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Article ; Online: Myeloid malignancies-related somatic mutations in aging individuals.

Coutinho, Diego F / Zalcberg, Ilana R / Monte-Mór, Bárbara C R

2019 Volume 7, Issue 6, Page(s) e683

Abstract: We search for the presence of somatic mutations in 12 genes related to MDS, MPN, and AML in a Brazilian cohort composed of 609 elderly individuals from a census-based sample. ...

Abstract	We search for the presence of somatic mutations in 12 genes related to MDS, MPN, and AML in a Brazilian cohort composed of 609 elderly individuals from a census-based sample.
MeSH term(s)	Age Factors ; Aged ; Aged, 80 and over ; Brazil/epidemiology ; Cohort Studies ; Female ; Hematopoiesis ; Humans ; Leukemia, Myeloid/blood ; Leukemia, Myeloid/epidemiology ; Leukemia, Myeloid/genetics ; Male ; Middle Aged ; Mutation ; Neoplasms/blood ; Neoplasms/epidemiology ; Neoplasms/genetics ; Whole Exome Sequencing/methods
Language	English
Publishing date	2019-04-21
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2734884-2
ISSN	2324-9269 ; 2324-9269
ISSN (online)	2324-9269
ISSN	2324-9269
DOI	10.1002/mgg3.683
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Article ; Online: Bromodomain 4 inhibition leads to MYCN downregulation in Wilms tumor.

Woods, Andrew D / Berlow, Noah E / Ortiz, Michael V / Dela Cruz, Filemon / Siddiquee, Armaan / Coutinho, Diego F / Purohit, Reshma / Freier, Katherine E Tranbarger / Michalek, Joel E / Lathara, Melvin / Matlock, Kevin / Srivivasa, Ganapati / Royer-Pokora, Brigitte / Veselska, Renata / Kung, Andrew L / Keller, Charles

Pediatric blood & cancer

2021 Volume 69, Issue 2, Page(s) e29401

Abstract: Background: Wilms tumor is the most common childhood kidney cancer. Two distinct histological subtypes of Wilms tumor have been described: tumors lacking anaplasia (the favorable subtype) and tumors displaying anaplastic features (the unfavorable ... ...

Abstract	Background: Wilms tumor is the most common childhood kidney cancer. Two distinct histological subtypes of Wilms tumor have been described: tumors lacking anaplasia (the favorable subtype) and tumors displaying anaplastic features (the unfavorable subtype). Children with favorable disease generally have a very good prognosis, whereas those with anaplasia are oftentimes refractory to standard treatments and suffer poor outcomes, leading to an unmet clinical need. MYCN dysregulation has been associated with a number of pediatric cancers including Wilms tumor. Procedures: In this context, we undertook a functional genomics approach to uncover novel therapeutic strategies for those patients with anaplastic Wilms tumor. Genomic analysis and in vitro experimentation demonstrate that cell growth can be reduced by modulating MYCN overexpression via bromodomain 4 (BRD4) inhibition in both anaplastic and nonanaplastic Wilms tumor models. Results: We observed a time-dependent reduction of MYCN and MYCC protein levels upon BRD4 inhibition in Wilms tumor cell lines, which led to cell death and proliferation suppression. BRD4 inhibition significantly reduced tumor volumes in Wilms tumor patient-derived xenograft (PDX) mouse models. Conclusions: We suggest that AZD5153, a novel dual-BRD4 inhibitor, can reduce MYCN levels in both anaplastic and nonanaplastic Wilms tumor cell lines, reduces tumor volume in Wilms tumor PDXs, and should be further explored for its therapeutic potential.
MeSH term(s)	Anaplasia/genetics ; Animals ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Child ; Down-Regulation ; Female ; Humans ; Kidney Neoplasms/drug therapy ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Male ; Mice ; N-Myc Proto-Oncogene Protein/genetics ; Nuclear Proteins/genetics ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Wilms Tumor/drug therapy ; Wilms Tumor/genetics ; Wilms Tumor/metabolism
Chemical Substances	BRD4 protein, human ; Cell Cycle Proteins ; MYCN protein, human ; N-Myc Proto-Oncogene Protein ; Nuclear Proteins ; Transcription Factors
Language	English
Publishing date	2021-10-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2131448-2
ISSN	1545-5017 ; 1545-5009
ISSN (online)	1545-5017
ISSN	1545-5009
DOI	10.1002/pbc.29401
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Zs.A 1131: Show issues

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Article ; Online: Validation of a non-oncogene encoded vulnerability to exportin 1 inhibition in pediatric renal tumors.

Med (New York, N.Y.)

2022 Volume 3, Issue 11, Page(s) 774–791.e7

Abstract: Background: Malignant rhabdoid tumors (MRTs) and Wilms' tumors (WTs) are rare and aggressive renal tumors of infants and young children comprising ∼5% of all pediatric cancers. MRTs are among the most genomically stable cancers, and although WTs are ... ...

Abstract	Background: Malignant rhabdoid tumors (MRTs) and Wilms' tumors (WTs) are rare and aggressive renal tumors of infants and young children comprising ∼5% of all pediatric cancers. MRTs are among the most genomically stable cancers, and although WTs are genomically heterogeneous, both generally lack therapeutically targetable genetic mutations. Methods: Comparative protein activity analysis of MRTs (n = 68) and WTs (n = 132) across TCGA and TARGET cohorts, using metaVIPER, revealed elevated exportin 1 (XPO1) inferred activity. In vitro studies were performed on a panel of MRT and WT cell lines to evaluate effects on proliferation and cell-cycle progression following treatment with the selective XPO1 inhibitor selinexor. In vivo anti-tumor activity was assessed in patient-derived xenograft (PDX) models of MRTs and WTs. Findings: metaVIPER analysis identified markedly aberrant activation of XPO1 in MRTs and WTs compared with other tumor types. All MRT and most WT cell lines demonstrated baseline, aberrant XPO1 activity with in vitro sensitivity to selinexor via cell-cycle arrest and induction of apoptosis. In vivo, XPO1 inhibitors significantly abrogated tumor growth in PDX models, inducing effective disease control with sustained treatment. Corroborating human relevance, we present a case report of a child with multiply relapsed WTs with prolonged disease control on selinexor. Conclusions: We report on a novel systems-biology-based comparative framework to identify non-genetically encoded vulnerabilities in genomically quiescent pediatric cancers. These results have provided preclinical rationale for investigation of XPO1 inhibitors in an upcoming investigator-initiated clinical trial of selinexor in children with MRTs and WTs and offer opportunities for exploration of inferred XPO1 activity as a potential predictive biomarker for response. Funding: This work was funded by CureSearch for Children's Cancer, Alan B. Slifka Foundation, NIH (U01 CA217858, S10 OD012351, and S10 OD021764), Michael's Miracle Cure, Hyundai Hope on Wheels, Cannonball Kids Cancer, Conquer Cancer the ASCO Foundation, Cycle for Survival, Paulie Strong Foundation, and the Grayson Fund.
MeSH term(s)	Child ; Humans ; Child, Preschool ; Cell Line, Tumor ; Xenograft Model Antitumor Assays ; Kidney Neoplasms/drug therapy ; Exportin 1 Protein
Chemical Substances	selinexor (31TZ62FO8F)
Language	English
Publishing date	2022-10-03
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2666-6340
ISSN (online)	2666-6340
DOI	10.1016/j.medj.2022.09.002
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Article ; Online: Myeloid neoplasias: what molecular analyses are telling us.

Gutiyama, Luciana M / Coutinho, Diego F / Lipkin, Marina V / Zalcberg, Ilana R

ISRN oncology

2012 Volume 2012, Page(s) 321246

Abstract: In the last decades, cytogenetic and molecular characterizations of hematological disorders at diagnosis and followup have been most valuable for guiding therapeutic decisions and prognosis. Genetic and epigenetic alterations detected by different ... ...

Abstract	In the last decades, cytogenetic and molecular characterizations of hematological disorders at diagnosis and followup have been most valuable for guiding therapeutic decisions and prognosis. Genetic and epigenetic alterations detected by different procedures have been associated to different cancer types and are considered important indicators for disease classification, differential diagnosis, prognosis, response, and individualization of therapy. The search for new biomarkers has been revolutionized by high-throughput technologies. At this point, it seems that we have overcome technological barriers, but we are still far from sorting the biological puzzle. Evidence based on translational research is required for validating novel genetic and epigenetic markers for routine clinical practice. We herein discuss the importance of genetic abnormalities and their molecular pathways in acute myeloid leukemia, myelodysplastic syndromes, and myeloproliferative neoplasms. We also discuss how novel genomic abnormalities may interact and reassess concepts and classifications of myeloid neoplasias.
Language	English
Publishing date	2012-09-27
Publishing country	Egypt
Document type	Journal Article
ZDB-ID	2612994-2
ISSN	2090-567X ; 2090-567X
ISSN (online)	2090-567X
ISSN	2090-567X
DOI	10.5402/2012/321246
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Article ; Online: TET2 mutations as a part of DNA dioxygenase deficiency in myelodysplastic syndromes.

Blood advances

2021 Volume 6, Issue 1, Page(s) 100–107

Abstract: Decrease in DNA dioxygenase activity generated by TET2 gene family is crucial in myelodysplastic syndromes (MDS). The general downregulation of 5-hydroxymethylcytosine (5-hmC) argues for a role of DNA demethylation in MDS beyond TET2 mutations, which ... ...

Abstract	Decrease in DNA dioxygenase activity generated by TET2 gene family is crucial in myelodysplastic syndromes (MDS). The general downregulation of 5-hydroxymethylcytosine (5-hmC) argues for a role of DNA demethylation in MDS beyond TET2 mutations, which albeit frequent, do not convey any prognostic significance. We investigated TETs expression to identify factors which can modulate the impact of mutations and thus 5-hmC levels on clinical phenotypes and prognosis of MDS patients. DNA/RNA-sequencing and 5-hmC data were collected from 1665 patients with MDS and 91 controls. Irrespective of mutations, a significant fraction of MDS patients exhibited lower TET2 expression, whereas 5-hmC levels were not uniformly decreased. In searching for factors explaining compensatory mechanisms, we discovered that TET3 was upregulated in MDS and inversely correlated with TET2 expression in wild-type cases. Although TET2 was reduced across all age groups, TET3 levels were increased in a likely feedback mechanism induced by TET2 dysfunction. This inverse relationship of TET2 and TET3 expression also corresponded to the expression of L-2-hydroxyglutarate dehydrogenase, involved in agonist/antagonist substrate metabolism. Importantly, elevated TET3 levels influenced the clinical phenotype of TET2 deficiency whereby the lack of compensation by TET3 (low TET3 expression) was associated with poor outcomes of TET2 mutant carriers.
MeSH term(s)	DNA ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Dioxygenases/genetics ; Humans ; Mutation ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/metabolism ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism
Chemical Substances	DNA-Binding Proteins ; Proto-Oncogene Proteins ; DNA (9007-49-2) ; Dioxygenases (EC 1.13.11.-) ; TET2 protein, human (EC 1.13.11.-)
Language	English
Publishing date	2021-11-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2021005418
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Article: Genetic Alterations in Essential Thrombocythemia Progression to Acute Myeloid Leukemia: A Case Series and Review of the Literature.

Ayres-Silva, Jackline P / Bonamino, Martin H / Gouveia, Maria E / Monte-Mor, Barbara C R / Coutinho, Diego F / Daumas, Adelmo H / Solza, Cristiana / Braggio, Esteban / Zalcberg, Ilana Renault

Frontiers in oncology

2018 Volume 8, Page(s) 32

Abstract: The genetic events associated with transformation of myeloproliferative neoplasms (MPNs) to secondary acute myeloid leukemia (sAML), particularly in the subgroup of essential thrombocythemia (ET) patients, remain incompletely understood. Deep studies ... ...

Abstract	The genetic events associated with transformation of myeloproliferative neoplasms (MPNs) to secondary acute myeloid leukemia (sAML), particularly in the subgroup of essential thrombocythemia (ET) patients, remain incompletely understood. Deep studies using high-throughput methods might lead to a better understanding of genetic landscape of ET patients who transformed to sAML. We performed array-based comparative genomic hybridization (aCGH) and whole exome sequencing (WES) to analyze paired samples from ET and sAML phases. We investigated five patients with previous history of MPN, which four had initial diagnosis of ET (one case harboring
Language	English
Publishing date	2018-02-19
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2018.00032
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Article ; Online: Bone marrow fibrosis at diagnosis is associated with TP53 overexpression and adverse prognosis in low-risk myelodysplastic syndrome.

Duarte, Fernando B / Barbosa, Maritza C / Jesus Dos Santos, Talyta E / Lemes, Romélia P G / Vasconcelos, João P / de Vasconcelos, Paulo R L / Rocha, Francisco D / Zalcberg, Ilana / Coutinho, Diego F

British journal of haematology

2017 Volume 181, Issue 4, Page(s) 547–549

MeSH term(s)	Aged ; Disease-Free Survival ; Female ; Gene Expression Regulation ; Humans ; Male ; Middle Aged ; Myelodysplastic Syndromes/diagnosis ; Myelodysplastic Syndromes/metabolism ; Myelodysplastic Syndromes/mortality ; Primary Myelofibrosis/diagnosis ; Primary Myelofibrosis/metabolism ; Primary Myelofibrosis/mortality ; Survival Rate ; Tumor Suppressor Protein p53/biosynthesis
Chemical Substances	TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2017-03-20
Publishing country	England
Document type	Letter
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/bjh.14656
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Article ; Online: Presence of CD34

Duarte, Fernando Barroso / DE Jesus Dos Santos, Talyta Ellen / Barbosa, Maritza Cavalcante / Moura, Anna Thawanny Gadelha / DE Vasconcelos, João Paulo Leitão / Rocha-Filho, Francisco Dário / Coutinho, Diego F / Zalcberg, Ilana / Vasconcelos, Paulo R L / Garcia, Yhasmine Delles Oliverira / Lemes, Romélia Pinheiro Gonçalves

In vivo (Athens, Greece)

2018 Volume 33, Issue 1, Page(s) 277–280

Abstract: Background/aim: Although risk stratification using the Prognostic Scores Systems (IPSS, WPSS and IPSS-R) incorporate key information about prognosis of patients with Myelodysplastic syndromes (MDS), patients classified as low-risk may evolve rapidly and ...

Abstract	Background/aim: Although risk stratification using the Prognostic Scores Systems (IPSS, WPSS and IPSS-R) incorporate key information about prognosis of patients with Myelodysplastic syndromes (MDS), patients classified as low-risk may evolve rapidly and aggressively, despite a "favorable" prognostic stratification. The aim of this study was to identify biomarkers for predicting prognosis, and for better stratification and management of these patients. Materials and methods: Expression of CD34 and p53 in megakaryocytes was examined by immunohistochemistry in 71 MDS patients classified as low-risk. Results: CD34 staining in megakaryocytes was associated with p53 expression (p=0.0166). CD34 and p53 expression were associated to worse overall survival in patients (p=0.0281). Conclusion: The presence of CD34 in megakaryocytes is associated with p53 expression and an adverse prognosis for MDS patients.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Antigens, CD34/genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Megakaryocytes/metabolism ; Megakaryocytes/pathology ; Middle Aged ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/metabolism ; Myelodysplastic Syndromes/pathology ; Prognosis ; Risk Assessment ; Risk Factors ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Antigens, CD34 ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2018-12-18
Publishing country	Greece
Document type	Journal Article
ZDB-ID	807031-3
ISSN	1791-7549 ; 0258-851X
ISSN (online)	1791-7549
ISSN	0258-851X
DOI	10.21873/invivo.11472
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Zs.A 2288: Show issues

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Article ; Online: Comprehensive Molecular Profiling of Desmoplastic Small Round Cell Tumor.

Slotkin, Emily K / Bowman, Anita S / Levine, Max F / Dela Cruz, Filemon / Coutinho, Diego F / Sanchez, Glorymar I / Rosales, Nestor / Modak, Shakeel / Tap, William D / Gounder, Mrinal M / Thornton, Katherine A / Bouvier, Nancy / You, Daoqi / Gundem, Gunes / Gerstle, Justin T / Heaton, Todd E / LaQuaglia, Michael P / Wexler, Leonard H / Meyers, Paul A /

Kung, Andrew L / Papaemmanuil, Elli / Zehir, Ahmet / Ladanyi, Marc / Shukla, Neerav

Molecular cancer research : MCR

2021 Volume 19, Issue 7, Page(s) 1146–1155

Abstract: Desmoplastic small round cell tumor (DSRCT) is characterized by ... ...

Abstract	Desmoplastic small round cell tumor (DSRCT) is characterized by the
MeSH term(s)	Adolescent ; Adult ; Cell Line, Tumor ; Child ; DNA Copy Number Variations/genetics ; Desmoplastic Small Round Cell Tumor/genetics ; Desmoplastic Small Round Cell Tumor/metabolism ; Desmoplastic Small Round Cell Tumor/pathology ; Female ; Gene Expression Profiling/methods ; Gene Expression Regulation, Neoplastic ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Male ; Middle Aged ; Multiplex Polymerase Chain Reaction/methods ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; RNA-Binding Protein EWS/genetics ; RNA-Binding Protein EWS/metabolism ; Receptor, Fibroblast Growth Factor, Type 4/genetics ; Receptor, Fibroblast Growth Factor, Type 4/metabolism ; WT1 Proteins/genetics ; WT1 Proteins/metabolism ; Young Adult
Chemical Substances	EWSR1 protein, human ; Oncogene Proteins, Fusion ; RNA-Binding Protein EWS ; WT1 Proteins ; WT1 protein, human ; FGFR4 protein, human (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 4 (EC 2.7.10.1)
Language	English
Publishing date	2021-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-20-0722
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Zs.A 5744: Show issues

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Article ; Online: TET2 expression level and 5-hydroxymethylcytosine are decreased in refractory cytopenia of childhood.

Coutinho, Diego F / Monte-Mór, Bárbara C R / Vianna, Danielle T / Rouxinol, Soraia T / Batalha, Anna Beatriz W / Bueno, Ana Paula S / Boulhosa, Alice M / Fernandez, Teresa S / Pombo-de-Oliveira, Maria S / Gutiyama, Luciana M / Abdelhay, Eliana / Zalcberg, Ilana R

Leukemia research

2015 Volume 39, Issue 10, Page(s) 1103–1108

Abstract: Myelodysplastic syndromes (MDS) are myeloid malignancies characterized by ineffective hematopoiesis, dysplasia, peripheral cytopenia and increased risk of progression to acute myeloid leukemia. Refractory cytopenia of childhood (RCC) is the most common ... ...

Abstract	Myelodysplastic syndromes (MDS) are myeloid malignancies characterized by ineffective hematopoiesis, dysplasia, peripheral cytopenia and increased risk of progression to acute myeloid leukemia. Refractory cytopenia of childhood (RCC) is the most common subtype of pediatric MDS and has overlapping clinical features with viral infections and autoimmune disorders. Mutations in TET2 gene are found in about 20-25% of adult MDS and are associated with a decrease in 5-hydroxymethylcytosine (5-hmC) content. TET2 deregulation and its malignant potential were reported in adult but not in pediatric MDS. We evaluated the gene expression and the presence of mutations in TET2 gene in 19 patients with RCC. TET2 expression level was correlated with 5-hmC amount in DNA and possible regulatory epigenetic mechanisms. One out of 19 pediatric patients with RCC was a carrier of a TET2 mutation. TET2 expression and 5-hmC levels were decreased in patients when compared to a disease-free group. Lower expression was not associated to the presence of mutation or with the status of promoter methylation, but a significant correlation with microRNA-22 expression was found. These findings suggested that TET2 downregulation and low levels of 5-hmC are inversely related to miR-22 expression. The existence of a regulatory loop between microRNA-22 and TET2 may play a role in MDS pathogenesis.
MeSH term(s)	5-Methylcytosine/analogs & derivatives ; Adolescent ; Case-Control Studies ; Child ; Child, Preschool ; Cytosine/analogs & derivatives ; Cytosine/biosynthesis ; DNA Mutational Analysis ; DNA-Binding Proteins/biosynthesis ; DNA-Binding Proteins/genetics ; Female ; Gene Expression Regulation/genetics ; High-Throughput Nucleotide Sequencing ; Humans ; Infant ; Male ; MicroRNAs/genetics ; Mutation ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/metabolism ; Polymerase Chain Reaction ; Proto-Oncogene Proteins/biosynthesis ; Proto-Oncogene Proteins/genetics ; Transcriptome
Chemical Substances	DNA-Binding Proteins ; MIRN22 microRNA, human ; MicroRNAs ; Proto-Oncogene Proteins ; 5-hydroxymethylcytosine (1123-95-1) ; 5-Methylcytosine (6R795CQT4H) ; Cytosine (8J337D1HZY) ; TET2 protein, human (EC 1.13.11.-)
Language	English
Publishing date	2015-07-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	752396-8
ISSN	1873-5835 ; 0145-2126
ISSN (online)	1873-5835
ISSN	0145-2126
DOI	10.1016/j.leukres.2015.07.005
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