficiency. OBJECTIVES/GOALS: Conventional approaches to creating isogenic knock-ins, to model disease-associated mutations, are limited by poor efficiency and loss of the mutant allele on extended culture. We present an optimized editing approach combining CRISPR/Cas9 with Adeno-associated virus, using mutant SF3B1 as a prototype. METHODS/STUDY POPULATION: Left and right homology arms for SF3B1 were PCR amplified and cloned into pAAV-SEPT-Acceptor plasmid (containing a chimeric intron, neomycin resistance cassette and polyA tail). The disease-associated K700E mutation was introduced by site-directed mutagenesis. Single guide RNA (sgRNA) complexed with recombinant Cas9 along with the AAV donor were delivered into K562 cells, G418 resistant clones selected, and screened for integration by PCR. Confirmed clones were then transduced with a doxycycline-inducible Cre-recombinase containing lentiviral vector. Inducible expression of Cre-recombinase and expression of the mutant allele were confirmed by Western blot and Sanger sequencing respectively. RESULTS/ANTICIPATED RESULTS: Targeted-integration efficiencies among the Neo-resistant clones, generated by AAV-alone and AAV+CRISPR/Cas9, were 16% and 94%, respectively. Single cell cloning after Cre-mediated excision of loxp was unsuccessful presumably due to toxicity of the K700E mutation. To overcome this limitation, clones were transduced with doxycycline-inducible Cre-recombinase lentiviral vector. Doxycycline induction of Cre-recombinase resulted in reliable excision of the loxp cassette and expression of mutant allele at about 50% variable allele frequency (as determined by Sanger sequencing). The approach was validated in additional cell lines and for introduction of ...
Keywords	Medicine ; R
Subject code	616
Language	English
Publishing date	2021-03-01T00:00:00Z
Publisher	Cambridge University Press
Document type	Article ; Online
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Article: Update on signal inhibitors in chronic lymphocytic leukemia.

Boddu, Prajwal / Jain, Nitin

Clinical advances in hematology & oncology : H&O

2018 Volume 16, Issue 4, Page(s) 279–288

Abstract: The last decade has seen major progress in our understanding of the pathobiology of chronic lymphocytic leukemia (CLL) and the identification of potential new therapeutic targets. As a result, researchers have developed novel targeted therapies, several ... ...

Abstract	The last decade has seen major progress in our understanding of the pathobiology of chronic lymphocytic leukemia (CLL) and the identification of potential new therapeutic targets. As a result, researchers have developed novel targeted therapies, several of which are already approved and many of which are in advanced stages of clinical development. These new agents are much less toxic than chemoimmunotherapy and may be preferred for their superior efficacy in patients with certain high-risk features, such as del(17p). The place of these therapies in CLL management is becoming better defined, and they are gradually replacing traditional forms of chemoimmunotherapy. This review provides an update on the clinical data regarding various signal transduction inhibitors in CLL.
MeSH term(s)	Animals ; Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/adverse effects ; Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/diagnosis ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/etiology ; Leukemia, Lymphocytic, Chronic, B-Cell/mortality ; Molecular Targeted Therapy ; Neoplasm Staging ; Prognosis ; Treatment Outcome
Chemical Substances	Antineoplastic Agents ; Biomarkers, Tumor
Language	English
Publishing date	2018-05-09
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2271951-9
ISSN	1543-0790
ISSN	1543-0790
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Article ; Online: Molecular pathogenesis of acquired aplastic anemia.

Boddu, Prajwal C / Kadia, Tapan M

European journal of haematology

2018 Volume 102, Issue 2, Page(s) 103–110

Abstract: The application of next-generation sequencing (NGS) has enhanced our understanding of the genetic landscape in acquired aplastic anemia (AA). Parallel progress has been in addressing aspects underlying immune dysregulation in disease pathogenesis. Novel ... ...

Abstract	The application of next-generation sequencing (NGS) has enhanced our understanding of the genetic landscape in acquired aplastic anemia (AA). Parallel progress has been in addressing aspects underlying immune dysregulation in disease pathogenesis. Novel insights into the molecular and biologic mechanisms have led to a shift in the paradigm of AA, from a solely autoimmune pathogenic concept toward its recognition as a multifaceted pathophysiology characterized by cytogenetic abnormalities, recurrent somatic mutations, telomere attrition, and immune dysregulation. The detection of recurrent driver mutations disrupting myelodysplastic syndrome (MDS)/acute myeloid leukemia (AML)-associated genes has suggested a pathophysiologic link between clonal hematopoiesis in AA and the later development of these clonal disorders. Further, certain AA-related somatic genetic alterations may have clinical implications on treatment response, disease progression, and survival following immunosuppressive therapy. Going forward, wider validation of these genetic abnormalities will allow for their incorporation into a more informative risk stratification system that does not rely solely on clinical factors.
MeSH term(s)	Anemia, Aplastic/blood ; Anemia, Aplastic/diagnosis ; Anemia, Aplastic/etiology ; Anemia, Aplastic/metabolism ; Animals ; Clonal Evolution/genetics ; Disease Susceptibility ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; Humans ; Immunogenetic Phenomena ; Mutation ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism
Language	English
Publishing date	2018-12-18
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	392482-8
ISSN	1600-0609 ; 0902-4441
ISSN (online)	1600-0609
ISSN	0902-4441
DOI	10.1111/ejh.13182
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Article ; Online: Prognostic Factors in the Era of Targeted Therapies in CLL.

Boddu, Prajwal / Ferrajoli, Alessandra

Current hematologic malignancy reports

2018 Volume 13, Issue 2, Page(s) 78–90

Abstract: Purpose of review: Chronic lymphocytic leukemia is heterogeneous disease characterized by a variable clinical course that is greatly influenced by various patient and disease characteristics. Over the last two decades, advent of new diagnostic ... ...

Abstract	Purpose of review: Chronic lymphocytic leukemia is heterogeneous disease characterized by a variable clinical course that is greatly influenced by various patient and disease characteristics. Over the last two decades, advent of new diagnostic methodologies has led to the identification of several factors of prognostic and predictive relevance. Furthermore, recent advances in next-generation sequencing techniques has identified recurrent novel mutations in NOTCH1, SF3B1, BIRC3, and ATM genes whose role as prognostic and predictive markers is currently being investigated. These biologic markers carry new prognostic information and their incorporation into prognostic scoring systems will likely lead to refined multi-parameter risk models. Recent findings: While the prognostic impact of many of the most commonly used markers on clinical outcomes in patients treated with chemo-immunotherapy is well documented, it is important to review their predictive and prognostic role in the era of novel targeted therapies. This article will discuss the currently available information on the clinical relevance of prognostic markers in patients treated with novel targeted therapies.
MeSH term(s)	Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; High-Throughput Nucleotide Sequencing ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/diagnosis ; Leukemia, Lymphocytic, Chronic, B-Cell/drug therapy ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Mutation ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Prognosis
Chemical Substances	Biomarkers, Tumor ; Neoplasm Proteins
Language	English
Publishing date	2018-02-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2229765-0
ISSN	1558-822X ; 1558-8211
ISSN (online)	1558-822X
ISSN	1558-8211
DOI	10.1007/s11899-018-0439-9
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Article ; Online: Updates on the pathophysiology and treatment of aplastic anemia: a comprehensive review.

Boddu, Prajwal Chaitanya / Kadia, Tapan Mahendra

Expert review of hematology

2017 Volume 10, Issue 5, Page(s) 433–448

Abstract: Introduction: The past decade or longer has witnessed an acceleration in our understanding of previously developed immune system and clonal evolution mechanisms, and the genesis of more novel concepts of telomere attrition. Many of these concepts are ... ...

Abstract	Introduction: The past decade or longer has witnessed an acceleration in our understanding of previously developed immune system and clonal evolution mechanisms, and the genesis of more novel concepts of telomere attrition. Many of these concepts are steadily finding their way into translation in various aspects of clinical practice, and provide prospects to improve AA management and inform therapeutic strategy development. In this review, we intend to discuss the pathophysiology and treatments with an emphasis on most recent developments to provide an update on our understanding of disease mechanisms. Areas covered: A literature search was undertaken addressing various aspects of pathophysiology with a focus on the role of immune system repertoire, telomeres and mutational events surrounding AA. We also reviewed upon the temporal evolution of treatment strategies in AA to the contemporary management of today and commented briefly upon the more recently investigated novel therapies and their expanding niche especially in the transplant and salvage setting. Expert commentary: Immune-mediated destruction of hematopoietic stem and progenitor cells, leading to a marrow devoid of hematopoietic elements, and peripheral pancytopenia are the hallmarks of AA. Recent studies have shed light on another facet of the disease - as a clonal disorder characterized by karyotypic abnormalities, genomic instability, telomere attrition, and recurrent somatic mutations reminiscent of myeloid malignancies. Further understanding of this underlying pathophysiology can help in improving prognostication and treatment of this disease.
MeSH term(s)	Abnormal Karyotype ; Anemia, Aplastic/genetics ; Anemia, Aplastic/metabolism ; Anemia, Aplastic/physiopathology ; Anemia, Aplastic/therapy ; Genomic Instability ; Hematopoietic Stem Cells/metabolism ; Humans ; Telomere/genetics ; Telomere/metabolism
Language	English
Publishing date	2017-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2516804-6
ISSN	1747-4094 ; 1747-4086
ISSN (online)	1747-4094
ISSN	1747-4086
DOI	10.1080/17474086.2017.1313700
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Article: Transcription elongation defects link oncogenic splicing factor mutations to targetable alterations in chromatin landscape.

Boddu, Prajwal C / Gupta, Abhishek / Roy, Rahul / De La Pena Avalos, Barbara / Herrero, Ane Olazabal / Neuenkirchen, Nils / Zimmer, Josh / Chandhok, Namrata / King, Darren / Nannya, Yashuhito / Ogawa, Seishi / Lin, Haifan / Simon, Matthew / Dray, Eloise / Kupfer, Gary / Verma, Amit K / Neugebauer, Karla M / Pillai, Manoj M

bioRxiv : the preprint server for biology

2023

Language	English
Publishing date	2023-02-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.02.25.530019
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Article ; Online: Hedgehog pathway inhibition as a therapeutic target in acute myeloid leukemia.

Shallis, Rory M / Bewersdorf, Jan Philipp / Boddu, Prajwal C / Zeidan, Amer M

Expert review of anticancer therapy

2019 Volume 19, Issue 8, Page(s) 717–729

Abstract: ... ...

Abstract	Introduction
MeSH term(s)	Adult ; Animals ; Antineoplastic Agents/pharmacology ; Benzimidazoles/pharmacology ; Hedgehog Proteins/metabolism ; Hematopoietic Stem Cells/cytology ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/pathology ; Molecular Targeted Therapy ; Phenylurea Compounds/pharmacology ; Signal Transduction/drug effects ; Stem Cells/cytology
Chemical Substances	Antineoplastic Agents ; Benzimidazoles ; Hedgehog Proteins ; Phenylurea Compounds ; glasdegib (K673DMO5H9)
Language	English
Publishing date	2019-08-17
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2112544-2
ISSN	1744-8328 ; 1473-7140
ISSN (online)	1744-8328
ISSN	1473-7140
DOI	10.1080/14737140.2019.1652095
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Article ; Online: The FANCI/FANCD2 complex links DNA damage response to R-loop regulation through SRSF1-mediated mRNA export.

Olazabal-Herrero, Anne / He, Boxue / Kwon, Youngho / Gupta, Abhishek K / Dutta, Arijit / Huang, Yuxin / Boddu, Prajwal / Liang, Zhuobin / Liang, Fengshan / Teng, Yaqun / Lan, Li / Chen, Xiaoyong / Pei, Huadong / Pillai, Manoj M / Sung, Patrick / Kupfer, Gary M

Cell reports

2024 Volume 43, Issue 1, Page(s) 113610

Abstract: Fanconi anemia (FA) is characterized by congenital abnormalities, bone marrow failure, and cancer susceptibility. The central FA protein complex FANCI/FANCD2 (ID2) is activated by monoubiquitination and recruits DNA repair proteins for interstrand ... ...

Abstract	Fanconi anemia (FA) is characterized by congenital abnormalities, bone marrow failure, and cancer susceptibility. The central FA protein complex FANCI/FANCD2 (ID2) is activated by monoubiquitination and recruits DNA repair proteins for interstrand crosslink (ICL) repair and replication fork protection. Defects in the FA pathway lead to R-loop accumulation, which contributes to genomic instability. Here, we report that the splicing factor SRSF1 and FANCD2 interact physically and act together to suppress R-loop formation via mRNA export regulation. We show that SRSF1 stimulates FANCD2 monoubiquitination in an RNA-dependent fashion. In turn, FANCD2 monoubiquitination proves crucial for the assembly of the SRSF1-NXF1 nuclear export complex and mRNA export. Importantly, several SRSF1 cancer-associated mutants fail to interact with FANCD2, leading to inefficient FANCD2 monoubiquitination, decreased mRNA export, and R-loop accumulation. We propose a model wherein SRSF1 and FANCD2 interaction links DNA damage response to the avoidance of pathogenic R-loops via regulation of mRNA export.
MeSH term(s)	Humans ; R-Loop Structures ; Active Transport, Cell Nucleus ; Fanconi Anemia/metabolism ; Fanconi Anemia Complementation Group Proteins/metabolism ; Fanconi Anemia Complementation Group D2 Protein/genetics ; Fanconi Anemia Complementation Group D2 Protein/metabolism ; Ubiquitination ; DNA Repair ; Neoplasms ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; DNA Damage ; Serine-Arginine Splicing Factors/genetics ; Serine-Arginine Splicing Factors/metabolism
Chemical Substances	Fanconi Anemia Complementation Group Proteins ; Fanconi Anemia Complementation Group D2 Protein ; RNA, Messenger ; FANCD2 protein, human ; FANCI protein, human ; SRSF1 protein, human ; Serine-Arginine Splicing Factors (170974-22-8)
Language	English
Publishing date	2024-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113610
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