1992
DOI: 10.1016/0140-6736(92)91528-g
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Urinary aflatoxin biomarkers and risk of hepatocellular carcinoma

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Cited by 631 publications
(349 citation statements)
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“…It has shown that the effects of exposure to aflatoxin and Hepatitis B virus (HBV) infection are significantly associated with the risk of death due to liver cancer. 71, 85 Ross et al 86 have revealed a strong statistical correlation between aflatoxin ingestion and incidence of HCC in several areas of the world.…”
Section: Role Of Aflatoxin B Causes Hepatocellular Carcinoma In Indiamentioning
confidence: 99%
“…It has shown that the effects of exposure to aflatoxin and Hepatitis B virus (HBV) infection are significantly associated with the risk of death due to liver cancer. 71, 85 Ross et al 86 have revealed a strong statistical correlation between aflatoxin ingestion and incidence of HCC in several areas of the world.…”
Section: Role Of Aflatoxin B Causes Hepatocellular Carcinoma In Indiamentioning
confidence: 99%
“…Among those, chronic hepatitis B (HBV) and C (HCV) viruses infections attribute to HCC development in more than 80% of the HCC cases worldwide . Other known risk factors of HCC, including dietary aflatoxin B 1 (AFB 1 ) intake, cigarette smoking or heavy alcohol consumption, can have synergistic effects (reviewed by Ross et al, 1992;Qian et al, 1994;Kew, 2003;Yu and Yuan, 2004). Besides these risk factors, there are several genetic disorders (Figure 2) such as hemochromatosis (an iron overload disease) that are associated with an increased risk of HCC Kowdley, 2004).…”
Section: Incidence and Etiology Of Hepatocellular Carcinomamentioning
confidence: 99%
“…Although chronic infection with hepatitis B virus (HBV) is now regarded as the major cause of HCC in high-incidence areas (Yeh et al, 1989;Chen et al, 1991;Ryder et al, 1992), ingestion of aflatoxin B 1 (AFB 1 ) has also been implicated as another major contributor to risk (Yeh et al, 1989;Ross et al, 1992;Wang et al, 1996a,b). Many studies have confirmed that parent compound AFB 1 is converted to its carcinogenic forms through metabolism by members of the endogenous cytochrome P-450 enzyme superfamily to reactive 8,9-epoxide metabolites, which can covalently interact with cellular DNA and proteins (International Agency for Research on Cancer, 1992;Gallagher et al, 1994;Guengerich et al, 1998).…”
mentioning
confidence: 99%