Response of negative estrogen-receptor hepatocarcinoma to tamoxifen, and survival of non-resectable patients

García-Leiva, Jorge; Gamboa‐Domínguez, Armando; Cerón-Lizárraga, T.; Morales-Espinosa, Daniela; Meza–Junco, Judith; Arrieta, Óscar

doi:10.1016/s1665-2681(19)31985-4

Cited by 5 publications

(3 citation statements)

References 16 publications

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“…In contrast, wildtype ER-␤ was expressed more often in HCV patients than in HBV patients (95.7% vs. 44.4%; p < 0.05). Within Western population, 33-46% of HCC samples showed overexpression of ER (Tsiambas et al, 2011;Garcia-Leiva et al, 2006;Moon et al, 2004). In summary, aberrant ER, both in Asian (Sheng et al, 2014) and Western (Villa et al, 1995) population have been described and shown to have an impact in patients prognosis.…”

Section: Hormone Receptorsmentioning

confidence: 96%

Hepatocellular carcinoma: Exploring the impact of ethnicity on molecular biology

Lamarca

Mendiola²,

Barriuso

2016

Critical Reviews in Oncology/Hematology

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Hepatocellular carcinoma (HCC) is the sixth most common cancer in the world and the third leading cause of cancer-related death. The high rate of diagnosis in non-curable stages and the lack of novel active treatments make it necessary to review all the possible sources of misleading results in this scenario. The incidence of HCC shows clear geographical variation with higher annual incidence in Asia and Africa than in Western countries; we aimed to review the literature to find if there are different trends in the main activated molecular pathways. Hyperactivation of RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signalling and epithelial to mesenchymal transition (EMT) process are more prevalent in the Western population; however, fibroblast growth factor (FGF), transforming growth factor β (TGFβ) and Notch pathways seems to be more relevant in Asian population. Whether these variations just reflect the distinct distribution of known causes of HCC or proper ethnical differences remain to be elucidated. Nevertheless, these clearly different patterns are relevant to regional or worldwide clinical trial design. If this information is neglected by sponsors and researchers the rate of failure in HCC trials will not improve.

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Section: Hormone Receptorsmentioning

confidence: 96%

Hepatocellular carcinoma: Exploring the impact of ethnicity on molecular biology

Lamarca

Mendiola²,

Barriuso

2016

Critical Reviews in Oncology/Hematology

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“…Oestrogen receptors have been found in up to 33% of HCC tumors. [72] Therefore, tamoxifen was investigated more than any other hormonal compound, as a possible systemic treatment for HCC. However, the results from the RCTs involving tamoxifen were disappointing.…”

Section: Hormonal Treatmentsmentioning

confidence: 99%

An overview of evidence-based management of hepatocellular carcinoma: A meta-analysis

Salhab

Canelo

2011

J Can Res Ther

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RFA should be the first-line treatment in patients with a single small HCC tumor ≤ 3 cm. Careful patient selection is crucial prior to transarterial chemoembolization (TACE), as the procedure may be associated with an increased risk of liver failure. Tamoxifen has no role to play in the treatment of HCC. Sorafenib should be the first-line treatment in patients with advanced and inoperable HCC. The role of Sorafenib in the management of early stage HCC remains to be determined.

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“…In particular, sex hormones, such as oestrogen receptors (ERα and β) and androgen receptor (AR), may be associated with the development of hepatocellular carcinoma . Epidemiological and animal studies have shown a close relationship between sexual hormones and HCC . Due to lower oestrogen and oestrogen receptor levels, men are more likely to develop HCC than women .…”

Section: Introductionmentioning

confidence: 99%

Fenofibrate induced PPAR alpha expression was attenuated by oestrogen receptor alpha overexpression in Hep3B cells

Jeng

Velmurugan

Hsu

et al. 2017

Environmental Toxicology

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The physiological regulation of Oestrogen receptor α (ERα) and peroxisome proliferator-activated receptor alpha (PPARα) in Hepatocellular carcinoma (HCC) remains unknown. The present study we first treat the cells with fenofibrate and further investigated the possible mechanisms of 17β-estradiol (E ) and/or ERα on regulating PPARα expression. We also found higher PPARα expression in the tumor area than adjacent areas and subsequently compared PPARα expression in four different hepatic cancer cell lines. Hep3B cells were found to express more PPARα than the other cell lines. Using the PPARα agonist fenofibrate, we found that fenofibrate increased Hep3B cell proliferation efficiency by increasing cell cycle proteins, such as cyclin D1 and PCNA, and inhibiting p27 and caspase 3 expressions. Next, we performed transient transfections and immuno-precipitation studies using the pTRE2/ERα plasmid to evaluate the interaction between ERα and PPARα. ERα interacted directly with PPARα and negatively regulated its function. Moreover, in Tet-on ERα over-expressed Hep3B cells, E treatment inhibited PPARα, its downstream gene acyl-CoA oxidase (ACO), cyclin D1 and PCNA expression and further increased p27 and caspase 3 expressions. However, over-expressed ERα plus 17-β-estradiol (10 M) reversed the fenofibrate effect and induced apoptosis, which was blocked in ICI/melatonin/fenofibrate-treated cells. This study illustrates that PPARα expression and function were negatively regulated by ERα expression in Hep3B cells.

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Response of negative estrogen-receptor hepatocarcinoma to tamoxifen, and survival of non-resectable patients

Cited by 5 publications

References 16 publications

Hepatocellular carcinoma: Exploring the impact of ethnicity on molecular biology

Hepatocellular carcinoma: Exploring the impact of ethnicity on molecular biology

An overview of evidence-based management of hepatocellular carcinoma: A meta-analysis

Fenofibrate induced PPAR alpha expression was attenuated by oestrogen receptor alpha overexpression in Hep3B cells

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