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Entity | Oral squamous cell carcinoma |
Note | HDAC1 overexpression was found in 55.10% of 49 mobile tongue squamous cell carcinoma evaluated whereas most of the cells from non-neoplastic epithelium presents negative immunoexpression for HDAC1 (Theocharis, et al. 2011). HDAC1 was overexpressed in 70% of lip squamous cell carcinoma (Fig.2) and in 77% of actinic cheilitis, with immunoexpression increasing in preneoplastic cases with severe epithelial dysplasia, and in neoplastic cases with poor differentiation (Chrun, et al. 2017). |
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| Fig. 2. Immunoexpression of HDAC1 in lip squamous cell carcinoma. |
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Entity | Esophageal cancer |
Note | Comparing H4 acetylation and HDAC1 expression, it was observed hyperacetylation of H4 and decreased HDAC1 expression from esophageal normal tissue through esophageal carcinoma, suggesting that the equilibrium between HDAC and HAT is interrupted in this carcinoma (Toh, et al. 2003). Few cases of esophageal cancer were reported with HDAC1 overexpression when compared to normal esophageal mucosa (15%) (Nakagawa, et al. 2007). Esophageal adenocarcinoma also presented subexpression in majority of cases and was not associated to prognostic factor (Langer, et al. 2010). |
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Entity | Thyroid cancer |
Note | HDAC1 immunoexpression was found in 99% of 47 thyroid malignances (papillary, follicular, medullary, and anaplastic thyroid carcinomas) and 23 benign thyroid tumors, with significant relation to tumor size, without difference in expression between malignant and benign thyroid tumors (Giaginis, et al. 2014). Nakagawa and collaborators reported immunoreactivity in all evaluated cases of papillary thyroid tumors (Nakagawa, et al. 2007). |
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Entity | Gastric cancer |
Note | HDAC1 overexpression was detected by semi-quantitative RT-PCR, immunoblot analysis, and immunohistochemistry in gastric cancer tissues compared to its corresponding normal tissue (Choi, et al. 2001; Nakagawa, et al. 2007). Sudo and colleagues found association between HDAC expression and aggressive behavior of primary gastric cancer. In this study, HDAC1 overexpression was found by quantitative reverse transcription-PCR in gastric cancer tissue in 77% of the cases, with higher expression correlated to lymph vessel and vascular vessel permeations, advanced stage of the disease, and lymph node metastasis (Sudo, et al. 2011). |
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Entity | Colorectal cancer |
Note | When comparing colorectal carcinoma cells and normal colonic mucosa by reverse transcription (RT)-PCR (Ishihama, et al. 2007) and immunohistochemistry (Nakagawa, et al. 2007) there was a greater HDAC1 expression in cancer than in normal colonic epithelium. Bernard and collaborators evaluated tissue microarray (TMA) with 254 colorectal adenocarcinomas samples and 50 normal colorectal tissues, showing no significant difference between normal and cancerous tissues, but suggested combination of higher HDAC expression and clinical outcomes for these patients (Benard, et al. 2015). |
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Entity | Pancreatic cancer |
Note | HDAC1 with HDAC2 and SIN3A were recognized as complex silencing regulators of CDH1 (E-cadherin), thus involved in pancreatic adenocarcinoma metastasis (von Burstin, et al. 2009; Aghdassi, et al. 2012). Several HDACs were evaluated in (pNET): higher expression of HDAC1 was observed in high grade pNET and its expression showed positive correlation with mitotic (pHH3) and proliferation (Ki-67) index (Klieser, et al. 2017). |
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Entity | Lymphomas |
Note | Hodgkin`s lymphoma exhibited higher immunoexpression of HDAC1 when analysing 283 TMA (Adams, et al. 2010). In diffuse large B-cell lymphomas (DLBCL) HDAC1 immunoexpression was higher in comparison to reactive lymphoid hyperplasia which was correlated to cell proliferation index (Ki67) in the development of DLBCL, and associated with aggressiveness/poor survival of DLBCL patients (Min, et al. 2012). On the other hand, Lee and colleagues found faintly nuclear staining in few cases of 91 DLBCL samples submitted to immunohistochemistry (Lee, et al. 2014). |
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Entity | Leukemias |
Note | Moreno and collaborators evaluated 94 cases of childhood acute lymphoblastic leukaemia (ALL) and found HDAC1 mRNA increased expression in T-cell ALL when compared to B-cell ALL. Yang et al. also found higher HDAC1 mRNA in ALL. (Moreno, et al. 2010). Quantitative real-time polymerase chain reaction also revealed higher HDAC1 expression in ALL (Yang, et al. 2015). Clinicopathological parameters indicated that overexpression of HDAC1 may be related to unfavourable prognosis of childhood ALL (Gruhn, et al. 2013). |
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Entity | Lung cancer |
Note | HDAC1 is highly expressed in lung cancer (Nakagawa, et al. 2007). A correlation between HDAC1 mRNA and protein levels showed that HDAC1 gene expression might be involved with lung cancer progression (Sasaki, et al. 2004). |
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Entity | Prostate cancer |
Note | Up-regulation of HDAC1 in prostate cancer compared to benign prostatic hyperplasia was demonstrated by immunohistochemistry (Patra, et al. 2001; Nakagawa, et al. 2007). Weichert and collaborators achieved immunohistochemistry for Class I HDAC isoforms in prostate carcinomas, showing HDAC1, HDAC2 and HDAC3 stronger expression accompanied by tumor cell proliferation raising (Weichert, et al. 2008). Overexpression of HDAC1 was also related to major increase of hormone refractory in prostate cancer and augmentation of proliferation (Halkidou, et al. 2004). |
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Entity | Breast cancer |
Note | HDAC1 was evaluated in TMA from 238 patients with primary breast cancer and presented wide variation in positive imunnoexpression (Muller, et al. 2013). While Nakagawa (Nakagawa, et al. 2007) and Ververis (Ververis and Karagiannis 2012) showed higher expression of HDAC1 by immunohistochemistry and immunofluorescence respectively. Suzuki and colleagues detected a decrease in its expression from normal tissue through invasive ductal carcinoma, and from high grade through intermediate/low grade carcinoma (Suzuki, et al. 2009). Higher expression of HDAC1 was related to molecular subtypes (Luminal A, Luminal B, HER overexpressed, and triple-negative) and with improved overall survival (Seo, et al. 2014). |
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Entity | Ovarian cancer |
Note | HDAC1 immunoexpression showed positive correlation with Ki-67 and inverse correlation with E-cadherin in 115 cases of ovarian tumors, suggesting an important participation of HDAC1 in cellular proliferation. Its overexpression was also associated with poor outcome (Hayashi, et al. 2010). Immunoreactivity for HDAC1 was sighted in 95% of cases evaluated, but without significant difference between histological subtypes of ovarian cancer (Nakagawa, et al. 2007). By immunohistochemistry and qRT-PCR, HDAC1 and DNMT3B revealed positive correlation in ovarian cancer; HDAC1 was highly expressed in comparison to normal ovarian tissue (Gu, et al. 2013). In a population-based cohort of 465 ovarian carcinomas, Weichert and collaborators observed higher level expression of HDAC1 and positive correlation with Ki67, indicating its participation in cell proliferation without significant interference in prognostic (Weichert 2009). |
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Entity | Endometrial cancer |
Note | Strong HDAC1 immunoexpression was observed in endometrial stromal sarcoma, and it was suggested that this expression is linked to lower than 10 years disease free survival (Baek, et al. 2016). Endometrial adenocarcinomas compared to normal endometrium exhibited reduction in HDAC1 expression (Krusche, et al. 2005). However, in other research, endometrial carcinomas presented higher HDAC1 expression in comparison to normal endometrial tissue (Fakhry, et al. 2010). Weichert and colleagues evaluated 149 endometrial carcinomas and showed a higher level of HDAC1 expression that was positively correlated with cell proliferation indicator (Ki-67) and associated to 10 years survival decrease (Weichert 2009). |
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