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Article ; Online: High Expression of TIM 3 and Galectin 9 on Immunohistochemistry Staining of Tumor Specimen at Diagnosis in Pediatric Patients with Ewing Sarcoma.

Si, Stephanie J / Wertheim, Gerald B / Barrett, David M

Journal of cancer immunology

2022 Volume 3, Issue 3, Page(s) 163–176

Abstract: Significant progress has been made in the advancement of immune system modulation for cancer treatment in recent years. In particular, immune checkpoint inhibitors and chimeric antigen receptor (CAR) T-cell therapy have demonstrated remarkable clinical ... ...

Abstract	Significant progress has been made in the advancement of immune system modulation for cancer treatment in recent years. In particular, immune checkpoint inhibitors and chimeric antigen receptor (CAR) T-cell therapy have demonstrated remarkable clinical benefit in relapsed/refractory cancers. However, our understanding of the immuno-oncologic landscape in pediatric solid tumors remains limited and is a barrier to continued progress. We examined the immunohistochemical expression of checkpoint receptors PD-1, TIM-3, LAG-3 and their respective ligands in various pediatric cancers at diagnosis and found high expression of TIM-3/Galectin-9 in the infiltrating cells of Ewing sarcoma. Location of checkpoint receptor/ligand expressions is important, as some staining patterns were only seen along tumor borders. Finally, peripheral T cell function varied significantly among different tumors supporting a complex relationship between the tumor microenvironment and the global immune system.
Language	English
Publishing date	2022-08-03
Publishing country	United States
Document type	Journal Article
ISSN	2689-968X
ISSN (online)	2689-968X
DOI	10.33696/cancerimmunol.3.053
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Article ; Online: Maturational dyssynchrony in benign B-cell precursors following lymphocyte depleting chemotherapy: A potential pitfall for B-lymphoblastic leukemia minimal/measurable residual disease (MRD) flow cytometry analysis.

Placek, Alexander / Lockhart, Brian / Miller, Karin P / Wertheim, Gerald B / Maude, Shannon L / Wood, Brent L / Kovach, Alexandra E

Cytometry. Part B, Clinical cytometry

2024 Volume 106, Issue 2, Page(s) 138–141

MeSH term(s)	Humans ; Flow Cytometry ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cells, B-Lymphoid ; Neoplasm, Residual
Language	English
Publishing date	2024-01-21
Publishing country	United States
Document type	Letter
ZDB-ID	2099657-3
ISSN	1552-4957 ; 1552-4949 ; 0196-4763
ISSN (online)	1552-4957
ISSN	1552-4949 ; 0196-4763
DOI	10.1002/cyto.b.22161
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Zs.A 1688: Show issues

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Article ; Online: NPM1 for MRD? Droplet Like It's Hot!

Wertheim, Gerald B W / Bagg, Adam

The Journal of molecular diagnostics : JMD

2017 Volume 19, Issue 4, Page(s) 498–501

Abstract: This commentary highlights the article by Mencia-Trinchant et al that describes a novel digital PCR assay for sensitive detection of minimal residual disease in NPM1 mutated acute myeloid leukemia. ...

Abstract	This commentary highlights the article by Mencia-Trinchant et al that describes a novel digital PCR assay for sensitive detection of minimal residual disease in NPM1 mutated acute myeloid leukemia.
MeSH term(s)	DNA Mutational Analysis/methods ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Neoplasm, Residual/diagnosis ; Neoplasm, Residual/genetics ; Nuclear Proteins/genetics ; Polymerase Chain Reaction/methods
Chemical Substances	Nuclear Proteins ; nucleophosmin (117896-08-9)
Language	English
Publishing date	2017-06-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2000060-1
ISSN	1943-7811 ; 1525-1578
ISSN (online)	1943-7811
ISSN	1525-1578
DOI	10.1016/j.jmoldx.2017.04.008
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Zs.A 5146: Show issues

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Article ; Online: Condensate-promoting ENL mutation drives tumorigenesis in vivo through dynamic regulation of histone modifications and gene expression.

Liu, Yiman / Li, Qinglan / Song, Lele / Gong, Chujie / Tang, Sylvia / Budinich, Krista A / Vanderbeck, Ashley / Mathias, Kaeli M / Wertheim, Gerald B / Nguyen, Son C / Outen, Riley / Joyce, Eric F / Maillard, Ivan / Wan, Liling

Cancer discovery

2024

Abstract: Gain-of-function mutations in the histone acetylation 'reader' ENL, found in AML and Wilms tumor, are known to drive condensate formation and gene activation in cellular systems. However, their role in tumorigenesis remains unclear. Using a conditional ... ...

Abstract	Gain-of-function mutations in the histone acetylation 'reader' ENL, found in AML and Wilms tumor, are known to drive condensate formation and gene activation in cellular systems. However, their role in tumorigenesis remains unclear. Using a conditional knock-in mouse model, we show that mutant ENL perturbs normal hematopoiesis, induces aberrant expansion of myeloid progenitors, and triggers rapid onset of aggressive AML. Mutant ENL alters developmental and inflammatory gene programs in part by remodeling histone modifications. Mutant ENL forms condensates in hematopoietic stem/progenitor cells at key leukemogenic genes, and disrupting condensate formation via mutagenesis impairs its chromatin and oncogenic function. Moreover, treatment with an acetyl-binding inhibitor of mutant ENL displaces these condensates from target loci, inhibits mutant ENL-induced chromatin changes, and delays AML initiation and progression in vivo. Our study elucidates the function of ENL mutations in chromatin regulation and tumorigenesis, and demonstrates the potential of targeting pathogenic condensates in cancer treatment.
Language	English
Publishing date	2024-04-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-23-0876
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Zs.A 6916: Show issues

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Article ; Online: FLT3 tyrosine kinase inhibition modulates PRC2 and promotes differentiation in acute myeloid leukemia.

Sung, Pamela J / Selvam, Murugan / Riedel, Simone S / Xie, Hongbo M / Bryant, Katie / Manning, Bryan / Wertheim, Gerald B / Kulej, Katarzyna / Pham, Lucie / Bowman, Robert L / Peresie, Jennifer / Nemeth, Michael J / Levine, Ross L / Garcia, Benjamin A / Meyer, Sara E / Sidoli, Simone / Bernt, Kathrin M / Carroll, Martin

Leukemia

2024 Volume 38, Issue 2, Page(s) 291–301

Abstract: Internal tandem duplication mutations in fms-like tyrosine kinase 3 (FLT3-ITD) are recurrent in acute myeloid leukemia (AML) and increase the risk of relapse. Clinical responses to FLT3 inhibitors (FLT3i) include myeloid differentiation of the FLT3-ITD ... ...

Abstract	Internal tandem duplication mutations in fms-like tyrosine kinase 3 (FLT3-ITD) are recurrent in acute myeloid leukemia (AML) and increase the risk of relapse. Clinical responses to FLT3 inhibitors (FLT3i) include myeloid differentiation of the FLT3-ITD clone in nearly half of patients through an unknown mechanism. We identified enhancer of zeste homolog 2 (EZH2), a component of polycomb repressive complex 2 (PRC2), as a mediator of this effect using a proteomic-based screen. FLT3i downregulated EZH2 protein expression and PRC2 activity on H3K27me3. FLT3-ITD and loss-of-function mutations in EZH2 are mutually exclusive in human AML. We demonstrated that FLT3i increase myeloid maturation with reduced stem/progenitor cell populations in murine Flt3-ITD AML. Combining EZH1/2 inhibitors with FLT3i increased terminal maturation of leukemic cells and reduced leukemic burden. Our data suggest that reduced EZH2 activity following FLT3 inhibition promotes myeloid differentiation of FLT3-ITD leukemic cells, providing a mechanistic explanation for the clinical observations. These results demonstrate that in addition to its known cell survival and proliferation signaling, FLT3-ITD has a second, previously undefined function to maintain a myeloid stem/progenitor cell state through modulation of PRC2 activity. Our findings support exploring EZH1/2 inhibitors as therapy for FLT3-ITD AML.
MeSH term(s)	Humans ; Animals ; Mice ; Protein-Tyrosine Kinases/genetics ; Polycomb Repressive Complex 2/genetics ; Proteomics ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Mutation ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; fms-Like Tyrosine Kinase 3/genetics ; fms-Like Tyrosine Kinase 3/therapeutic use
Chemical Substances	Protein-Tyrosine Kinases (EC 2.7.10.1) ; Polycomb Repressive Complex 2 (EC 2.1.1.43) ; Protein Kinase Inhibitors ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1) ; FLT3 protein, human (EC 2.7.10.1)
Language	English
Publishing date	2024-01-05
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-023-02131-4
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Zs.A 2295: Show issues

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Article ; Online: Cytochemical Staining.

Paessler, Michele E / Helfrich, Marybeth / Wertheim, Gerald B W

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1633, Page(s) 19–32

Abstract: Historically, the diagnosis and classification of acute leukemia involved morphologic review of blasts in the peripheral blood and bone marrow smears and cytochemical staining. Cytochemical stains, which are enzymatic colorimetric reactions that occur in ...

Abstract	Historically, the diagnosis and classification of acute leukemia involved morphologic review of blasts in the peripheral blood and bone marrow smears and cytochemical staining. Cytochemical stains, which are enzymatic colorimetric reactions that occur in the cells of interest, were necessary to assign and confirm myeloid and lymphoid lineage. In the current WHO 2008 Classification of leukemia, immunophenotyping and cytogenetic analysis have largely replaced cytochemical staining in the characterization of acute leukemias. Nonetheless, cytochemical testing remains a useful adjunct assay for the proper classification of acute leukemia in a number of diagnostic settings. This chapter reviews the principles of the most common cytochemical stains, their procedures and guides to interpretation, and results in acute myeloid leukemia.
MeSH term(s)	Humans ; Immunophenotyping/methods ; Leukemia, Myeloid, Acute/classification ; Leukemia, Myeloid, Acute/diagnosis ; Staining and Labeling/methods
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7142-8_2
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Article: Co-Occurrence of Pallister-Killian Syndrome and Burkitt Lymphoma in a Patient with Near-Normal Neurocognitive Development.

Izumi, Kosuke / Ganetzky, Rebecca D / Wertheim, Gerald B W / Skraban, Cara M / Bedoukian, Emma C / Wilkens, Alisha / Fincher, Christopher / Thomas, Nina H / Ginsberg, Jill P / Rheingold, Susan R / Conlin, Laura K / Deardorff, Matthew A

Molecular syndromology

2023 Volume 14, Issue 4, Page(s) 303–309

Abstract: Background: Pallister-Killian syndrome (PKS) is typically recognized by its features that include developmental delay, seizures, sparse temporal hair, and facial dysmorphisms. PKS is most frequently caused by mosaic supernumerary isochromosome 12p.: ... ...

Abstract	Background: Pallister-Killian syndrome (PKS) is typically recognized by its features that include developmental delay, seizures, sparse temporal hair, and facial dysmorphisms. PKS is most frequently caused by mosaic supernumerary isochromosome 12p. Case presentation: Here, we report a patient with PKS who was subsequently diagnosed with Burkitt lymphoma. Following the successful treatment of lymphoma, this patient demonstrated very mild intellectual disability despite the diagnosis of PKS, which is usually associated with severe developmental delay. Discussion: This is the first reported patient with PKS and a hematologic malignancy. Although there is no significant reported association of tetrasomy 12p with cancer, the co-occurrence of two rare findings in this patient suggests a potential relationship. The localization of
Language	English
Publishing date	2023-05-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2546218-0
ISSN	1661-8777 ; 1661-8769
ISSN (online)	1661-8777
ISSN	1661-8769
DOI	10.1159/000530197
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Article ; Online: Identification of TP53 germline variants in pediatric patients undergoing tumor testing: strategy and prevalence.

Luo, Minjie / Wong, Derek / Zelley, Kristin / Wu, Jinhua / Schubert, Jeffery / Denenberg, Elizabeth H / Fanning, Elizabeth A / Chen, Jiani / Gallo, Daniel / Golenberg, Netta / Patel, Maha / Conlin, Laura K / Maxwell, Kara N / Wertheim, Gerald B / Surrey, Lea F / Zhong, Yiming / Brodeur, Garrett M / MacFarland, Suzanne P / Li, Marilyn M

Journal of the National Cancer Institute

2024

Abstract: Background: TP53 alterations are common in certain pediatric cancers, making identification of putative germline variants through tumor genomic profiling crucial for patient management.: Methods: We analyzed TP53 alterations in 3123 tumors from 2788 ... ...

Abstract	Background: TP53 alterations are common in certain pediatric cancers, making identification of putative germline variants through tumor genomic profiling crucial for patient management. Methods: We analyzed TP53 alterations in 3123 tumors from 2788 pediatric patients sequenced using tumor-only or tumor-normal paired panels. Germline confirmatory testing was performed when indicated. Somatic and germline variants were classified following published guidelines. Results: In 248 tumors from 222 patients, 284 Tier 1/2 TP53 sequence and small copy number variants were detected. Following germline classification, 73.9% of 142 unique variants were pathogenic/likely pathogenic (P/LP). Confirmatory testing on 118 patients revealed germline TP53 variants in 28 patients (23 P/LP and 5 uncertain significance), suggesting a minimum Li-Fraumeni syndrome (LFS) incidence of 0.8% (23/2788) in this cohort, 10.4% (23/222) in patients with TP53 variant-carrying tumors, and 19.5% (23/118) with available normal samples. About 25% (7/28) of patients with germline TP53 variants did not meet LFS diagnostic/testing criteria while 20.9% (28/134) with confirmed or inferred somatic origins did. TP53 biallelic inactivation occurred in 75% of germline carrier tumors and was also prevalent in other groups, causing an elevated tumor-observed variant allelic fraction (VAF). However, somatic evidence including low VAF correctly identified only 27.8% (25/90) of patients with confirmed somatic TP53 variants. Conclusion: The high incidence and variable phenotype of LFS in this cohort highlights the importance of assessing germline status of TP53 variants identified in all pediatric tumors. Without clear somatic evidence, distinguishing somatic from germline origins is challenging. Classifying germline and somatic variants should follow appropriate guidelines.
Language	English
Publishing date	2024-05-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	2992-0
ISSN	1460-2105 ; 0027-8874 ; 0198-0157
ISSN (online)	1460-2105
ISSN	0027-8874 ; 0198-0157
DOI	10.1093/jnci/djae102
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Article ; Online: Reinfusion of CD19 CAR T cells for relapse prevention and treatment in children with acute lymphoblastic leukemia.

Blood advances

2024 Volume 8, Issue 9, Page(s) 2182–2192

Abstract: Abstract: Relapse after CD19-directed chimeric antigen receptor (CAR)-modified T cells remains a substantial challenge. Short CAR T-cell persistence contributes to relapse risk, necessitating novel approaches to prolong durability. CAR T-cell reinfusion ...

Abstract	Abstract: Relapse after CD19-directed chimeric antigen receptor (CAR)-modified T cells remains a substantial challenge. Short CAR T-cell persistence contributes to relapse risk, necessitating novel approaches to prolong durability. CAR T-cell reinfusion (CARTr) represents a potential strategy to reduce the risk of or treat relapsed disease after initial CAR T-cell infusion (CARTi). We conducted a retrospective review of reinfusion of murine (CTL019) or humanized (huCART19) anti-CD19/4-1BB CAR T cells across 3 clinical trials or commercial tisagenlecleucel for relapse prevention (peripheral B-cell recovery [BCR] or marrow hematogones ≤6 months after CARTi), minimal residual disease (MRD) or relapse, or nonresponse to CARTi. The primary endpoint was complete response (CR) at day 28 after CARTr, defined as complete remission with B-cell aplasia. Of 262 primary treatments, 81 were followed by ≥1 reinfusion (investigational CTL019, n = 44; huCART19, n = 26; tisagenlecleucel, n = 11), representing 79 patients. Of 63 reinfusions for relapse prevention, 52% achieved CR (BCR, 15/40 [38%]; hematogones, 18/23 [78%]). Lymphodepletion was associated with response to CARTr for BCR (odds ratio [OR], 33.57; P = .015) but not hematogones (OR, 0.30; P = .291). The cumulative incidence of relapse was 29% at 24 months for CR vs 61% for nonresponse to CARTr (P = .259). For MRD/relapse, CR rate to CARTr was 50% (5/10), but 0/8 for nonresponse to CARTi. Toxicity was generally mild, with the only grade ≥3 cytokine release syndrome (n = 6) or neurotoxicity (n = 1) observed in MRD/relapse treatment. Reinfusion of CTL019/tisagenlecleucel or huCART19 is safe, may reduce relapse risk in a subset of patients, and can reinduce remission in CD19+ relapse.
MeSH term(s)	Humans ; Child ; Antigens, CD19/immunology ; Antigens, CD19/therapeutic use ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Immunotherapy, Adoptive/methods ; Immunotherapy, Adoptive/adverse effects ; Child, Preschool ; Female ; Male ; Receptors, Chimeric Antigen/therapeutic use ; Adolescent ; Recurrence ; Retrospective Studies ; Infant ; Receptors, Antigen, T-Cell/therapeutic use ; Treatment Outcome ; T-Lymphocytes/immunology
Language	English
Publishing date	2024-02-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2024012885
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Zs.A 7153: Show issues

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Article ; Online: Incidental EBV-positivity in paediatric post-transplant specimens demonstrates the need for stringent criteria for diagnosing post-transplant lymphoproliferative disorders.

King, Rebecca L / Paessler, Michele E / Howard, Matthew T / Wertheim, Gerald B

Journal of clinical pathology

2017 Volume 70, Issue 3, Page(s) 270–273

Abstract: Aims: To examine the need for minimal diagnostic criteria for post-transplant lymphoproliferative disorders (PTLD) in children, we sought to determine the rate of incidental Epstein-Barr virus (EBV)-positivity in tissues from organ transplant recipients ...

Abstract	Aims: To examine the need for minimal diagnostic criteria for post-transplant lymphoproliferative disorders (PTLD) in children, we sought to determine the rate of incidental Epstein-Barr virus (EBV)-positivity in tissues from organ transplant recipients (OTR). Methods: EBV in situ hybridisation (ISH) was done retrospectively on tissue from 34 paediatric autopsies of OTR and paediatric tonsillectomy specimens from non-OTR (96) and OTR (6). Patients with a history of PTLD were excluded from both data sets. Results: EBV-positivity was found incidentally in 2/34 autopsy cases (5.9%). Median time from transplant to death for all patients was 12.8 months (range 0.1-153 months). Median time between transplant and death in EBV-positive cases was 34 months. EBV was positive in 26/102 tonsils (25%). Among tonsils from OTR, 4/6 (67%) were EBV-positive. Conclusions: These findings reinforce the need for strict morphological and clinical criteria, other than EBV-positivity, when diagnosing PTLD in the paediatric population.
MeSH term(s)	Adolescent ; Adult ; Child ; Child, Preschool ; Epstein-Barr Virus Infections/epidemiology ; Female ; Humans ; Incidental Findings ; Infant ; Lymphoproliferative Disorders/diagnosis ; Lymphoproliferative Disorders/virology ; Male ; Organ Transplantation ; Palatine Tonsil/pathology ; Palatine Tonsil/virology ; Postoperative Complications/diagnosis ; Postoperative Complications/virology ; Pseudolymphoma/diagnosis ; Pseudolymphoma/pathology ; Pseudolymphoma/virology ; Young Adult
Language	English
Publishing date	2017-03
Publishing country	England
Document type	Journal Article
ZDB-ID	80261-x
ISSN	1472-4146 ; 0021-9746
ISSN (online)	1472-4146
ISSN	0021-9746
DOI	10.1136/jclinpath-2016-203924
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