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Article ; Online: Oncogene Up-Regulation after Hypomethylating Therapy. Reply.

Voso, Maria T / Tenen, Daniel G / Chai, Li

2022 Volume 387, Issue 5, Page(s) 476–477

MeSH term(s)	Azacitidine/therapeutic use ; Demethylation ; Humans ; Myelodysplastic Syndromes/therapy ; Oncogenes ; Up-Regulation
Chemical Substances	Azacitidine (M801H13NRU)
Language	English
Publishing date	2022-07-26
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMc2208134
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Article ; Online: The Interplay between Transcription Factor SALL4 and Histone Modifiers in Hematopoietic Stem and Progenitor Cells.

Tatetsu, Hiro / Tenen, Daniel G / Chai, Li

Journal of cellular immunology

2021 Volume 3, Issue 1, Page(s) 26–30

Language	English
Publishing date	2021-04-21
Publishing country	United States
Document type	Journal Article
ISSN	2689-2812
ISSN (online)	2689-2812
DOI	10.33696/immunology.3.073
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Article ; Online: SALL4: An Intriguing Therapeutic Target in Cancer Treatment.

Moein, Shiva / Tenen, Daniel G / Amabile, Giovanni / Chai, Li

Cells

2022 Volume 11, Issue 16

Abstract: Spalt-Like Transcription Factor 4 (SALL4) is a critical factor for self-renewal ability and pluripotency of stem cells. On the other hand, various reports show tight relation of SALL4 to cancer occurrence and metastasis. SALL4 exerts its effects not only ...

Abstract	Spalt-Like Transcription Factor 4 (SALL4) is a critical factor for self-renewal ability and pluripotency of stem cells. On the other hand, various reports show tight relation of SALL4 to cancer occurrence and metastasis. SALL4 exerts its effects not only by inducing gene expression but also repressing a large cluster of genes through interaction with various epigenetic modifiers. Due to high expression of SALL4 in cancer cells and its silence in almost all adult tissues, it is an ideal target for cancer therapy. However, targeting SALL4 meets various challenges. SALL4 is a transcription factor and designing appropriate drug to inhibit this intra-nucleus component is challenging. On the other hand, due to lack of our knowledge on structure of the protein and the suitable active sites, it becomes more difficult to reach the appropriate drugs against SALL4. In this review, we have focused on approaches applied yet to target this oncogene and discuss the potential of degrader systems as new therapeutics to target oncogenes.
MeSH term(s)	Adult ; Gene Expression Regulation ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Stem Cells/metabolism ; Transcription Factors/metabolism
Chemical Substances	SALL4 protein, human ; Transcription Factors
Language	English
Publishing date	2022-08-20
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11162601
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Article: Chromatin structure and 3D architecture define differential functions of

Qiu, Kevin / Vu, Duc / Wang, Leran / Bookstaver, Anna / Dinh, Thang N / Goldfarb, Adam N / Tenen, Daniel G / Trinh, Bon Q

bioRxiv : the preprint server for biology

2024

Abstract: The precise spatio-temporal expression of the hematopoietic ETS transcription ... ...

Abstract	The precise spatio-temporal expression of the hematopoietic ETS transcription factor
Language	English
Publishing date	2024-01-01
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.01.573782
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Article ; Online: Emerging therapies for inv(16) AML.

Surapally, Sridevi / Tenen, Daniel G / Pulikkan, John A

Blood

2021 Volume 137, Issue 19, Page(s) 2579–2584

Abstract: The core binding factor composed of CBFβ and RUNX subunits plays a critical role in most hematopoietic lineages and is deregulated in acute myeloid leukemia (AML). The fusion oncogene CBFβ-SMMHC expressed in AML with the chromosome inversion inv(16)( ... ...

Abstract	The core binding factor composed of CBFβ and RUNX subunits plays a critical role in most hematopoietic lineages and is deregulated in acute myeloid leukemia (AML). The fusion oncogene CBFβ-SMMHC expressed in AML with the chromosome inversion inv(16)(p13q22) acts as a driver oncogene in hematopoietic stem cells and induces AML. This review focuses on novel insights regarding the molecular mechanisms involved in CBFβ-SMMHC-driven leukemogenesis and recent advances in therapeutic approaches to target CBFβ-SMMHC in inv(16) AML.
MeSH term(s)	Animals ; Antineoplastic Agents, Immunological/therapeutic use ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Cell Transformation, Neoplastic/genetics ; Chromosome Inversion ; Chromosomes, Human, Pair 16/genetics ; Chromosomes, Human, Pair 16/ultrastructure ; Combined Modality Therapy ; Core Binding Factor Alpha 2 Subunit/deficiency ; Core Binding Factor Alpha 2 Subunit/metabolism ; Core Binding Factor beta Subunit/genetics ; Core Binding Factor beta Subunit/physiology ; Forecasting ; Gemtuzumab/therapeutic use ; Gene Expression Regulation, Leukemic ; Gene Knock-In Techniques ; Hematopoiesis/drug effects ; Hematopoiesis/genetics ; Humans ; Immunotherapy/methods ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Mice ; Molecular Targeted Therapy ; Myosin Heavy Chains/genetics ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Oncogene Proteins, Fusion/antagonists & inhibitors ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/physiology ; T-Lymphocytes/immunology ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents, Immunological ; CBFB protein, human ; CBFbeta-MYH11 fusion protein ; Cbfb protein, mouse ; Core Binding Factor Alpha 2 Subunit ; Core Binding Factor beta Subunit ; MYH11 protein, human ; Oncogene Proteins, Fusion ; RUNX1 protein, human ; Runx1 protein, mouse ; Gemtuzumab (93NS566KF7) ; Myosin Heavy Chains (EC 3.6.4.1)
Language	English
Publishing date	2021-03-30
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.2020009933
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Article ; Online: EGFR signaling pathway as therapeutic target in human cancers.

Levantini, Elena / Maroni, Giorgia / Del Re, Marzia / Tenen, Daniel G

Seminars in cancer biology

2022 Volume 85, Page(s) 253–275

Abstract: Epidermal Growth Factor Receptor (EGFR) enacts major roles in the maintenance of epithelial tissues. However, when EGFR signaling is altered, it becomes the grand orchestrator of epithelial transformation, and hence one of the most world-wide studied ... ...

Abstract	Epidermal Growth Factor Receptor (EGFR) enacts major roles in the maintenance of epithelial tissues. However, when EGFR signaling is altered, it becomes the grand orchestrator of epithelial transformation, and hence one of the most world-wide studied tyrosine kinase receptors involved in neoplasia, in several tissues. In the last decades, EGFR-targeted therapies shaped the new era of precision-oncology. Despite major advances, the dream of converting solid tumors into a chronic disease is still unfulfilled, and long-term remission eludes us. Studies investigating the function of this protein in solid malignancies have revealed numerous ways how tumor cells dysregulate EGFR function. Starting from preclinical models (cell lines, organoids, murine models) and validating in clinical specimens, EGFR-related oncogenic pathways, mechanisms of resistance, and novel avenues to inhibit tumor growth and metastatic spread enriching the therapeutic portfolios, were identified. Focusing on non-small cell lung cancer (NSCLC), where EGFR mutations are major players in the adenocarcinoma subtype, we will go over the most relevant discoveries that led us to understand EGFR and beyond, and highlight how they revolutionized cancer treatment by expanding the therapeutic arsenal at our disposal.
MeSH term(s)	Humans ; Mice ; Animals ; Carcinoma, Non-Small-Cell Lung/genetics ; Lung Neoplasms/genetics ; Protein Kinase Inhibitors/pharmacology ; Drug Resistance, Neoplasm/genetics ; Mutation ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Signal Transduction
Chemical Substances	Protein Kinase Inhibitors ; ErbB Receptors (EC 2.7.10.1) ; EGFR protein, human (EC 2.7.10.1)
Language	English
Publishing date	2022-04-12
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1033980-2
ISSN	1096-3650 ; 1044-579X
ISSN (online)	1096-3650
ISSN	1044-579X
DOI	10.1016/j.semcancer.2022.04.002
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Article: Metabolic alterations and vulnerabilities in hepatocellular carcinoma.

Tenen, Daniel G / Chai, Li / Tan, Justin L

Gastroenterology report

2020 Volume 9, Issue 1, Page(s) 1–13

Abstract: Liver cancer is a serious disease. It is ranked as the cancer with the second highest number of cancer-related deaths worldwide. Hepatocellular carcinoma (HCC), which arises from transformed hepatocytes, is the major subtype of liver cancer. It accounts ... ...

Abstract	Liver cancer is a serious disease. It is ranked as the cancer with the second highest number of cancer-related deaths worldwide. Hepatocellular carcinoma (HCC), which arises from transformed hepatocytes, is the major subtype of liver cancer. It accounts for 85% of total liver-cancer cases. An important aspect of HCC that has been actively studied is its metabolism. With the liver as the primary site of numerous metabolic processes in the body, it has been shown that the metabolism of HCC cells is highly dysregulated compared to that of normal hepatocytes. It is therefore crucial to understand the metabolic alterations caused by HCC and the underlying mechanisms for these alterations. This deeper understanding will allow diagnostic and therapeutic advancements in the treatment of HCC. In this review, we will summarize the current literature in HCC metabolic alterations, induced vulnerabilities, and potential therapeutic interventions.
Language	English
Publishing date	2020-11-18
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2710871-5
ISSN	2052-0034
ISSN	2052-0034
DOI	10.1093/gastro/goaa066
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Article ; Online: Diverse functions of long noncoding RNAs in acute myeloid leukemia: emerging roles in pathophysiology, prognosis, and treatment resistance.

Mishra, Srishti / Liu, Jun / Chai, Li / Tenen, Daniel G

Current opinion in hematology

2021 Volume 29, Issue 1, Page(s) 34–43

Abstract: Purpose of review: Advancements in the next-generation sequencing technologies have identified rare transcripts of long noncoding RNAs (lncRNAs) in the genome of cancers, including in acute myeloid leukemia (AML). The purpose of this review is to ... ...

Abstract	Purpose of review: Advancements in the next-generation sequencing technologies have identified rare transcripts of long noncoding RNAs (lncRNAs) in the genome of cancers, including in acute myeloid leukemia (AML). The purpose of this review is to highlight the contribution of lncRNAs in AML pathogenesis, prognosis, and chemoresistance. Recent findings: Several studies have recently reported that deregulated lncRNAs are novel key players in the development of AML and are associated with AML pathophysiology and may serve as prognostic indicators. A few aberrantly expressed lncRNAs that correlated with the recurrent genetic mutations in AML such as NPM1 and RUNX1 have recently been characterized. Moreover, a few lncRNAs in MLL-rearranged leukemia have been described. Additionally, the involvement of lncRNAs in AML chemoresistance has been postulated. Summary: Investigating the functional roles of the noncoding regions including lncRNAs, may provide novel insights into the pathophysiology, refine the prognostic schema, and provide novel therapeutic treatment strategies in AML.
MeSH term(s)	High-Throughput Nucleotide Sequencing ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/drug therapy ; Leukemia, Myeloid, Acute/genetics ; Mutation ; Prognosis ; RNA, Long Noncoding/genetics
Chemical Substances	RNA, Long Noncoding
Language	English
Publishing date	2021-11-28
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.0000000000000692
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Article ; Online: Long noncoding RNA-mediated activation of PROTOR1/PRR5-AKT signaling shunt downstream of PI3K in triple-negative breast cancer.

Tu, Zhenbo / Hu, Yi / Raizada, Devesh / Bassal, Mahmoud A / Tenen, Daniel G / Karnoub, Antoine E

Proceedings of the National Academy of Sciences of the United States of America

2022 Volume 119, Issue 43, Page(s) e2203180119

Abstract: The phosphoinositide 3-kinase (PI3K) pathway represents the most hyperactivated oncogenic pathway in triple-negative breast cancer (TNBC), a highly aggressive tumor subtype encompassing ∼15% of breast cancers and which possesses no targeted therapeutics. ...

Abstract	The phosphoinositide 3-kinase (PI3K) pathway represents the most hyperactivated oncogenic pathway in triple-negative breast cancer (TNBC), a highly aggressive tumor subtype encompassing ∼15% of breast cancers and which possesses no targeted therapeutics. Despite critical contributions of its signaling arms to disease pathogenesis, PI3K pathway inhibitors have not achieved expected clinical responses in TNBC, owing largely to a still-incomplete understanding of the compensatory cascades that operate downstream of PI3K. Here, we investigated the contributions of long noncoding RNAs (lncRNAs) to PI3K activities in clinical and experimental TNBC and discovered a prominent role for LINC01133 as a PI3K-AKT signaling effector. We found that LINC01133 exerted protumorigenic roles in TNBC and that it governed a previously undescribed mTOR Complex 2 (mTORC2)-dependent pathway that activated AKT in a PI3K-independent manner. Mechanistically, LINC01133 induced the expression of the mTORC2 component PROTOR1/PRR5 by competitively coupling away its negative messenger RNA (mRNA) regulator, the heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2B1). PROTOR1/PRR5 in turn was sufficient and necessary for LINC01133-triggered functions, casting previously unappreciated roles for this Rictor-binding protein in cellular signaling and growth. Notably, LINC01133 antagonism undermined cellular growth, and we show that the LINC01133-PROTOR1/PRR5 pathway was tightly associated with TNBC poor patient survival. Altogether, our findings uncovered a lncRNA-driven signaling shunt that acts as a critical determinant of malignancy downstream of the PI3K pathway and as a potential RNA therapeutic target in clinical TNBC management.
MeSH term(s)	Humans ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Triple Negative Breast Neoplasms/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphatidylinositol 3-Kinase/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Cell Proliferation/genetics ; Phosphoinositide-3 Kinase Inhibitors ; Mechanistic Target of Rapamycin Complex 2/metabolism ; RNA, Messenger ; Heterogeneous-Nuclear Ribonucleoproteins ; Cell Line, Tumor
Chemical Substances	RNA, Long Noncoding ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Phosphoinositide-3 Kinase Inhibitors ; Mechanistic Target of Rapamycin Complex 2 (EC 2.7.11.1) ; RNA, Messenger ; Heterogeneous-Nuclear Ribonucleoproteins
Language	English
Publishing date	2022-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2203180119
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Article ; Online: Repurposing RNA sequencing for discovery of RNA modifications in clinical cohorts.

Tan, Kar-Tong / Ding, Ling-Wen / Wu, Chan-Shuo / Tenen, Daniel G / Yang, Henry

Science advances

2021 Volume 7, Issue 32

Abstract: The study of RNA modifications in large clinical cohorts can reveal relationships between the epitranscriptome and human diseases, although this is especially challenging. We developed ModTect (https://github.com/ktan8/ModTect), a statistical framework ... ...

Abstract	The study of RNA modifications in large clinical cohorts can reveal relationships between the epitranscriptome and human diseases, although this is especially challenging. We developed ModTect (https://github.com/ktan8/ModTect), a statistical framework to identify RNA modifications de novo by standard RNA-sequencing with deletion and mis-incorporation signals. We show that ModTect can identify both known (
MeSH term(s)	Base Sequence ; High-Throughput Nucleotide Sequencing ; Humans ; Neoplasms/genetics ; RNA/genetics ; RNA/metabolism ; RNA Processing, Post-Transcriptional ; Sequence Analysis, RNA
Chemical Substances	RNA (63231-63-0)
Language	English
Publishing date	2021-08-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.abd2605
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