Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (775 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A hepatic carcinogen whose mechanism of activation involves N-hydroxylation to the aryl hydroxamic acid followed by enzymatic sulfonation to sulfoxyfluorenylacetamide. It is used to study the carcinogenicity and mutagenicity of aromatic amines.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: 2 Acetylaminofluorene; 2-Acetamidofluorene; 2 Acetamidofluorene; 2-Fluorenylacetamide; 2 Fluorenylacetamide; Fluoren-2-ylacetamide; Fluoren 2 ylacetamide; 2-AAF.
Where it fits in the MeSH classification
- Broader topics
- Acetamides; Fluorenes
- Narrower topics
- Acetoxyacetylaminofluorene; Hydroxyacetylaminofluorene
Research landscape
PubMed indexes 2,669 records tagged with the MeSH heading “2-Acetylaminofluorene” (counts retrieved 2026-10-31). 22 of them (0.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,265 records.
Reviews account for 68 records (2.5%) and meta-analyses for 0. Randomized controlled trials number 0 (0.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,265 |
| 2000-2009 | 281 |
| 2010-2019 | 101 |
| 2020 onward | 22 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 68 | 2.5% |
| Meta-analyses | 0 | 0.0% |
| Randomized controlled trials | 0 | 0.0% |
Method: PubMed query "2-Acetylaminofluorene"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Development of Asialoglycoprotein Receptor-Targeted Nanoparticles for Selective Delivery of Gemcitabine to Hepatocellular Carcinoma [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Selective targeting of anticancer drugs to the tumor site is beneficial in the pharmacotherapy of hepatocellular carcinoma (HCC).
- Closing excerpt
- In conclusion, this study demonstrated site-specific delivery and enhanced in vivo anti-HCC efficacy of gemcitabine by G4, which could function as promising carrier in hepatoma.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (192 words)
Selective targeting of anticancer drugs to the tumor site is beneficial in the pharmacotherapy of hepatocellular carcinoma (HCC). This study evaluated the prospective of galactosylated chitosan nanoparticles as a liver-specific carrier to improve the therapeutic efficacy of gemcitabine in HCC by targeting asialoglycoprotein receptors expressed on hepatocytes. Nanoparticles were formulated (G1-G5) by an ionic gelation method and evaluated for various physicochemical characteristics. Targeting efficacy of formulation G4 was evaluated in rats. Physicochemical characteristics exhibited by nanoparticles were optimal for administering and targeting gemcitabine effectively to the liver. The biphasic release behavior observed with G4 can provide higher drug concentration and extend the pharmacotherapy in the liver target site. Rapid plasma clearance of gemcitabine (70% in 30 min) from G4 was noticed in rats with HCC as compared to pure drug (p p < 0.0001) demonstrated excellent liver targeting by G4, while mitigating systemic toxicity. Morphological, biochemical, and histopathological examination as well as blood levels of the tumor marker, alpha-fetoprotein, in rats confirmed the curative effect of G4. In conclusion, this study demonstrated site-specific delivery and enhanced in vivo anti-HCC efficacy of gemcitabine by G4, which could function as promising carrier in hepatoma.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31847085 · DOI · PMC6943439
Oval cell response is attenuated by depletion of liver resident macrophages in the 2-AAF/partial hepatectomy rat [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Background/aimsMacrophages are known to play an important role in hepatocyte mediated liver regeneration by secreting inflammatory mediators.
- Closing excerpt
- ConclusionsThese data indicate that macrophages play an important role in oval cell mediated liver regeneration in the 2-AAF/PH model.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (254 words)
Background/aimsMacrophages are known to play an important role in hepatocyte mediated liver regeneration by secreting inflammatory mediators. However, there is little information available on the role of resident macrophages in oval cell mediated liver regeneration. In the present study we aimed to investigate the role of macrophages in oval cell expansion induced by 2-acetylaminofluorene/partial hepatectomy (2-AAF/PH) in rats.Methodology/principal findingsWe depleted macrophages in the liver of 2-AAF/PH treated rats by injecting liposome encapsulated clodronate 48 hours before PH. Regeneration of remnant liver mass, as well as proliferation and differentiation of oval cells were measured. We found that macrophage-depleted rats suffered higher mortality and liver transaminase levels. We also showed that depletion of macrophages yielded a significant decrease of EPCAM and PCK positive oval cells in immunohistochemical stained liver sections 9 days after PH. Meanwhile, oval cell differentiation was also attenuated as a result of macrophage depletion, as large foci of small basophilic hepatocytes were observed by day 9 following hepatectomy in control rats whereas they were almost absent in macrophage depleted rats. Accordingly, real-time polymerase chain reaction analysis showed lower expression of albumin mRNA in macrophage depleted livers. Then we assessed whether macrophage depletion may affect hepatic production of stimulating cytokines for liver regeneration. We showed that macrophage-depletion significantly inhibited hepatic expression of tumor necrosis factor-α and interleukin-6, along with a lack of signal transducer and activator of transcription 3 phosphorylation during the early period following hepatectomy.ConclusionsThese data indicate that macrophages play an important role in oval cell mediated liver regeneration in the 2-AAF/PH model.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 22514719 · DOI · PMC3325996
Carcinogenic adducts induce distinct DNA polymerase binding orientations [3]
Abstract reading summary — source excerpts
- Opening excerpt
- DNA polymerases must accurately replicate DNA to maintain genome integrity.
- Closing excerpt
- Finally, we have directly observed an adduct- and mismatch-induced intermediate state, which may be an obligatory step in the DNA polymerase proofreading mechanism.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (139 words)
DNA polymerases must accurately replicate DNA to maintain genome integrity. Carcinogenic adducts, such as 2-aminofluorene (AF) and N-acetyl-2-aminofluorene (AAF), covalently bind DNA bases and promote mutagenesis near the adduct site. The mechanism by which carcinogenic adducts inhibit DNA synthesis and cause mutagenesis remains unclear. Here, we measure interactions between a DNA polymerase and carcinogenic DNA adducts in real-time by single-molecule fluorescence. We find the degree to which an adduct affects polymerase binding to the DNA depends on the adduct location with respect to the primer terminus, the adduct structure and the nucleotides present in the solution. Not only do the adducts influence the polymerase dwell time on the DNA but also its binding position and orientation. Finally, we have directly observed an adduct- and mismatch-induced intermediate state, which may be an obligatory step in the DNA polymerase proofreading mechanism.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23814187 · DOI · PMC3763543
Conformation-Dependent Lesion Bypass and Mutagenicity of Bulky 2-Acetylaminofluorene-Guanine DNA Adduct in Epigenetically Relevant Sequence Contexts [4]
Abstract reading summary — source excerpts
- Opening excerpt
- DNA base cytosine can be modified epigenetically by adding a methyl group to form 5-methylcytosine (5mC).
- Closing excerpt
- Our findings provide a new perspective on the role of epigenetic markers in DNA replication and could help to develop methods to identify mutation patterns associated with specific mutational signatures or spectra in cancer.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (190 words)
DNA base cytosine can be modified epigenetically by adding a methyl group to form 5-methylcytosine (5mC). 5mC in DNA CpG islands plays a crucial role in mammalian cell development and epigenetic regulation. While 5mC does not block DNA replication and is not mutagenic, the biological consequences of 5mC affecting the flanking guanine with a bulky modification during DNA replication are not well understood. This paper examined the lesion bypass and mutagenicity of the 2-acetylaminofluorene-modified guanine DNA adduct (dG-AAF) in epigenetically relevant sequence contexts in Escherichia coli. The C/5mC context exhibited significantly different bypass and mutagenicity profiles for dG-AAF. The biological outcomes also varied depending on the nature of the 3' flanking base and the lesion bulkiness. In addition, we extensively observed a unique type of -1 G deletion when the lesion was flanked by 3' purines, possibly due to the formation of a stacked slipped mutagenic intermediate. However, there was no such deletion with 3' pyrimidines. Our findings provide a new perspective on the role of epigenetic markers in DNA replication and could help to develop methods to identify mutation patterns associated with specific mutational signatures or spectra in cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40613893 · DOI · PMC12422539
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Genetic toxicity of 2-acetylaminofluorene, 2-aminofluorene and some of their metabolites and model metabolites [5]
- Research article 2-Acetylaminofluorene mechanistic data and risk assessment: DNA reactivity, enhanced cell proliferation and tumor initiation [6]
- Research article DNA adduct measurements and tumor incidence during chronic carcinogen exposure in rodents [7]
- Research article Relationship of DNA adducts derived from 2-acetylaminofluorene to cell proliferation and the induction of rodent liver and bladder tumors [8]
- Research article Sulfuric acid esters as ultimate electrophilic and carcinogenic metabolites of some alkenylbenzenes and aromatic amines in mouse liver [9]
- Research article Carcinogen-modified DNA and specific humoral immunity toward carcinogen-DNA adducts. A review [10]
References
- Nair AB, Shah J, Al-Dhubiab BE, Patel SS, Morsy MA, Patel V, et al.. Development of Asialoglycoprotein Receptor-Targeted Nanoparticles for Selective Delivery of Gemcitabine to Hepatocellular Carcinoma. . 2019. PMID 31847085 · DOI · PMC6943439
- Xiang S, Dong HH, Liang HF, He SQ, Zhang W, Li CH, et al.. Oval cell response is attenuated by depletion of liver resident macrophages in the 2-AAF/partial hepatectomy rat. . 2012. PMID 22514719 · DOI · PMC3325996
- Vrtis KB, Markiewicz RP, Romano LJ, Rueda D. Carcinogenic adducts induce distinct DNA polymerase binding orientations. . 2013. PMID 23814187 · DOI · PMC3763543
- Chen YT, Qi R, Cai A, Cho BP, Li D. Conformation-Dependent Lesion Bypass and Mutagenicity of Bulky 2-Acetylaminofluorene-Guanine DNA Adduct in Epigenetically Relevant Sequence Contexts. . 2025. PMID 40613893 · DOI · PMC12422539
- Heflich RH, Neft RE. Genetic toxicity of 2-acetylaminofluorene, 2-aminofluorene and some of their metabolites and model metabolites. Mutat Res. 1994. PMID 7521935 · DOI
- Verna L, Whysner J, Williams GM. 2-Acetylaminofluorene mechanistic data and risk assessment: DNA reactivity, enhanced cell proliferation and tumor initiation. Pharmacol Ther. 1996. PMID 8910950 · DOI
- Poirier MC, Beland FA. DNA adduct measurements and tumor incidence during chronic carcinogen exposure in rodents. Environ Health Perspect. 1994. PMID 7889840 · DOI · PMC1566867
- Cohen SM, Ellwein LB. Relationship of DNA adducts derived from 2-acetylaminofluorene to cell proliferation and the induction of rodent liver and bladder tumors. Toxicol Pathol. 1995. PMID 7569667 · DOI
- Miller EC, Miller JA, Boberg EW, Delclos KB, Lai CC, Fennell TR, et al.. Sulfuric acid esters as ultimate electrophilic and carcinogenic metabolites of some alkenylbenzenes and aromatic amines in mouse liver. Carcinog Compr Surv. 1985. PMID 3904999
- Verdina A. Carcinogen-modified DNA and specific humoral immunity toward carcinogen-DNA adducts. A review. Ann Ist Super Sanita. 2006. PMID 17033140
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.