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Samuel A Miller et al.
Molecular cancer research : MCR, 18(2), 264-277 (2019-11-11)
Activation of the epithelial-to-mesenchymal transition (EMT) program is a critical mechanism for initiating cancer progression and migration. Colorectal cancers contain many genetic and epigenetic alterations that can contribute to EMT. Mutations activating the PI3K/AKT signaling pathway are observed in >40%
Catherine Lee et al.
Nature communications, 10(1), 332-332 (2019-01-20)
Drugs that modify the epigenome are powerful tools for treating cancer, but these drugs often have pleiotropic effects, and identifying patients who will benefit from them remains a major clinical challenge. Here we show that medulloblastomas driven by the transcription
Robert Kleszcz et al.
Cellular oncology (Dordrecht), 42(4), 505-520 (2019-05-16)
Activation of the Wnt pathway contributes to the development of head and neck squamous cell carcinomas (HNSCC) and its inhibition has recently emerged as a promising therapeutic strategy. Here, we aimed at identifying suitable molecular targets for down-regulation of canonical
Xuan Zhang et al.
Frontiers in oncology, 11, 748730-748730 (2021-10-30)
The development of resistance to 5-fluorouracil (5FU) chemotherapy is a major handicap for sustained effective treatment in peritoneal carcinomatosis (PC) of colorectal cancer (CRC). Metabolic reprogramming of adipocytes, a component of the tumor microenvironment and the main composition of peritoneum
Kimberly N Smitheman et al.
Haematologica, 104(6), 1156-1167 (2018-12-06)
Lysine specific demethylase 1 (LSD1) is a histone modifying enzyme that suppresses gene expression through demethylation of lysine 4 on histone H3. The anti-tumor activity of GSK2879552 and GSK-LSD1, potent, selective irreversible inactivators of LSD1, has previously been described. Inhibition
Cavan P Bailey et al.
Frontiers in immunology, 11, 2196-2196 (2020-10-13)
Cell therapies such as chimeric-antigen receptor (CAR) T-cells and NK cells are cutting-edge methods for treating cancer and other diseases. There is high interest in optimizing drug treatment regimens to best work together with emerging cell therapies, such as targeting
Isuru R Kumarasinghe et al.
European journal of medicinal chemistry, 148, 210-220 (2018-02-21)
Lysine-specific demethylase 1 (LSD1) is a chromatin-remodeling enzyme that plays an important role in cancer. Over-expression of LSD1 decreases methylation at histone 3 lysine 4, and aberrantly silences tumor suppressor genes. Inhibitors of LSD1 have been designed as chemical probes
Chaeyoon Oh et al.
BMB reports, 53(7), 385-390 (2020-04-23)
Inflammatory Bowel Disease is caused by an acute or chronic dysfunction of the mucosal inflammatory system in the intestinal tract. In line with the results of our previous study, wherein we found that the PKCα-LSD1-NF-κB signaling plays a critical role
PKCα-LSD1-NF-κB-Signaling Cascade Is Crucial for Epigenetic Control of the Inflammatory Response
Kim D, et al.
Molecular Cell, 69(3), 398-411 (2018)
Agatheeswaran Subramaniam et al.
Blood, 136(19), 2151-2161 (2020-06-26)
Culture conditions in which hematopoietic stem cells (HSCs) can be expanded for clinical benefit are highly sought after. Here, we report that inhibition of the epigenetic regulator lysine-specific histone demethylase 1A (LSD1) induces a rapid expansion of human cord blood-derived
Ryan S Stowers et al.
Nature biomedical engineering, 3(12), 1009-1019 (2019-07-10)
In breast cancer, the increased stiffness of the extracellular matrix is a key driver of malignancy. Yet little is known about the epigenomic changes that underlie the tumorigenic impact of extracellular matrix mechanics. Here, we show in a three-dimensional culture
Shinji Takagi et al.
Cancer research, 77(17), 4652-4662 (2017-07-02)
T-3775440 is an irreversible inhibitor of the chromatin demethylase LSD1, which exerts antiproliferative effects by disrupting the interaction between LSD1 and GFI1B, a SNAG domain transcription factor, inducing leukemia cell transdifferentiation. Here, we describe the anticancer effects and mechanism of
Joy E Kirkpatrick et al.
Epigenetics, 13(5), 557-572 (2018-06-22)
Periodontal disease (PD) afflicts 46% of Americans with no effective adjunctive therapies available. While most pharmacotherapy for PD targets bacteria, the host immune response is responsible for driving tissue damage and bone loss in severe disease. Herein, we establish that
Donglim Esther Park et al.
Nature cell biology, 22(5), 603-615 (2020-04-15)
Merkel cell carcinoma (MCC)-a neuroendocrine cancer of the skin-is caused by the integration of Merkel cell polyomavirus and persistent expression of large T antigen and small T antigen. We report that small T antigen in complex with MYCL and the
Xiaomu Wei et al.
Cancer research, 78(10), 2747-2759 (2018-03-22)
Given the frequent and largely incurable occurrence of multiple myeloma, identification of germline genetic mutations that predispose cells to multiple myeloma may provide insight into disease etiology and the developmental mechanisms of its cell of origin, the plasma cell (PC).
HIV-1 infection of microglial cells in a reconstituted humanized mouse model and identification of compounds that selectively reverse HIV latency
Llewellyn GN, et al.
Journal of Neurovirology, 1-12 (2017)
Antonio Romo-Morales et al.
Pediatric blood & cancer, 66(9), e27888-e27888 (2019-06-18)
Ewing sarcoma and desmoplastic small round cell tumors (DSRCT) are rare and clinically aggressive sarcomas usually characterized by oncogenic fusion proteins involving EWS. Emerging studies of Ewing sarcoma have demonstrated EWS-FLI1-driven chromatin remodeling as a key aspect of tumorigenicity. In
Anne-Claire Guénantin et al.
The Journal of clinical investigation, 131(1) (2021-01-05)
LMNA mutations in patients are responsible for a dilated cardiomyopathy. Molecular mechanisms underlying the origin and development of the pathology are unknown. Herein, using mouse pluripotent embryonic stem cells (ESCs) and a mouse model both harboring the p.H222P Lmna mutation
Michael E Vinyard et al.
Nature chemical biology, 15(5), 529-539 (2019-04-18)
Understanding the mechanism of small molecules is a critical challenge in chemical biology and drug discovery. Medicinal chemistry is essential for elucidating drug mechanism, enabling variation of small molecule structure to gain structure-activity relationships (SARs). However, the development of complementary
Nicholas K Vinckier et al.
Nature communications, 11(1), 2082-2082 (2020-05-01)
Developmental progression depends on temporally defined changes in gene expression mediated by transient exposure of lineage intermediates to signals in the progenitor niche. To determine whether cell-intrinsic epigenetic mechanisms contribute to signal-induced transcriptional responses, here we manipulate the signalling environment
Theodore P Braun et al.
Proceedings of the National Academy of Sciences of the United States of America, 117(24), 13670-13679 (2020-05-31)
Acute myeloid leukemia (AML) is a deadly hematologic malignancy with poor prognosis, particularly in the elderly. Even among individuals with favorable-risk disease, approximately half will relapse with conventional therapy. In this clinical circumstance, the determinants of relapse are unclear, and
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