Histone Deacetylase Inhibitors in Cutaneous T-cell Lymphoma

McCann, Sue; Story, Sara K.

doi:10.1097/jdn.0000000000000007

Cited by 4 publications

(6 citation statements)

References 10 publications

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“…Microarray analyses showed that a unique set of genes related to apoptosis, immune regulation, and angiogenesis were altered after Panobinostat treatment 115 . A phase II trial of oral Panobinostat in patients with refractory cutaneous T-cell lymphoma (CTCL) failed at least two systemic therapies with relatively low response rates and short time to progression (CRs: 15 of 95 patients) 123 . In a phase II trial of oral Panobinostat in a total number of 139 patients with MF/SS refractory to 2 standard therapies, the median TTRs was 2.3 months in bexarotene-exposed group (n=79), while 2.8 months in bexarotene-naïve group (n=60); the median DORs of bexarotent -exposed group was 5.6 months; the median PFS rates of bexarotent -exposed group was 4.2 months and 3.7 months for bexarotene-naïve group 113 .…”

Section: Therapeutic Strategies Targeting Hdacsmentioning

confidence: 99%

Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas

et al. 2019

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T-cell lymphomas are a heterogeneous group of cancers with different pathogenesis and poor prognosis. Histone deacetylases (HDACs) are epigenetic modifiers that modulate many key biological processes. In recent years, HDACs have been fully investigated for their roles and potential as drug targets in T-cell lymphomas. In this review, we have deciphered the modes of action of HDACs, HDAC inhibitors as single agents, and HDACs guided combination therapies in T-cell lymphomas. The overview of HDACs on the stage of T-cell lymphomas, and HDACs guided therapies both as single agents and combination regimens endow great opportunities for the cure of T-cell lymphomas.

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Section: Therapeutic Strategies Targeting Hdacsmentioning

confidence: 99%

Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas

et al. 2019

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“…Mitra et al (2018) also reported the similar observation that hdac1 is essential for MGPC proliferation during zebrafish retinal regeneration (63). In case of zebrafish spinal cord, a recent study observed that Hdac1 induce newborn motor neuron formation by activating ERG proliferation (75). Thus, it has been obvious that histone acetylation and deacetylation play an essential role in injury-induced regenerative responses in zebrafish CNS.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic cross-talk between Sirt1 and Dnmt1 promotes axonal regeneration after spinal cord injury in zebrafish

Gupta,

Hui

2024

Preprint

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Though spinal cord injury (SCI) causes irreversible sensory and motor impairments in human, adult zebrafish retain the potent regenerative capacity by injury-induced proliferation of central nervous system (CNS)-resident progenitor cells to develop new functional neurons at the lesion site. The hallmark of SCI in zebrafish lies in a series of changes in the epigenetic landscape, specifically DNA methylation and histone modifications. Decoding the post-SCI epigenetic modifications is therefore critical for the development of therapeutic remedies that boost SCI recovery process. Here, we have studied on Sirtuin1 (Sirt1), a non-classical histone deacetylase that potentially play a critical role in neural progenitor cells (NPCs) proliferation and axonal regrowth following SCI in zebrafish. We investigated the role of Sirt1 in NPC proliferation and axonal regrowth in response to injury in the regenerating spinal cord and found that Sirt1 is involved in the induction of NPC proliferation along with glial bridging during spinal cord regeneration. We also demonstrate that Sirt1 plays a pivotal role in regulating the HIPPO pathway through deacetylation-mediated inactivation of Dnmt1 and subsequent hypomethylation of yap1 promoter, leading to the induction of ctgfa expression, which drives the NPC proliferation and axonal regrowth to complete the regenerative process. In conclusion, our study reveals a novel cross-talk between two important epigenetic effectors, Sirt1 and Dnmt1, in the context of spinal cord regeneration, establishing a previously undisclosed relation between Sirt1 and Yap1 which provides a deeper understanding of the underlying mechanisms governing injury-induced NPC proliferation and axonal regrowth. Therefore, we have identified Sirt1 as a novel, major epigenetic regulator of spinal cord regeneration by modulating the HIPPO pathway in zebrafish.

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“…In a recent study, the role of Hdac1 in the ERG during spinal cord regeneration in zebrafish was investigated [ 111 ]. After spinal cord transection in larval zebrafish, the reduced expression of Hdac1 in ERGs by a potential Hdac1 inhibitor decreased the numbers of both newborn motor neurons and total newborn neurons ( Figure 1 C) [ 111 ]. This decrease was observed to be caused by a reduction in the ERG proliferation driven by a lesion.…”

Section: Epigenetic Regulation Of Regeneration-competent Animals Afte...mentioning

confidence: 99%

“…12, x 12 of 23unaffected by increased deacetylation caused by Hdac1 overexpression or global Hat inhibition in the ERG[111].…”

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confidence: 99%

Regenerative Potential of Injured Spinal Cord in the Light of Epigenetic Regulation and Modulation

Gupta

Dutta

Hui

2023

Cells

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A spinal cord injury is a form of physical harm imposed on the spinal cord that causes disability and, in many cases, leads to permanent mammalian paralysis, which causes a disastrous global issue. Because of its non-regenerative aspect, restoring the spinal cord’s role remains one of the most daunting tasks. By comparison, the remarkable regenerative ability of some regeneration-competent species, such as some Urodeles (Axolotl), Xenopus, and some teleost fishes, enables maximum functional recovery, even after complete spinal cord transection. During the last two decades of intensive research, significant progress has been made in understanding both regenerative cells’ origins and the molecular signaling mechanisms underlying the regeneration and reconstruction of damaged spinal cords in regenerating organisms and mammals, respectively. Epigenetic control has gradually moved into the center stage of this research field, which has been helped by comprehensive work demonstrating that DNA methylation, histone modifications, and microRNAs are important for the regeneration of the spinal cord. In this review, we concentrate primarily on providing a comparison of the epigenetic mechanisms in spinal cord injuries between non-regenerating and regenerating species. In addition, we further discuss the epigenetic mediators that underlie the development of a regeneration-permissive environment following injury in regeneration-competent animals and how such mediators may be implicated in optimizing treatment outcomes for spinal cord injurie in higher-order mammals. Finally, we briefly discuss the role of extracellular vesicles (EVs) in the context of spinal cord injury and their potential as targets for therapeutic intervention.

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Histone Deacetylase Inhibitors in Cutaneous T-cell Lymphoma

Cited by 4 publications

References 10 publications

Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas

Histone Deacetylases (HDACs) Guided Novel Therapies for T-cell lymphomas

Epigenetic cross-talk between Sirt1 and Dnmt1 promotes axonal regeneration after spinal cord injury in zebrafish

Regenerative Potential of Injured Spinal Cord in the Light of Epigenetic Regulation and Modulation

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