# Aflatoxin and Liver Cancer in China: The Evolving Research Landscape

**Authors:** Jian-Guo Chen, Thomas W. Kensler, Gui-Ju Sun, Jian Zhu, Jian-Hua Lu, Da Pan, Yong-Hui Zhang, John D. Groopman

PMC · DOI: 10.3390/toxins18020061 · Toxins · 2026-01-25

## TL;DR

Aflatoxin exposure is strongly linked to liver cancer in China, and efforts to reduce contamination have successfully lowered cancer rates through dietary changes and policy.

## Contribution

The paper synthesizes China's long-term research on aflatoxin-related liver cancer and proposes an integrated prevention framework.

## Key findings

- Biomarkers like AFB1–N7–guanine and TP53 R249S establish a causal link between aflatoxin exposure and HCC.
- Dietary shifts and food governance reduced aflatoxin biomarkers and HCC mortality in endemic regions.
- Chemoprevention strategies like oltipraz and broccoli sprout beverages can lower aflatoxin burdens in exposed populations.

## Abstract

Aflatoxins, particularly aflatoxin B1 (AFB1), are among the most potent naturally occurring carcinogens and remain a major food-borne hazard in parts of Asia and Africa. China has generated a uniquely cohesive body of evidence connecting aflatoxin contamination to hepatocellular carcinoma (HCC), especially in settings where chronic hepatitis B virus (HBV) infection is highly prevalent and acts synergistically with aflatoxin exposure. Over five decades, field investigations and laboratory innovations—exemplified by long-term work in Qidong—have assembled a multi-layered causal chain spanning the following: (i) contamination monitoring in staple foods; (ii) quantification of internal dose and biologically effective dose using validated biomarkers (e.g., urinary AFB1–N7–guanine, AFM1, and serum AFB1–lysine albumin adducts); (iii) a characteristic molecular fingerprint in tumors and circulation (TP53 R249S); (iv) reversibility demonstrated through randomized intervention trials and policy-driven natural experiments. Chemoprevention and dietary interception studies (e.g., oltipraz, chlorophyllin, and broccoli sprout beverages) showed that enhancing detoxication pathways can lower biomarker burdens in exposed populations. At the population level, a sustained dietary transition from maize to rice, together with strengthened food governance, was accompanied by marked decreases in biomarker distributions and subsequent declines in HCC mortality in endemic regions. Nevertheless, regional heterogeneity, multi-mycotoxin co-exposure, and climate variability are expected to increase exposure volatility and complicate surveillance. Here, we translate and synthesize the Chinese evidence base, highlight biomarker-enabled monitoring and policy evaluation, and propose an integrated “5+1” prevention framework spanning source control, process detoxification, tiered governance, short-course interception, precision follow-up of high-risk individuals, and climate-sensitive early warning along the climate–agriculture–storage–processing–population (CAT–CSPP) chain.

## Linked entities

- **Genes:** TP53 (tumor protein p53) [NCBI Gene 7157]
- **Chemicals:** aflatoxin B1 (PubChem CID 186907), AFB1 (PubChem CID 186907), AFM1 (PubChem CID 15558498), oltipraz (PubChem CID 47318), chlorophyllin (PubChem CID 123798)
- **Diseases:** hepatocellular carcinoma (MONDO:0007256), HCC (MONDO:0007256)

## Full-text entities

- **Genes:** TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** cancer (MESH:D009369), HBV infection (MESH:D006509), injury to (MESH:D014947), chronic liver disease (MESH:D008107), inflammation (MESH:D007249), carcinogenesis (MESH:D063646), toxicosis (MESH:C565846), Toxicity (MESH:D064420), hepatitis C virus (HCV) infection (MESH:D006526), carcinogenic (MESH:D011230), Instability (MESH:D043171), tumor-related (MESH:D000072716), HCC (MESH:D006528), liver-function abnormalities (MESH:D056486), chronic hepatitis B virus (HBV) infection (MESH:D019694)
- **Chemicals:** sulforaphane (MESH:C016766), chlorophyll (MESH:D002734), AFB1 (MESH:D016604), vegetable oils (MESH:D010938), chlorophyllin (MESH:C007020), Aflatoxin (MESH:D000348), corn oil (MESH:D003314), Oil (MESH:D009821), glucoraphanin (MESH:C119494), montmorillonite (MESH:D001546), AFB1-N7 (-), fumonisins (MESH:D037341), ZEN (MESH:D015025), oltipraz (MESH:C026209), lys (MESH:D008239), AFM1 (MESH:D016607), lipid (MESH:D008055)
- **Species:** Arachis hypogaea (goober, species) [taxon 3818], A. flavus [taxon 315677], Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606], Brassica oleracea var. italica (asparagus broccoli, varietas) [taxon 36774], Oryza sativa (Asian cultivated rice, species) [taxon 4530]
- **Mutations:** G-->T in codon 249, 249 AGG, R249S

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12944938/full.md

## References

94 references — full list in the complete paper: https://tomesphere.com/paper/PMC12944938/full.md

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Source: https://tomesphere.com/paper/PMC12944938