ArticleAnti-cancer drugs2018
Clinicopathological features and prediction values of HDAC1, HDAC2, HDAC3, and HDAC11 in classical Hodgkin lymphoma.
Article in Anti-cancer drugs, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- The Epigenetic Architecture of Classical Hodgkin Lymphoma: Lineage Erasure, Immune Escape, and Therapeutic Reprogramming.Medicina (Kaunas, Lithuania) · 2026Review
- HDAC11 Deacetylates BRAF to Regulate Kinase Activity and Cell Proliferation.ACS chemical biology · 2025Article
- Review
- LncRNA EGFR‑AS1 promotes lung cancer cell proliferation, invasion and metastasis via regulation of miR‑449a/HDAC1.Experimental and therapeutic medicine · 2025Article
- Review
- HDAC11 is related to breast cancer prognosis and inhibits invasion and proliferation of breast cancer cells.International journal of clinical and experimental pathology · 2023Article
- New molecular targets in Hodgkin and Reed-Sternberg cells.Frontiers in immunology · 2023Review
- Targeting pancreatic cancer immune evasion by inhibiting histone deacetylases.World journal of gastroenterology · 2022Review
- Tambulin Targets Histone Deacetylase 1 Inhibiting Cell Growth and Inducing Apoptosis in Human Lung Squamous Cell Carcinoma.Frontiers in pharmacology · 2020Article
- MGCD0103 induces apoptosis and simultaneously increases the expression of NF-κB and PD-L1 in classical Hodgkin's lymphoma.Experimental and therapeutic medicine · 2018Article
- Prognosis Analysis of Histone Deacetylases mRNA Expression in Ovarian Cancer Patients.Journal of Cancer · 2018Article
- Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials.Signal transduction and targeted therapyReview
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylases (HDACs) are involved in multiple physical and pathological processes in classical Hodgkin lymphoma (cHL). The prognostic value of HDACs in cHL patients has not been discussed. The aim of the current study is to investigate the HDAC1, HDAC2, HDAC3, and HDAC11 expressions, and to evaluate the correlation of HDAC1, HDAC2, HDAC3, and HDAC11 expressions with the survival rate in cHL patients. We retrospectively analyzed clinicopathological data of 28 patients who were diagnosed with cHL between August 2002 and March 2010. Immunohistochemistry was used to detect the expression of HDAC1, HDAC2, HDAC3, and HDAC11 in these patients. The results showed that HDAC1, HDAC3, and HDAC11 were expressed at a higher level in Hodgkin Reed-Sternberg cells, whereas HDAC2 was expressed at a lower level in Hodgkin Reed-Sternberg cells. The expression of HDAC2 had a relationship with pathological type (P=0.012). There was also a correlation between the expression of HDAC11 and the erythrocyte sedimentation rate (P=0.054). Other clinicopathological parameters had no significant correlation with the expression of HDAC1, HDAC2, HDAC3, and HDAC11 in terms of survival (P>0.05). The 10-year total survival rate by Cox multivariate analysis, after taking into account all clinical and pathologic factors, showed that bulky disease retained significance (P=0.028). Higher expression of HDAC1 predicted shorter progression-free survival and overall survival (OS) in cHL patients (P<0.05, in both cases), and higher expression of HDAC11 might be correlated with lower OS (P=0.05). The study showed that the expressions of HDAC2 and HDAC11 have a particular relationship with the pathologic subtype. Increased expression of HDAC1 was correlated negatively with progression-free survival and OS, and increased expression of HDAC11 had a borderline relationship with the OS rate in patients with cHL.
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