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Article: Gene expression and epigenetic deregulation.

Shaknovich, Rita

Advances in experimental medicine and biology

2013 Volume 792, Page(s) 133–150

Abstract: The last decade resulted in many scientific discoveries illuminating epigenetic mechanisms of gene regulation and genome organization. DNA methylation emerged as playing a pivotal role in development and cancer. Genome-wide changes in DNA methylation, ... ...

Abstract	The last decade resulted in many scientific discoveries illuminating epigenetic mechanisms of gene regulation and genome organization. DNA methylation emerged as playing a pivotal role in development and cancer. Genome-wide changes in DNA methylation, including hypermethylation of tumor suppressor genes and genome-wide loss of methylation, are two dominant mechanisms that deregulate gene expression and contribute to chromosomal instability. In this chapter we give an overview of how methylation patterns are established during B-cell development and what machinery is necessary to maintain those patterns. We summarize the current state of knowledge of aberrant changes taking place during and contributing to lymphoid transformation in general and to the development of CLL in particular. We discuss key deregulated biomarkers extensively studied using single-gene approaches and give an overview of a wealth of data that became available from genome-wide approaches, focusing on pathways that are critical for lymphomagenesis. We also highlight epigenetic differences between known prognostic groups of CLL.
MeSH term(s)	Chromatin Assembly and Disassembly ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation, Leukemic ; Gene Silencing ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/etiology ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics
Language	English
Publishing date	2013
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-1-4614-8051-8_6
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Article ; Online: Author Correction: A purine scaffold Hsp90 inhibitor destabilizes BCL-6 and has specific antitumor activity in BCL-6-dependent B cell lymphomas.

Cerchietti, Leandro C / Lopes, Eloisi C / Yang, Shao Ning / Hatzi, Katerina / Bunting, Karen L / Tsikitas, Lucas A / Mallik, Alka / Robles, Ana I / Walling, Jennifer / Varticovski, Lyuba / Shaknovich, Rita / Bhalla, Kapil N / Chiosis, Gabriela / Melnick, Ari

Nature medicine

2024

Language	English
Publishing date	2024-04-03
Publishing country	United States
Document type	Published Erratum
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/s41591-024-02957-0
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Article: Epigenetic function of activation-induced cytidine deaminase and its link to lymphomagenesis.

Dominguez, Pilar M / Shaknovich, Rita

Frontiers in immunology

2014 Volume 5, Page(s) 642

Abstract: Activation-induced cytidine deaminase (AID) is essential for somatic hypermutation and class switch recombination of immunoglobulin (Ig) genes during B cell maturation and immune response. Expression of AID is tightly regulated due to its mutagenic and ... ...

Abstract	Activation-induced cytidine deaminase (AID) is essential for somatic hypermutation and class switch recombination of immunoglobulin (Ig) genes during B cell maturation and immune response. Expression of AID is tightly regulated due to its mutagenic and recombinogenic potential, which is known to target not only Ig genes, but also non-Ig genes, contributing to lymphomagenesis. In recent years, a new epigenetic function of AID and its link to DNA demethylation came to light in several developmental systems. In this review, we summarize existing evidence linking deamination of unmodified and modified cytidine by AID to base-excision repair and mismatch repair machinery resulting in passive or active removal of DNA methylation mark, with the focus on B cell biology. We also discuss potential contribution of AID-dependent DNA hypomethylation to lymphomagenesis.
Language	English
Publishing date	2014
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2014.00642
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Article ; Online: The new frontier of epigenetic heterogeneity in B-cell neoplasms.

Dominguez, Pilar M / Teater, Matt / Shaknovich, Rita

Current opinion in hematology

2017 Volume 24, Issue 4, Page(s) 402–408

Abstract: Purpose of review: There is mounting evidence that heterogeneity of the epigenome is a feature of many cancers, including B-cell lymphomas, and presents important clinical implications. The purpose of this review is to explain the biological and ... ...

Abstract	Purpose of review: There is mounting evidence that heterogeneity of the epigenome is a feature of many cancers, including B-cell lymphomas, and presents important clinical implications. The purpose of this review is to explain the biological and clinical relevance of this epigenetic phenomenon in B-cell neoplasms. Recent findings: Here, we summarize new findings demonstrating that B-cell lymphomas display increased DNA methylation heterogeneity compared to their normal counterparts. This plasticity of cytosine methylation manifests both as intertumor and intratumor heterogeneity and is associated with worse prognosis and poor clinical outcome in lymphoma patients. Recent studies of different subtypes of B-cell lymphomas have revealed that epigenetic aberrations and heterogeneous cytosine methylation patterning are common features of all neoplasms derived from B-lymphocytes, irrespective of maturation stage. With regard to mechanisms driving this process, recent reports suggest that cytosine methylation heterogeneity arises through passive and active processes. One factor implicated in active generation of cytosine methylation heterogeneity is activation-induced cytidine deaminase, which mediates DNA methylation changes and introduces epigenetic heterogeneity in normal germinal center B cells, the cells of origin of mature B-cell neoplasms such as diffuse large B-cell lymphoma and follicular lymphoma. Summary: Understanding the scope and mechanism of epigenetic heterogeneity in cancer is of paramount importance to our understanding of clonal plasticity and treatment responses in B-cell lymphomas.
MeSH term(s)	Animals ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Genetic Heterogeneity ; Germinal Center/metabolism ; Humans ; Leukemia, B-Cell/diagnosis ; Leukemia, B-Cell/genetics ; Leukemia, B-Cell/metabolism ; Lymphoma, B-Cell/diagnosis ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/metabolism ; Signal Transduction
Language	English
Publishing date	2017-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000348
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Article ; Online: Epigenetics and B-cell lymphoma.

Shaknovich, Rita / Melnick, Ari

Current opinion in hematology

2011 Volume 18, Issue 4, Page(s) 293–299

Abstract: Purpose of review: It has only recently become apparent that mutations in epigenetic mechanisms and perturbation of epigenomic patterning are frequent events in B-cell lymphomas. The purpose of this review is to highlight these new findings and provide ... ...

Abstract	Purpose of review: It has only recently become apparent that mutations in epigenetic mechanisms and perturbation of epigenomic patterning are frequent events in B-cell lymphomas. The purpose of this review is to highlight these new findings and provide a conceptual framework for understanding how epigenetic modifications might contribute to lymphomagenesis. Recent findings: Somatic mutations affecting histone methyltransferases such as enhancer of zeste 2 and mixed lineage leukemia 2, histone demethylases including ubiquitously transcribed X chromosome tetratricopeptide repeat and Jumonji domain-containing 2C, and histone acetyltransferases including CBP and p300 are recurrent and common in lymphomas. These mutations result in disruption of chromatin structure and functions of other proteins, ultimately causing aberrant transcriptional programming affecting multiple gene networks. Widespread perturbation of cytosine methylation patterning now appears to be a hallmark of B-cell lymphomas and occurs in specific patterns that can distinguish disease subtypes. Therapeutic targeting strategies can overcome abnormal epigenetic mechanisms and potently kill lymphoma cells. Summary: Newly discovered epigenetic lesions may provide critical insights into the genesis of B-cell lymphomas, but further studies are required to understand how they affect biological mechanism. Epigenetic lesions offer tremendous opportunities for the development of improved biomarkers and treatments.
MeSH term(s)	Animals ; DNA Methylation ; Epigenesis, Genetic ; Humans ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/pathology
Language	English
Publishing date	2011-06-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0b013e32834788cf
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Article: Epigenetic diversity in hematopoietic neoplasms.

Shaknovich, Rita / De, Subhajyoti / Michor, Franziska

Biochimica et biophysica acta

2014 Volume 1846, Issue 2, Page(s) 477–484

Abstract: Tumor cell populations display a remarkable extent of variability in non-genetic characteristics such as DNA methylation, histone modification patterns, and differentiation levels of individual cells. It remains to be elucidated whether non-genetic ... ...

Abstract	Tumor cell populations display a remarkable extent of variability in non-genetic characteristics such as DNA methylation, histone modification patterns, and differentiation levels of individual cells. It remains to be elucidated whether non-genetic heterogeneity is simply a byproduct of tumor evolution or instead a manifestation of a higher-order tissue organization that is maintained within the neoplasm to establish a differentiation hierarchy, a favorable microenvironment, or a buffer against changing selection pressures during tumorigenesis. Here, we review recent findings on epigenetic diversity, particularly heterogeneity in DNA methylation patterns in hematologic malignancies. We also address the implications of epigenetic heterogeneity for the clonal evolution of tumors and discuss its effects on gene expression and other genome functions in cancer.
MeSH term(s)	Clonal Evolution ; DNA Methylation ; Epigenesis, Genetic ; Hematologic Neoplasms/genetics ; Humans ; Lymphoma/genetics
Language	English
Publishing date	2014-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbcan.2014.09.003
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Article ; Online: Mechanisms of epigenetic deregulation in lymphoid neoplasms.

Jiang, Yanwen / Hatzi, Katerina / Shaknovich, Rita

Blood

2013 Volume 121, Issue 21, Page(s) 4271–4279

MeSH term(s)	Animals ; Epigenesis, Genetic/physiology ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/physiopathology ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/physiopathology
Language	English
Publishing date	2013-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2012-12-451799
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Article ; Online: Single-cell spatial analysis of tumor immune architecture in diffuse large B-cell lymphoma.

Colombo, Anthony R / Hav, Monirath / Singh, Mohan / Xu, Alexander / Gamboa, Alicia / Lemos, Tucker / Gerdtsson, Erik / Chen, Denaly / Houldsworth, Jane / Shaknovich, Rita / Aoki, Tomohiro / Chong, Lauren / Takata, Katsuyoshi / Chavez, Elizabeth A / Steidl, Christian / Hicks, James / Kuhn, Peter / Siddiqi, Imran / Merchant, Akil

Blood advances

2022 Volume 6, Issue 16, Page(s) 4675–4690

Abstract: Multiplexed immune cell profiling of the tumor microenvironment (TME) in cancer has improved our understanding of cancer immunology, but complex spatial analyses of tumor-immune interactions in lymphoma are lacking. Here, we used imaging mass cytometry ( ... ...

Abstract	Multiplexed immune cell profiling of the tumor microenvironment (TME) in cancer has improved our understanding of cancer immunology, but complex spatial analyses of tumor-immune interactions in lymphoma are lacking. Here, we used imaging mass cytometry (IMC) on 33 cases of diffuse large B-cell lymphoma (DLBCL) to characterize tumor and immune cell architecture and correlate it to clinicopathological features such as cell of origin, gene mutations, and responsiveness to chemotherapy. To understand the poor response of DLBCL to immune checkpoint inhibitors (ICI), we compared our results to IMC data from Hodgkin lymphoma, a cancer highly responsive to ICI, and observed differences in the expression of PD-L1, PD-1, and TIM-3. We created a spatial classification of tumor cells and identified tumor-centric subregions of immune activation, immune suppression, and immune exclusion within the topology of DLBCL. Finally, the spatial analysis allowed us to identify markers such as CXCR3, which are associated with penetration of immune cells into immune desert regions, with important implications for engineered cellular therapies. This is the first study to integrate tumor mutational profiling, cell of origin classification, and multiplexed immuno-phenotyping of the TME into a spatial analysis of DLBCL at the single-cell level. We demonstrate that, far from being histopathologically monotonous, DLBCL has a complex tumor architecture, and that changes in tumor topology can be correlated with clinically relevant features. This analysis identifies candidate biomarkers and therapeutic targets such as TIM-3, CCR4, and CXCR3 that are relevant for combination treatment strategies in immuno-oncology and cellular therapies.
MeSH term(s)	Hepatitis A Virus Cellular Receptor 2 ; Hodgkin Disease ; Humans ; Lymphoma, Large B-Cell, Diffuse/pathology ; Spatial Analysis ; Tumor Microenvironment/genetics
Chemical Substances	Hepatitis A Virus Cellular Receptor 2
Language	English
Publishing date	2022-06-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2022007493
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Article: The PATHFINDER Study: Assessment of the Implementation of an Investigational Multi-Cancer Early Detection Test into Clinical Practice.

Nadauld, Lincoln D / McDonnell, Charles H / Beer, Tomasz M / Liu, Minetta C / Klein, Eric A / Hudnut, Andrew / Whittington, Richard A / Taylor, Bruce / Oxnard, Geoffrey R / Lipson, Jafi / Lopatin, Margarita / Shaknovich, Rita / Chung, Karen C / Fung, Eric T / Schrag, Deborah / Marinac, Catherine R

Cancers

2021 Volume 13, Issue 14

Abstract: To examine the extent of the evaluation required to achieve diagnostic resolution and the test performance characteristics of a targeted methylation cell-free DNA (cfDNA)-based multi-cancer early detection (MCED) test, ~6200 participants ≥50 years with ( ... ...

Abstract	To examine the extent of the evaluation required to achieve diagnostic resolution and the test performance characteristics of a targeted methylation cell-free DNA (cfDNA)-based multi-cancer early detection (MCED) test, ~6200 participants ≥50 years with (cohort A) or without (cohort B) ≥1 of 3 additional specific cancer risk factors will be enrolled in PATHFINDER (NCT04241796), a prospective, longitudinal, interventional, multi-center study. Plasma cfDNA from blood samples will be analyzed to detect abnormally methylated DNA associated with cancer (i.e., cancer "signal") and a cancer signal origin (i.e., tissue of origin). Participants with a "signal detected" will undergo further diagnostic evaluation per guiding physician discretion; those with a "signal not detected" will be advised to continue guideline-recommended screening. The primary objective will be to assess the number and types of subsequent diagnostic tests needed for diagnostic resolution. Based on microsimulations (using estimates of cancer incidence and dwell times) of the typical risk profiles of anticipated participants, the median (95% CI) number of participants with a "signal detected" result is expected to be 106 (87-128). Subsequent diagnostic evaluation is expected to detect 52 (39-67) cancers. The positive predictive value of the MCED test is expected to be 49% (39-58%). PATHFINDER will evaluate the integration of a cfDNA-based MCED test into existing clinical cancer diagnostic pathways. The study design of PATHFINDER is described here.
Language	English
Publishing date	2021-07-13
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13143501
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Article ; Online: Prognostic Significance of Blood-Based Multi-cancer Detection in Plasma Cell-Free DNA.

Chen, Xiaoji / Dong, Zhao / Hubbell, Earl / Kurtzman, Kathryn N / Oxnard, Geoffrey R / Venn, Oliver / Melton, Collin / Clarke, Christina A / Shaknovich, Rita / Ma, Ting / Meixiong, Gerry / Seiden, Michael V / Klein, Eric A / Fung, Eric T / Liu, Minetta C

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

2021 Volume 27, Issue 15, Page(s) 4221–4229

Abstract: Purpose: We recently reported the development of a cell-free DNA (cfDNA) targeted methylation (TM)-based sequencing approach for a multi-cancer early detection (MCED) test that includes cancer signal origin prediction. Here, we evaluated the prognostic ... ...

Abstract	Purpose: We recently reported the development of a cell-free DNA (cfDNA) targeted methylation (TM)-based sequencing approach for a multi-cancer early detection (MCED) test that includes cancer signal origin prediction. Here, we evaluated the prognostic significance of cancer detection by the MCED test using longitudinal follow-up data. Experimental design: As part of a Circulating Cell-free Genome Atlas (CCGA) substudy, plasma cfDNA samples were sequenced using a TM approach, and machine learning classifiers predicted cancer status and cancer signal origin. Overall survival (OS) of cancer participants in the first 3 years of follow-up was evaluated in relation to cancer detection by the MCED test and clinical characteristics. Results: Cancers not detected by the MCED test had significantly better OS ( Conclusions: Cancer detection by the MCED test was prognostic beyond clinical stage and method of diagnosis. Cancers not detected by the MCED test had better prognosis than cancers detected and SEER-based expected survival. Cancer detection and prognosis may be linked by the underlying biological factor of tumor fraction in cfDNA.
MeSH term(s)	Aged ; Circulating Tumor DNA/blood ; Early Detection of Cancer/methods ; Female ; Follow-Up Studies ; Humans ; Longitudinal Studies ; Male ; Middle Aged ; Neoplasms/blood ; Neoplasms/mortality ; Prognosis ; Survival Rate
Chemical Substances	Circulating Tumor DNA
Language	English
Publishing date	2021-06-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-21-0417
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