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Article: Predicting leukemic transformation in myelodysplastic syndrome using a transcriptomic signature.

Guo, Chao / Gao, Ya-Yue / Li, Zhen-Ling

2023 Volume 14, Page(s) 1235315

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2023-10-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2023.1235315
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Article: Chromothripsis orchestrates leukemic transformation in blast phase MPN through targetable amplification of

Brierley, C K / Yip, B H / Orlando, G / Goyal, H / Wen, S / Wen, J / Levine, M F / Jakobsdottir, G M / Rodriguez-Meira, A / Adamo, A / Bashton, M / Hamblin, A / Clark, S A / O'Sullivan, J / Murphy, L / Olijnik, A A / Cotton, A / Narina, S / Pruett-Miller, S M /

Enshaei, A / Harrison, C / Drummond, M / Knapper, S / Tefferi, A / Antony-Debré, I / Thongjuea, S / Wedge, D C / Constantinescu, S / Papaemmanuil, E / Psaila, B / Crispino, J D / Mead, A J

bioRxiv : the preprint server for biology

2023

Abstract: Chromothripsis, the process of catastrophic shattering and haphazard repair of chromosomes, is a common event in cancer. Whether chromothripsis might constitute an actionable molecular event amenable to therapeutic targeting remains an open question. We ... ...

Abstract	Chromothripsis, the process of catastrophic shattering and haphazard repair of chromosomes, is a common event in cancer. Whether chromothripsis might constitute an actionable molecular event amenable to therapeutic targeting remains an open question. We describe recurrent chromothripsis of chromosome 21 in a subset of patients in blast phase of a myeloproliferative neoplasm (BP-MPN), which alongside other structural variants leads to amplification of a region of chromosome 21 in ∼25% of patients ('chr21amp'). We report that chr21amp BP-MPN has a particularly aggressive and treatment-resistant phenotype. The chr21amp event is highly clonal and present throughout the hematopoietic hierarchy.
Language	English
Publishing date	2023-12-10
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.12.08.570880
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Article ; Online: Oncogenic RAS promotes leukemic transformation of CUX1-deficient cells.

An, Ningfei / Khan, Saira / Imgruet, Molly K / Jueng, Lia / Gurbuxani, Sandeep / McNerney, Megan E

Oncogene

2023 Volume 42, Issue 12, Page(s) 881–893

Abstract: 7/del(7q) is prevalent across subtypes of myeloid neoplasms. CUX1, located on 7q22, encodes a homeodomain-containing transcription factor, and, like -7/del(7q), CUX1 inactivating mutations independently carry a poor prognosis. As with loss of 7q, CUX1 ... ...

Abstract	-7/del(7q) is prevalent across subtypes of myeloid neoplasms. CUX1, located on 7q22, encodes a homeodomain-containing transcription factor, and, like -7/del(7q), CUX1 inactivating mutations independently carry a poor prognosis. As with loss of 7q, CUX1 mutations often occur early in disease pathogenesis. We reported that CUX1 deficiency causes myelodysplastic syndrome in mice but was insufficient to drive acute myeloid leukemia (AML). Given the known association between -7/del(7q) and RAS pathway mutations, we mined cancer genome databases and explicitly linked CUX1 mutations with oncogenic RAS mutations. To determine if activated RAS and CUX1 deficiency promote leukemogenesis, we generated mice bearing Nras
MeSH term(s)	Mice ; Animals ; Phosphatidylinositol 3-Kinases/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Mutation ; Hematopoietic Stem Cells/metabolism
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Transcription Factors
Language	English
Publishing date	2023-02-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-023-02612-x
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Zs.A 2218: Show issues

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Article ; Online: Galectin-9, a pro-survival factor inducing immunosuppression, leukemic cell transformation and expansion.

Yıldırım, Cansu

Molecular biology reports

2024 Volume 51, Issue 1, Page(s) 571

Abstract: ... in tumor immune evasion. Galectin-9 (Gal-9) is one of the key proteins that leukemic cells express, secrete, and use ... enabling leukemic cells to evade immune surveillance. The present review provides the molecular mechanisms ... by Gal-9 expressing leukemic cells will enable the identification of novel therapeutic strategies ...

Abstract	Leukemia is a malignancy of the bone marrow and blood originating from self-renewing cancerous immature blast cells or transformed leukocytes. Despite improvements in treatments, leukemia remains still a serious disease with poor prognosis because of disease heterogeneity, drug resistance and relapse. There is emerging evidence that differentially expression of co-signaling molecules play a critical role in tumor immune evasion. Galectin-9 (Gal-9) is one of the key proteins that leukemic cells express, secrete, and use to proliferate, self-renew, and survive. It also suppresses host immune responses controlled by T and NK cells, enabling leukemic cells to evade immune surveillance. The present review provides the molecular mechanisms of Gal-9-induced immune evasion in leukemia. Understanding the complex immune evasion machinery driven by Gal-9 expressing leukemic cells will enable the identification of novel therapeutic strategies for efficient immunotherapy in leukemic patients. Combined treatment approaches targeting T-cell immunoglobulin and mucin domain-3 (Tim-3)/Gal-9 and other immune checkpoint pathways can be considered, which may enhance the efficacy of host effector cells to attack leukemic cells.
MeSH term(s)	Humans ; Galectins/metabolism ; Leukemia/immunology ; Hepatitis A Virus Cellular Receptor 2/metabolism ; Cell Transformation, Neoplastic/immunology ; Cell Transformation, Neoplastic/genetics ; Animals ; Immune Tolerance ; Signal Transduction ; Tumor Escape ; Cell Proliferation ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism
Chemical Substances	Galectins ; LGALS9 protein, human ; Hepatitis A Virus Cellular Receptor 2 ; HAVCR2 protein, human
Language	English
Publishing date	2024-04-25
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-024-09563-w
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Zs.A 1140: Show issues

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Article ; Online: Risk of thrombosis, hemorrhage and leukemic transformation in patients with myeloproliferative neoplasms: A nationwide longitudinal cohort study.

Hur, Joon Young / Choi, Nayeon / Choi, Jung Hye / Kim, Jiyeong / Won, Young-Woong

Thrombosis research

2024 Volume 236, Page(s) 209–219

Abstract: ... of thrombosis, hemorrhage, leukemic transformation in patients with myeloproliferative neoplasms (MPNs ... were enrolled. The risk of thrombosis, hemorrhage, leukemic transformation was estimated using a Cox ... thrombosis, hemorrhage, leukemic transformation was higher in MPN patients (adjusted hazard ratio [aHR] 1.695 ...

Abstract	Introduction: There are few large-scale, population-based studies detailing the risks of thrombosis, hemorrhage, leukemic transformation in patients with myeloproliferative neoplasms (MPNs), including essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF). Methods: We performed a nationwide longitudinal cohort study using the Korean National Health Insurance System (NHIS) database. MPN patients (n = 11,991) and their 1:4 age- and sex-matched controls (n = 47,964) were enrolled. The risk of thrombosis, hemorrhage, leukemic transformation was estimated using a Cox proportional hazards regression, and stratified analyses were performed for related factors. Results: During a median of 7.8 years of follow-up, 30.1 % of MPN patients (3614/11,991) and 19.0 % of the matched controls (9141/47,964) developed arterial thrombosis, 11.6 % of MPN patients (1397/11,991) and 6.4 % of the matched controls (3099/47,964) developed venous thrombosis and 18.7 % of MPN patients (2251/11,991) and 12.1 % of the matched controls (5836/47,964) developed hemorrhage. 4.9 % of MPN patients (597/11,991) and 0.1 % of matched controls (50/47,964) developed leukemia. The overall risk of developing thrombosis, hemorrhage, leukemic transformation was higher in MPN patients (adjusted hazard ratio [aHR] 1.695, 95 % confidence interval [CI]: 1.629-1.765 for arterial thrombosis, aHR 1.963, 95 % CI: 1.838-2.096 for venous thrombosis, and aHR 1.714, 95 % CI: 1.630-1.802 for hemorrhage) than in the controls. Patients with MPNs had a 10-year cumulative incidence of leukemic transformation of 6.2 %. Conclusion: The patients with MPNs have a higher risk of thrombosis, hemorrhage, and leukemic transformation than matched controls. Strategies are warranted to reduce the risk of thrombosis, hemorrhage, and leukemic transformation in MPN patients.
MeSH term(s)	Humans ; Longitudinal Studies ; Myeloproliferative Disorders/complications ; Thrombosis/etiology ; Polycythemia Vera/epidemiology ; Hemorrhage/etiology ; Hemorrhage/epidemiology ; Cohort Studies ; Venous Thrombosis
Language	English
Publishing date	2024-03-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	121852-9
ISSN	1879-2472 ; 0049-3848
ISSN (online)	1879-2472
ISSN	0049-3848
DOI	10.1016/j.thromres.2024.03.008
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Zs.A 863: Show issues

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Article ; Online: Enhanced MAPK signaling induced by CSF3R mutants confers dependence to DUSP1 for leukemic transformation.

Kesarwani, Meenu / Kincaid, Zachary / Azhar, Mohammad / Azam, Mohammad

Blood advances

2024 Volume 8, Issue 11, Page(s) 2765–2776

Abstract: ... role of DUSP1 in leukemic transformation driven by enhanced MAPK signaling and advocate ... in leukemic context causes activation of JNK1/2 that results in induced expression of BIM and P53 ... while suppressing the expression of BCL2 that selectively triggers apoptotic response in leukemic cells ...

Abstract	Abstract: Elevated MAPK and the JAK-STAT signaling play pivotal roles in the pathogenesis of chronic neutrophilic leukemia and atypical chronic myeloid leukemia. Although inhibitors targeting these pathways effectively suppress the diseases, they fall short in providing enduring remission, largely attributed to the cytostatic nature of these drugs. Even combinations of these drugs are ineffective in achieving sustained remission. Enhanced MAPK signaling besides promoting proliferation and survival triggers a proapoptotic response. Consequently, malignancies reliant on elevated MAPK signaling use MAPK feedback regulators to intricately modulate the signaling output, prioritizing proliferation and survival while dampening the apoptotic stimuli. Herein, we demonstrate that enhanced MAPK signaling in granulocyte colony-stimulating factor 3 receptor (CSF3R)-driven leukemia upregulates the expression of dual specificity phosphatase 1 (DUSP1) to suppress the apoptotic stimuli crucial for leukemogenesis. Consequently, genetic deletion of Dusp1 in mice conferred synthetic lethality to CSF3R-induced leukemia. Mechanistically, DUSP1 depletion in leukemic context causes activation of JNK1/2 that results in induced expression of BIM and P53 while suppressing the expression of BCL2 that selectively triggers apoptotic response in leukemic cells. Pharmacological inhibition of DUSP1 by BCI (a DUSP1 inhibitor) alone lacked antileukemic activity due to ERK1/2 rebound caused by off-target inhibition of DUSP6. Consequently, a combination of BCI with a MEK inhibitor successfully cured CSF3R-induced leukemia in a preclinical mouse model. Our findings underscore the pivotal role of DUSP1 in leukemic transformation driven by enhanced MAPK signaling and advocate for the development of a selective DUSP1 inhibitor for curative treatment outcomes.
MeSH term(s)	Animals ; Mice ; Dual Specificity Phosphatase 1/metabolism ; Dual Specificity Phosphatase 1/genetics ; Humans ; Receptors, Colony-Stimulating Factor/genetics ; Receptors, Colony-Stimulating Factor/metabolism ; MAP Kinase Signaling System/drug effects ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Mutation ; Apoptosis ; Leukemia/metabolism ; Leukemia/genetics ; Gene Expression Regulation, Leukemic
Chemical Substances	Dual Specificity Phosphatase 1 (EC 3.1.3.48) ; Receptors, Colony-Stimulating Factor ; CSF3R protein, human ; DUSP1 protein, human (EC 3.1.3.48)
Language	English
Publishing date	2024-03-26
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.2023010830
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Article: Broad de-regulated U2AF1 splicing is prognostic and augments leukemic transformation via protein arginine methyltransferase activation.

bioRxiv : the preprint server for biology

2024

Abstract: The role of splicing dysregulation in cancer is underscored by splicing factor mutations; however, its impact in the absence of such rare mutations is poorly understood. To reveal complex patient subtypes and putative regulators of pathogenic splicing in ...

Abstract	The role of splicing dysregulation in cancer is underscored by splicing factor mutations; however, its impact in the absence of such rare mutations is poorly understood. To reveal complex patient subtypes and putative regulators of pathogenic splicing in Acute Myeloid Leukemia (AML), we developed a new approach called OncoSplice. Among diverse new subtypes, OncoSplice identified a biphasic poor prognosis signature that partially phenocopies
Language	English
Publishing date	2024-02-08
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.04.578798
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Article ; Online: Phase Separation Mediates NUP98 Fusion Oncoprotein Leukemic Transformation.

Chandra, Bappaditya / Michmerhuizen, Nicole L / Shirnekhi, Hazheen K / Tripathi, Swarnendu / Pioso, Brittany J / Baggett, David W / Mitrea, Diana M / Iacobucci, Ilaria / White, Michael R / Chen, Jingjing / Park, Cheon-Gil / Wu, Huiyun / Pounds, Stanley / Medyukhina, Anna / Khairy, Khaled / Gao, Qingsong / Qu, Chunxu / Abdelhamed, Sherif / Gorman, Scott D /

Bawa, Simranjot / Maslanka, Carolyn / Kinger, Swati / Dogra, Priyanka / Ferrolino, Mylene C / Di Giacomo, Danika / Mecucci, Cristina / Klco, Jeffery M / Mullighan, Charles G / Kriwacki, Richard W

Cancer discovery

2021 Volume 12, Issue 4, Page(s) 1152–1169

Abstract: ... associated with aberrant transcriptional activity and transformation of hematopoietic stem and ...

Abstract	NUP98 fusion oncoproteins (FO) are drivers in pediatric leukemias and many transform hematopoietic cells. Most NUP98 FOs harbor an intrinsically disordered region from NUP98 that is prone to liquid-liquid phase separation (LLPS) in vitro. A predominant class of NUP98 FOs, including NUP98-HOXA9 (NHA9), retains a DNA-binding homeodomain, whereas others harbor other types of DNA- or chromatin-binding domains. NUP98 FOs have long been known to form puncta, but long-standing questions are how nuclear puncta form and how they drive leukemogenesis. Here we studied NHA9 condensates and show that homotypic interactions and different types of heterotypic interactions are required to form nuclear puncta, which are associated with aberrant transcriptional activity and transformation of hematopoietic stem and progenitor cells. We also show that three additional leukemia-associated NUP98 FOs (NUP98-PRRX1, NUP98-KDM5A, and NUP98-LNP1) form nuclear puncta and transform hematopoietic cells. These findings indicate that LLPS is critical for leukemogenesis by NUP98 FOs. Significance: We show that homotypic and heterotypic mechanisms of LLPS control NUP98-HOXA9 puncta formation, modulating transcriptional activity and transforming hematopoietic cells. Importantly, these mechanisms are generalizable to other NUP98 FOs that share similar domain structures. These findings address long-standing questions on how nuclear puncta form and their link to leukemogenesis. This article is highlighted in the In This Issue feature, p. 873.
MeSH term(s)	Carcinogenesis ; Cell Nucleus ; Child ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Humans ; Leukemia/genetics ; Nuclear Pore Complex Proteins/genetics ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; Retinoblastoma-Binding Protein 2
Chemical Substances	Homeodomain Proteins ; Nuclear Pore Complex Proteins ; Nup98 protein, human ; Oncogene Proteins, Fusion ; PRRX1 protein, human ; nuclear pore complex protein 98 ; KDM5A protein, human (EC 1.14.11.-) ; Retinoblastoma-Binding Protein 2 (EC 1.14.11.27)
Language	English
Publishing date	2021-12-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-21-0674
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Zs.A 6916: Show issues

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Article: Myelofibrotic and leukemic transformation in 2016 WHO-defined Philadelphia-negative myeloproliferative neoplasm.

Song, Ik-Chan / Yeon, Sang Hoon / Lee, Myung-Won / Ryu, Hyewon / Lee, Hyo-Jin / Yun, Hwan-Jung / Kim, Seon Young / Jo, Deog-Yeon

Blood research

2022 Volume 57, Issue 1, Page(s) 59–68

Abstract: Background: Information on myelofibrotic and leukemic transformations in Korean ... of myelofibrotic and leukemic transformations in Korean patients with Ph ...

Abstract	Background: Information on myelofibrotic and leukemic transformations in Korean Philadelphia chromosome- negative myeloproliferative neoplasms (Ph Methods: This study retrospectively analyzed transformations in patients diagnosed with essential thrombocythemia (ET), polycythemia vera (PV) prefibrotic/early primary myelofibrosis (pre-PMF), or overt primary myelofibrosis (PMF) based on the 2016 World Health Organization criteria between January 1996 and December 2020 at Chungam National University Hospital, Daejeon, Korea. Results: A total of 351 patients (144 with ET, 131 with PV, 45 with pre-PMF, and 31 with PMF; 204 men and 147 women) with a median age of 64 years (range, 15‒91 years) were followed for a median of 4.6 years (range, 0.2‒24.8 years). The 10-year incidence of overt myelofibrosis was higher in pre-PMF than in ET (31.3% and 13.7%, respectively; Conclusion: The rates and clinical courses of myelofibrotic and leukemic transformations in Korean patients with Ph
Language	English
Publishing date	2022-03-31
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	2711910-5
ISSN	2288-0011 ; 2287-979X
ISSN (online)	2288-0011
ISSN	2287-979X
DOI	10.5045/br.2021.2021209
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Article: PHF6 suppresses self-renewal of leukemic stem cells in AML.

Jalnapurkar, Sapana S / Pawar, Aishwarya / George, Subin S / Antony, Charles / Grana, Jason / Gurbuxani, Sandeep / Paralkar, Vikram R

bioRxiv : the preprint server for biology

2024

Abstract: ... HSC self-renewal without malignant transformation. We report here that ...

Abstract	Acute myeloid leukemia is characterized by uncontrolled proliferation of self-renewing myeloid progenitors. PHF6 is a chromatin-binding protein mutated in myeloid leukemias, and its loss increases mouse HSC self-renewal without malignant transformation. We report here that
Language	English
Publishing date	2024-01-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.06.573649
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