Rare complication of hepatocellular carcinoma in Wilson's disease

Ohkoshi-Yamada, Marina; Kamimura, Kenya; Kamimura, Hiroteru; Terai, Shuji

doi:10.1002/jgh3.12648

Cited by 10 publications

(7 citation statements)

References 14 publications

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“…Genetic mutations involved in hereditary hemochromatosis, glycogen storage diseases, and Wilson disease have been associated with greater risk of HCC. 8 – 10 While case reports exist on patients with these genetic diseases developing concurrent leukemias or lymphomas, there is no strong evidence of any genetic mutations that are common to individuals with HCC and individuals with CLL/SLL. 11 Some causes of chronic liver disease, including hepatitis B, hepatitis C and iron overload, have been postulated to be associated with greater risk of non-Hodgkin lymphoma.…”

Section: Discussionmentioning

confidence: 99%

Hepatocellular Carcinoma With Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma in the Absence of Cirrhosis

Tu,

Khalyfa,

Bellizzi

et al. 2024

ACG Case Rep J

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This report describes a rare case of hepatocellular carcinoma (HCC) concurrent with chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) without traditional risk factors, such as hepatic fibrosis or chronic hepatitis. Initially presenting with hematuria, incidental imaging revealed a liver lesion, later diagnosed as moderately differentiated HCC. Notably, the patient had no history of well-established risk factors of HCC including viral hepatitis or liver cirrhosis. CLL/SLL was unexpectedly discovered in the surgical specimen during the hepatectomy. This case challenges traditional perceptions of HCC etiology, suggesting a potential link between HCC and CLL/SLL even without established risk factors.

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Section: Discussionmentioning

confidence: 99%

Hepatocellular Carcinoma With Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma in the Absence of Cirrhosis

Tu,

Khalyfa,

Bellizzi

et al. 2024

ACG Case Rep J

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“…D-penicillamine is widely utilized as a therapeutic agent for Wilson’s disease to improve Cu deposition in the liver. Surprisingly, patients who are treated with d-penicillamine have an increased risk of HCC development because the administration of d-penicillamine often causes iron accumulation and synergistic radical formation in the liver [ 127 ].…”

Section: Coppermentioning

confidence: 99%

Current Trends on the Involvement of Zinc, Copper, and Selenium in the Process of Hepatocarcinogenesis

Himoto,

Masaki

2024

Nutrients

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Numerous nutritional factors increase the risk of hepatocellular carcinoma (HCC) development. The dysregulation of zinc, copper, and selenium homeostasis is associated with the occurrence of HCC. The impairment of the homeostasis of these essential trace elements results in oxidative stress, DNA damage, cell cycle progression, and angiogenesis, finally leading to hepatocarcinogenesis. These essential trace elements can affect the microenvironment in HCC. The carrier proteins for zinc and copper and selenium-containing enzymes play important roles in the prevention or progression of HCC. These trace elements enhance or alleviate the chemosensitivity of anticancer agents in patients with HCC. The zinc, copper, or selenium may affect the homeostasis of other trace elements with each other. Novel types of cell death including ferropotosis and cupropotosis are also associated with hepatocarcinogenesis. Therapeutic strategies for HCC that target these carrier proteins for zinc and copper or selenium-containing enzymes have been developed in in vitro and in vivo studies. The use of zinc-, copper- or selenium-nanoparticles has been considered as novel therapeutic agents for HCC. These results indicate that zinc, copper, and selenium may become promising therapeutic targets in patients with HCC. The clinical application of these agents is an urgent unmet requirement. This review article highlights the correlation between the dysregulation of the homeostasis of these essential trace elements and the development of HCC and summarizes the current trends on the roles of these essential trace elements in the pathogenesis of hepatocarcinogenesis.

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“…Several other conditions of iron and copper overload also exist as a result of increased gastrointestinal absorption, such as of iron in idiopathic hemochromatosis and copper in Wilson's disease [21,49,50]. Chronic metal overload in the latter two diseases of increased metal absorption could eventually lead to metal overload, serious toxicities and fatalities, including many cases of hepatocellular carcinoma [21,[50][51][52].…”

Section: Targeting Aspects Of Chelator Interactions With Ironmentioning

confidence: 99%

New Iron Metabolic Pathways and Chelation Targeting Strategies Affecting the Treatment of All Types and Stages of Cancer

Kontoghiorghes¹

2022

IJMS

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There is new and increasing evidence from in vitro, in vivo and clinical studies implicating the pivotal role of iron and associated metabolic pathways in the initiation, progression and development of cancer and in cancer metastasis. New metabolic and toxicity mechanisms and pathways, as well as genomic, transcription and other factors, have been linked to cancer and many are related to iron. Accordingly, a number of new targets for iron chelators have been identified and characterized in new anticancer strategies, in addition to the classical restriction of/reduction in iron supply, the inhibition of transferrin iron delivery, the inhibition of ribonucleotide reductase in DNA synthesis and high antioxidant potential. The new targets include the removal of excess iron from iron-laden macrophages, which affects anticancer activity; the modulation of ferroptosis; ferritin iron removal and the control of hyperferritinemia; the inhibition of hypoxia related to the role of hypoxia-inducible factor (HIF); modulation of the function of new molecular species such as STEAP4 metalloreductase and the metastasis suppressor N-MYC downstream-regulated gene-1 (NDRG1); modulation of the metabolic pathways of oxidative stress damage affecting mitochondrial function, etc. Many of these new, but also previously known associated iron metabolic pathways appear to affect all stages of cancer, as well as metastasis and drug resistance. Iron-chelating drugs and especially deferiprone (L1), has been shown in many recent studies to fulfill the role of multi-target anticancer drug linked to the above and also other iron targets, and has been proposed for phase II trials in cancer patients. In contrast, lipophilic chelators and their iron complexes are proposed for the induction of ferroptosis in some refractory or recurring tumors in drug resistance and metastasis where effective treatments are absent. There is a need to readdress cancer therapy and include therapeutic strategies targeting multifactorial processes, including the application of multi-targeting drugs involving iron chelators and iron–chelator complexes. New therapeutic protocols including drug combinations with L1 and other chelating drugs could increase anticancer activity, decrease drug resistance and metastasis, improve treatments, reduce toxicity and increase overall survival in cancer patients.

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Rare complication of hepatocellular carcinoma in Wilson's disease

Cited by 10 publications

References 14 publications

Hepatocellular Carcinoma With Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma in the Absence of Cirrhosis

Hepatocellular Carcinoma With Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma in the Absence of Cirrhosis

Current Trends on the Involvement of Zinc, Copper, and Selenium in the Process of Hepatocarcinogenesis

New Iron Metabolic Pathways and Chelation Targeting Strategies Affecting the Treatment of All Types and Stages of Cancer

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