Absence of &amp;beta;&lt;i&gt;-catenin&lt;/i&gt; Mutations in Mouse Hepatoblastomas Induced by &lt;i&gt;N&lt;/i&gt;, &lt;i&gt;N&lt;/i&gt;-dimethylformamide

Kakuni, Masakazu; Senoh, Hideki; Morimura, Keiichirou; Wanibuchi, Hideki; Takaba, Katsumi; Nagano, Kasuke; Fukushima, Shoji

doi:10.1293/tox.17.261

Cited by 2 publications

(4 citation statements)

References 37 publications

(30 reference statements)

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“…There are many reports of high percentages of HBs with gene mutation and abnormal localization of β-catenin in mice (de La Coste et al, 1998; Devereux et al, 1999; Anna et al, 2000, 2003; Hayashi et al, 2003), in contrast to our previous (Kakuni et al, 2004) and present studies. The root causes are unclear, but it is likely that specificity regarding inducing compounds and strains of mice is involved.…”

Section: Discussioncontrasting

confidence: 94%

“…Chemically induced hepatocellular adenomas (HCAs) and HCCs in 2 studies had mutations in exon 2 of β-catenin (Hayashi et al, 2003;Huang et al, 2003), but were lacking in another investigation (Aydinlik et al, 2001). Concerning HBs, there have been many reports of high percentages of gene mutations and abnormal localization of β-catenin (de La Coste et al, 1998;Devereux et al, 1999;Anna et al, 2000Anna et al, , 2003Hayashi et al, 2003), but we earlier found no change in N,N-Dimethylformamide-induced HBs in mice (Kakuni et al, 2004).…”

Section: Introductionmentioning

confidence: 82%

“…While high percentages of carcinogen-induced HBs have been found with gene mutations and abnormal localization of β-catenin, in the majority of cases B6C3F1 mice were used (de La Coste et al, 1998;Devereux et al, 1999;Anna et al, 2000Anna et al, , 2003Hayashi et al, 2003). We employed Crj:BDF1 mice in our previous (Kakuni et al, 2004) and present study and there may be clear strain differences in gene mutations induced by carcinogens. Buchmann et al (1991) demonstrated a 56% incidence rate for mutations of the H-ras gene in liver tumors induced by N-nitrosodiethylamine, but none in equivalent lesions due to this carcinogen in C57BL/6 mice.…”

Section: Discussionmentioning

confidence: 99%

“…We employed Crj:BDF1 mice in our previous (Kakuni et al, 2004) and present study and there may be clear strain differences in gene mutations induced by carcinogens. Buchmann et al (1991) demonstrated a 56% incidence rate for mutations of the H-ras gene in liver tumors induced by N-nitrosodiethylamine, but none in equivalent lesions due to this carcinogen in C57BL/6 mice.…”

Section: Pcr-sscpmentioning

confidence: 99%

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Absence of β-Catenin Alteration in Hepatic Tumors Induced by p-Nitroanisole in Crj:BDF1 Mice

Kushida

Aiso²,

Morimura

et al. 2006

Toxicol Pathol

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In the present study, β-catenin localization in hepatocellular neoplasms and hepatoblastomas, induced by oral administration of p-Nitroanisole (pNA) in Crj:BDF1 for 2 years, was evaluated by immunohistochemistry along with genetic alterations in exon 2 of β-catenin by the polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) approach. Genomic DNA was isolated from paraffin sections of a total of 53 liver tumors. Immunohistochemical analysis revealed no abnormal accumulation of the β-catenin protein in any of the cases. No mutations (0/13), 20% silent mutations (3/15) and 8% silent plus 12% functional mutations (2 + 3/25), not in the multiple phosphorylation sites of β-catenin, were observed in hepatocellular adenomas, carcinomas and hepatoblastomas, respectively. The results indicate that β-catenin does not play an important role in development of hepatic tumors induced by pNA in Crj:BDF1 mice.

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Section: Discussioncontrasting

confidence: 94%

Section: Introductionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Pcr-sscpmentioning

confidence: 99%

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Absence of β-Catenin Alteration in Hepatic Tumors Induced by p-Nitroanisole in Crj:BDF1 Mice

Kushida

Aiso²,

Morimura

et al. 2006

Toxicol Pathol

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Toxicology of dimethyl and monomethyl derivatives of acetamide and formamide: a second update

Kennedy

2012

Critical Reviews in Toxicology

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Dimethylacetamide (DMAC) and dimethylformamide (DMF) continue to be important, widely used solvents involved in a wide variety of industrial applications. As liquids with relatively low vapor pressures, contact with both the integumentary and respiratory systems is the main source of human exposure. Although airborne control levels for the workplace have been established and industrial hygiene practices to limit dermal contact have been put in place, use of these chemicals has been associated with occupational illness, mainly in Asia where new and expanded uses have led to overexposures. Thus an update of the basic toxicology data including tables indicating the dose/exposure response characteristics of both DMAC and DMF is currently important. Both chemicals are similar from a toxicology perspective. Human experience has generally shown the materials to be without adverse effect except under conditions where airborne and dermal controls were not properly applied. The use of urinary metabolite monitoring has successfully been employed to measure integrated dermal and inhalation worker exposure. The chemicals are not particularly toxic following acute exposure but high doses can produce damage to the liver, the organ which is first affected by these two chemicals. Repeated dose/exposure studies have characterized both the targets of toxicity and the doses required to produce changes by various routes of exposure. Higher doses of these materials can produce changes in developing systems, infrequently in experiments at doses in which the maternal animal is unaffected, thus care needs to be taken when exposures are to women of child-bearing age. The chemicals appear to be low in genetic activity and inhalation exposures have not shown the materials to produce tumors in rodents except with DMF in a situation in which aerosol formation was encountered. This presentation extends the two previous reviews and, like those, includes updated information on acetamide and formamide and their monomethyl derivatives as well as the commercially important DMAC and DMF. Since a large portion of the newer information deals with effects in humans and biomonitoring, these sections are presented at the start of this review.

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Absence of β<i>-catenin</i> Mutations in Mouse Hepatoblastomas Induced by <i>N</i>, <i>N</i>-dimethylformamide

Cited by 2 publications

References 37 publications

Absence of β-Catenin Alteration in Hepatic Tumors Induced by p-Nitroanisole in Crj:BDF1 Mice

Absence of β-Catenin Alteration in Hepatic Tumors Induced by p-Nitroanisole in Crj:BDF1 Mice

Toxicology of dimethyl and monomethyl derivatives of acetamide and formamide: a second update

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