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. 2023 Sep 4;23(5):727-739.
doi: 10.17305/bb.2023.8791.

The role of chidamide in the treatment of B-cell non-Hodgkin lymphoma: An updated systematic review

Hastono Ridwansyah  1 , Indra Wijaya  2 , Muhammad Hasan Bashari  3 , Achmad Hussein Sundawa Kartamihardja  4 , Bethy Suryawathy Hernowo  5
Affiliations

The role of chidamide in the treatment of B-cell non-Hodgkin lymphoma: An updated systematic review

Hastono Ridwansyah et al. Biomol Biomed. .

Abstract

B-cell non-Hodgkin lymphoma (B-NHL) is a lymphoid malignancy derived from B-cells that remains difficult to treat. Moreover, relapses and refractory cases are common. Abnormalities in epigenetic mechanisms, such as imbalanced histone acetylation affecting certain genes, contribute to relapses and refractory cases. Chidamide (tucidinostat) is a novel histone deacetylase inhibitor that can reverse this epigenetic imbalance and has been approved for the treatment of T-cell malignancies. However, the use of chidamide for B-NHL remains limited, and the lack of relevant literature exacerbates this limitation. We conducted this review to summarize the anticancer activity of chidamide against B-NHL and its clinical applications to overcome drug resistance. This systematic review was conducted according to the PRISMA 2020 guidelines, using some keyword combinations from MEDLINE and EBSCO. The inclusion and exclusion criteria were also defined. Of the 131 records retrieved from databases, 16 were included in the review. Nine articles revealed that chidamide limited tumor progression by modifying the tumor microenvironment, stopping the cell cycle, inducing apoptosis and autophagy, and enhancing complement-dependent and antibody-dependent cell-mediated cytotoxicities.According to seven other studies, administering chidamide in combination with another existing therapeutic regimen may benefit not only patients with relapsed/refractory B-NHL, but also those with newly diagnosed B-NHL. Chidamide plays many important roles in limiting B-NHL progression through epigenetic modifications. Thus, combining chidamide with other anticancer drugs may be more beneficial for patients with newly diagnosed and relapsed/refractory B-NHL.

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Conflict of interest statement

Conflicts of interest: Authors declare no conflicts of interest.

Figures

Figure 1.
Figure 1.
A systematic literature search was conducted using a PRISMA flow diagram. Of the 131 articles retrieved, 16 were included in the review. PRISMA: Preferred Reporting Items for Systematic Reviews Meta-Analysis.
Figure 2.
Figure 2.
Risk of bias assessment summary using ROBINS-I. BC: Bias due to confounding; BSP: Bias in the selection of participants; COI: Bias in the classification of interventions; BDI: Bias due to deviations from the intended intervention; BMD: Bias due to missing data; BMO: Bias in the measurement of outcomes; BSR: Bias in the selection of the reported result; ROBINS-I: Risk of bias in non-randomized studies of interventions. Green: low risk of bias; yellow: moderate risk of bias; red: serious risk of bias; and white: no information.
Figure 3.
Figure 3.
Proposed mechanisms of action of chidamide in inducing cell cycle arrest in B-cell non-Hodgkin lymphoma. HDAC: Histone deacetylase; CKI: Cyclin-dependent kinase.
Figure 4.
Figure 4.
Mechanisms by which chidamide promotes cell death and modulates TME in B-cell non-Hodgkin lymphoma through various mechanisms. TME: Tumor microenvironment; HDAC: Histone deacetylase; MHC: Major histocompatibility complex; NF-κB: Nuclear factor kappa B; STAT3: Signal transducer and activator of transcription 3; BTG-1: B-cell translocation gene-1; NK: Natural killer.
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