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Article ; Online: Ablation of Wnt signaling in bone marrow stromal cells overcomes microenvironment-mediated drug resistance in acute myeloid leukemia.

Palani, Hamenth Kumar / Ganesan, Saravanan / Balasundaram, Nithya / Venkatraman, Arvind / Korula, Anu / Abraham, Aby / George, Biju / Mathews, Vikram

Scientific reports

2024 Volume 14, Issue 1, Page(s) 8404

Abstract: The survival of leukemic cells is significantly influenced by the bone marrow microenvironment, where stromal cells play a crucial role. While there has been substantial progress in understanding the mechanisms and pathways involved in this crosstalk, ... ...

Abstract	The survival of leukemic cells is significantly influenced by the bone marrow microenvironment, where stromal cells play a crucial role. While there has been substantial progress in understanding the mechanisms and pathways involved in this crosstalk, limited data exist regarding the impact of leukemic cells on bone marrow stromal cells and their potential role in drug resistance. In this study, we identify that leukemic cells prime bone marrow stromal cells towards osteoblast lineage and promote drug resistance. This biased differentiation of stroma is accompanied by dysregulation of the canonical Wnt signaling pathway. Inhibition of Wnt signaling in stroma reversed the drug resistance in leukemic cells, which was further validated in leukemic mice models. This study evaluates the critical role of leukemic cells in establishing a drug-resistant niche by influencing the bone marrow stromal cells. Additionally, it highlights the potential of targeting Wnt signaling in the stroma by repurposing an anthelmintic drug to overcome the microenvironment-mediated drug resistance.
MeSH term(s)	Animals ; Mice ; Wnt Signaling Pathway ; Leukemia, Myeloid, Acute/metabolism ; Bone Marrow/metabolism ; Stromal Cells/metabolism ; Mesenchymal Stem Cells/metabolism ; Drug Resistance ; Bone Marrow Cells ; Tumor Microenvironment/physiology
Language	English
Publishing date	2024-04-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-024-58860-8
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Article ; Online: Microenvironment and drug resistance in acute myeloid leukemia: Do we know enough?

Ganesan, Saravanan / Mathews, Vikram / Vyas, Neha

International journal of cancer

2021 Volume 150, Issue 9, Page(s) 1401–1411

Abstract: Acute myeloid leukemia (AMLs), as the name suggests, often develop suddenly and are very progressive forms of cancer. Unlike in acute promyelocytic leukemia, a subtype of AML, the outcomes in most other AMLs remain poor. This is mainly attributed to the ... ...

Abstract	Acute myeloid leukemia (AMLs), as the name suggests, often develop suddenly and are very progressive forms of cancer. Unlike in acute promyelocytic leukemia, a subtype of AML, the outcomes in most other AMLs remain poor. This is mainly attributed to the acquired drug resistance and lack of targeted therapy. Different studies across laboratories suggest that the cellular mechanisms to impart therapy resistance are often very dynamic and should be identified in a context-specific manner. Our review highlights the progress made so far in identifying the different cellular mechanisms of mutation-independent therapy resistance in AML. It reiterates that for more effective outcomes cancer therapies should acquire a more tailored approach where the protective interactions between the cancer cells and their niches are identified and targeted.
MeSH term(s)	Drug Resistance ; Humans ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Promyelocytic, Acute ; Mutation ; Tumor Microenvironment
Language	English
Publishing date	2021-12-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218257-9
ISSN	1097-0215 ; 0020-7136
ISSN (online)	1097-0215
ISSN	0020-7136
DOI	10.1002/ijc.33908
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Article ; Online: Genomic and functional impact of Trp53 inactivation in JAK2V617F myeloproliferative neoplasms.

Gou, Panhong / Liu, Duanya / Ganesan, Saravanan / Lauret, Evelyne / Maslah, Nabih / Parietti, Veronique / Zhang, Wenchao / Meignin, Véronique / Kiladjian, Jean-Jacques / Cassinat, Bruno / Giraudier, Stephane

Blood cancer journal

2024 Volume 14, Issue 1, Page(s) 1

Abstract: Classical myeloproliferative neoplasms (MPNs) are characterized by the proliferation of myeloid cells and the risk of transformation into myelofibrosis or acute myeloid leukemia (AML) and TP53 mutations in MPN patients are linked to AML. However, ... ...

Abstract	Classical myeloproliferative neoplasms (MPNs) are characterized by the proliferation of myeloid cells and the risk of transformation into myelofibrosis or acute myeloid leukemia (AML) and TP53 mutations in MPN patients are linked to AML. However, JAK2V617F has been reported to impact the TP53 response to DNA damage, suggesting potential overlapping role of TP53 inactivation in MPN. We established a mouse model showing that JAK2V617F/Vav-Cre/Trp53
MeSH term(s)	Humans ; Mice ; Animals ; Tumor Suppressor Protein p53/genetics ; Janus Kinase 2/genetics ; Janus Kinase 2/metabolism ; Myeloproliferative Disorders/drug therapy ; Myeloproliferative Disorders/genetics ; Mutation ; Interferon-alpha/pharmacology ; Leukemia, Myeloid, Acute ; Genomics
Chemical Substances	Tumor Suppressor Protein p53 ; Janus Kinase 2 (EC 2.7.10.2) ; Interferon-alpha
Language	English
Publishing date	2024-01-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2600560-8
ISSN	2044-5385 ; 2044-5385
ISSN (online)	2044-5385
ISSN	2044-5385
DOI	10.1038/s41408-023-00969-6
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Article ; Online: GoT-Splice protocol for multi-omics profiling of gene expression, cell-surface proteins, mutational status, and RNA splicing in human cells.

Ganesan, Saravanan / Cortés-López, Mariela / Swett, Ariel D / Dai, Xiaoguang / Hickey, Scott / Chamely, Paulina / Hawkins, Allegra G / Juul, Sissel / Landau, Dan A / Gaiti, Federico

STAR protocols

2024 Volume 5, Issue 2, Page(s) 102966

Abstract: Studying RNA splicing factor mutations is challenging due to difficulties in distinguishing wild-type and mutant cells within complex human tissues and inaccuracies associated with reconstructing splicing signals from short-read sequencing data. Here, we ...

Abstract	Studying RNA splicing factor mutations is challenging due to difficulties in distinguishing wild-type and mutant cells within complex human tissues and inaccuracies associated with reconstructing splicing signals from short-read sequencing data. Here, we present Genotyping of Transcriptomes (GoT)-Splice, a protocol that overcomes these limitations by combining GoT with enhanced long-read single-cell transcriptome and cell-surface proteomics profiling. We describe steps for long-read library preparation and analysis, followed by cDNA re-amplification, enrichment of mutation of interest, sample indexing, and GoT library preparation. For complete details on the use and execution of this protocol, please refer to Cortés-López et al.
Language	English
Publishing date	2024-03-20
Publishing country	United States
Document type	Journal Article
ISSN	2666-1667
ISSN (online)	2666-1667
DOI	10.1016/j.xpro.2024.102966
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Article ; Online: Cystatin F a potential diagnostic biomarker in acute promyelocytic leukemia.

Palani, Hamenth Kumar / Ganesan, Saravanan / Balasundaram, Nithya / Venkatraman, Arvind / Kulkarni, Uday / Korula, Anu / Nair, Sukesh C / Mani, Thenmozhi / Balasubramanian, Poonkuzhali / Abraham, Aby / Puttamallesh, Vinuth N / Gowda, Harsha / Mathews, Vikram

Annals of hematology

2024 Volume 103, Issue 6, Page(s) 2181–2183

MeSH term(s)	Humans ; Biomarkers, Tumor/blood ; Leukemia, Promyelocytic, Acute/diagnosis ; Leukemia, Promyelocytic, Acute/blood ; Leukocytes, Mononuclear/metabolism
Language	English
Publishing date	2024-03-01
Publishing country	Germany
Document type	Letter
ZDB-ID	1064950-5
ISSN	1432-0584 ; 0939-5555 ; 0945-8077
ISSN (online)	1432-0584
ISSN	0939-5555 ; 0945-8077
DOI	10.1007/s00277-024-05673-4
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Article ; Online: Combination Lenalidomide/Bortezomib Treatment Synergistically Induces Calpain-Dependent Ikaros Cleavage and Apoptosis in Myeloma Cells.

Ganesan, Saravanan / Palani, Hamenth Kumar / Balasundaram, Nithya / David, Sachin / Devasia, Anup J / George, Biju / Mathews, Vikram

Molecular cancer research : MCR

2020 Volume 18, Issue 4, Page(s) 529–536

Abstract: Multiple myeloma had been successfully treated by combining lenalidomide and bortezomib with reports suggesting benefits of such a combination even in relapsed/refractory cases. Recently, it was demonstrated that Ikaros degradation by lenalidomide ... ...

Abstract	Multiple myeloma had been successfully treated by combining lenalidomide and bortezomib with reports suggesting benefits of such a combination even in relapsed/refractory cases. Recently, it was demonstrated that Ikaros degradation by lenalidomide happens via proteasome-dependent pathway and this process is critical for the eradication of myeloma cells. On the basis of this, an antagonistic effect should be observed if a combination of both these agents were used, which however is not the observation seen in the clinical setting. Our study demonstrates that when these agents are combined they exhibit a synergistic activity against myeloma cells and degradation of Ikaros happens by a proteasome-independent calcium-induced calpain pathway. Our study identifies the crucial role of calcium-induced calpain pathway in inducing apoptosis of myeloma cells when this combination or lenalidomide and bortezomib is used. We also report that this combination enhanced the expression of CD38 compared with lenalidomide alone. Thus, data from our study would establish the rationale for the addition of daratumumab along with this combination to further enhance therapeutic activity against multiple myeloma. IMPLICATIONS: Lenalidomide and bortezomib combination degrades IKZF1 in multiple myeloma through a calcium-dependent calpain and caspase pathway. VISUAL OVERVIEW: http://mcr.aacrjournals.org/content/molcanres/18/4/529/F1.large.jpg.
MeSH term(s)	Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Apoptosis/drug effects ; Bortezomib/pharmacology ; Bortezomib/therapeutic use ; Humans ; Immunologic Factors/pharmacology ; Immunologic Factors/therapeutic use ; Lenalidomide/pharmacology ; Lenalidomide/therapeutic use ; Multiple Myeloma/drug therapy
Chemical Substances	Immunologic Factors ; Bortezomib (69G8BD63PP) ; Lenalidomide (F0P408N6V4)
Language	English
Publishing date	2020-01-08
Publishing country	United States
Document type	Journal Article ; 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-19-0431
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Article ; Online: Mapping genotypes to chromatin accessibility profiles in single cells.

Izzo, Franco / Myers, Robert M / Ganesan, Saravanan / Mekerishvili, Levan / Kottapalli, Sanjay / Prieto, Tamara / Eton, Elliot O / Botella, Theo / Dunbar, Andrew J / Bowman, Robert L / Sotelo, Jesus / Potenski, Catherine / Mimitou, Eleni P / Stahl, Maximilian / El Ghaity-Beckley, Sebastian / Arandela, JoAnn / Raviram, Ramya / Choi, Daniel C / Hoffman, Ronald /

Chaligné, Ronan / Abdel-Wahab, Omar / Smibert, Peter / Ghobrial, Irene M / Scandura, Joseph M / Marcellino, Bridget / Levine, Ross L / Landau, Dan A

Nature

2024

Abstract: In somatic tissue differentiation, chromatin accessibility changes govern priming and precursor commitment towards cellular ... ...

Abstract	In somatic tissue differentiation, chromatin accessibility changes govern priming and precursor commitment towards cellular fates
Language	English
Publishing date	2024-05-08
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-024-07388-y
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Article: Breast Cancer Macrophage Heterogeneity and Self-renewal are Determined by Spatial Localization.

bioRxiv : the preprint server for biology

2023

Abstract: Tumor-infiltrating macrophages support critical steps in tumor progression, and their accumulation in the tumor microenvironment (TME) is associated with adverse outcomes and therapeutic resistance across human cancers. In the TME, macrophages adopt ... ...

Abstract	Tumor-infiltrating macrophages support critical steps in tumor progression, and their accumulation in the tumor microenvironment (TME) is associated with adverse outcomes and therapeutic resistance across human cancers. In the TME, macrophages adopt diverse phenotypic alterations, giving rise to heterogeneous immune activation states and induction of cell cycle. While the transcriptional profiles of these activation states are well-annotated across human cancers, the underlying signals that regulate macrophage heterogeneity and accumulation remain incompletely understood. Here, we leveraged a novel
Language	English
Publishing date	2023-10-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.10.24.563749
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Article ; Online: Metabolic adaptation drives arsenic trioxide resistance in acute promyelocytic leukemia.

Balasundaram, Nithya / Ganesan, Saravanan / Chendamarai, Ezhilarasi / Palani, Hamenth Kumar / Venkatraman, Arvind / Alex, Ansu Abu / David, Sachin / Kumar, Swathy Palani / Radhakrishnan, Nair Reeshma / Yasar, Mohammed / Krishna, Sanjeev / Korula, Anu / Kulkarni, Uday / Janet, Nancy Beryl / Balasubramanian, Poonkuzhali / Mathews, Vikram

Blood advances

2021 Volume 6, Issue 2, Page(s) 652–663

Abstract: Acquired genetic mutations can confer resistance to arsenic trioxide (ATO) in the treatment of acute promyelocytic leukemia (APL). However, such resistance-conferring mutations are rare and do not explain most disease recurrence seen in the clinic. We ... ...

Abstract	Acquired genetic mutations can confer resistance to arsenic trioxide (ATO) in the treatment of acute promyelocytic leukemia (APL). However, such resistance-conferring mutations are rare and do not explain most disease recurrence seen in the clinic. We have generated stable ATO-resistant promyelocytic cell lines that are less sensitive to all-trans retinoic acid (ATRA) and the combination of ATO and ATRA compared with the sensitive cell line. Characterization of these resistant cell lines that were generated in-house showed significant differences in immunophenotype, drug transporter expression, anti-apoptotic protein dependence, and promyelocytic leukemia-retinoic acid receptor alpha (PML-RARA) mutation. Gene expression profiling revealed prominent dysregulation of the cellular metabolic pathways in these ATO-resistant APL cell lines. Glycolytic inhibition by 2-deoxyglucose (2-DG) was sufficient and comparable to the standard of care (ATO) in targeting the sensitive APL cell line. 2-DG was also effective in the in vivo transplantable APL mouse model; however, it did not affect the ATO-resistant cell lines. In contrast, the resistant cell lines were significantly affected by compounds targeting mitochondrial respiration when combined with ATO, irrespective of the ATO resistance-conferring genetic mutations or the pattern of their anti-apoptotic protein dependency. Our data demonstrate that combining mitocans with ATO can overcome ATO resistance. We also show that this combination has potential for treating non-M3 acute myeloid leukemia (AML) and relapsed APL. The translation of this approach in the clinic needs to be explored further.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins ; Arsenic Trioxide/pharmacology ; Arsenic Trioxide/therapeutic use ; Arsenicals/pharmacology ; Arsenicals/therapeutic use ; Leukemia, Promyelocytic, Acute/genetics ; Mice ; Oxides/pharmacology ; Oxides/therapeutic use ; Tretinoin/pharmacology ; Tretinoin/therapeutic use
Chemical Substances	Apoptosis Regulatory Proteins ; Arsenicals ; Oxides ; Tretinoin (5688UTC01R) ; Arsenic Trioxide (S7V92P67HO)
Language	English
Publishing date	2021-10-08
Publishing country	United States
Document type	Journal Article ; 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.2021005300
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Article ; Online: Single-cell multi-omics defines the cell-type-specific impact of splicing aberrations in human hematopoietic clonal outgrowths.

Cortés-López, Mariela / Chamely, Paulina / Hawkins, Allegra G / Stanley, Robert F / Swett, Ariel D / Ganesan, Saravanan / Mouhieddine, Tarek H / Dai, Xiaoguang / Kluegel, Lloyd / Chen, Celine / Batta, Kiran / Furer, Nili / Vedula, Rahul S / Beaulaurier, John / Drong, Alexander W / Hickey, Scott / Dusaj, Neville / Mullokandov, Gavriel / Stasiw, Adam M /

Su, Jiayu / Chaligné, Ronan / Juul, Sissel / Harrington, Eoghan / Knowles, David A / Potenski, Catherine J / Wiseman, Daniel H / Tanay, Amos / Shlush, Liran / Lindsley, Robert C / Ghobrial, Irene M / Taylor, Justin / Abdel-Wahab, Omar / Gaiti, Federico / Landau, Dan A

Cell stem cell

2023 Volume 30, Issue 9, Page(s) 1262–1281.e8

Abstract: RNA splicing factors are recurrently mutated in clonal blood disorders, but the impact of dysregulated splicing in hematopoiesis remains unclear. To overcome technical limitations, we integrated genotyping of transcriptomes (GoT) with long-read single- ... ...

Abstract	RNA splicing factors are recurrently mutated in clonal blood disorders, but the impact of dysregulated splicing in hematopoiesis remains unclear. To overcome technical limitations, we integrated genotyping of transcriptomes (GoT) with long-read single-cell transcriptomics and proteogenomics for single-cell profiling of transcriptomes, surface proteins, somatic mutations, and RNA splicing (GoT-Splice). We applied GoT-Splice to hematopoietic progenitors from myelodysplastic syndrome (MDS) patients with mutations in the core splicing factor SF3B1. SF3B1
MeSH term(s)	Humans ; RNA Splice Sites ; Multiomics ; RNA Splicing/genetics ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/metabolism ; RNA Splicing Factors/genetics ; RNA Splicing Factors/metabolism ; Mutation/genetics ; Phosphoproteins/genetics ; Phosphoproteins/metabolism
Chemical Substances	RNA Splice Sites ; RNA Splicing Factors ; Phosphoproteins
Language	English
Publishing date	2023-08-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2023.07.012
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