Publications by authors named "Johan G de Boer"

Background: The products of cyp19, dax, foxl2, mis, sf1 and sox9 have each been associated with sex-determining processes among vertebrates. We provide evidence for expression of these regulators very early in salmonid development and in tissues outside of the hypothalamic-pituitary-adrenal/gonadal (HPAG) axis. Although the function of these factors in sexual differentiation have been defined, their roles in early development before sexual fate decisions and in tissues beyond the brain or gonad are essentially unknown.

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Analogues of the gonadotropin releasing hormone (GnRH) inhibit the hypothalamic-pituitary-gonadal axis. This has provided treatment modalities for advanced and metastatic prostate cancer. The latest group of analogues, the GnRH antagonists, make promising treatments available that avoid the transient surge in testosterone that occurs with the use of GnRH agonists.

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Purpose: We review the effect of diet and dietary supplement interventions on prostate cancer progression, recurrence and survival.

Materials And Methods: A literature search was conducted in MEDLINE, EMBASE and CINAHL to identify diet and dietary supplement intervention studies in men with prostate cancer using prostate specific antigen or prostate specific antigen doubling time as a surrogate serum biomarker of prostate cancer recurrence and/or survival.

Results: Of the 32 studies identified 9 (28%) were randomized controlled trials and the focus of this review.

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Background: Several genome duplications have occurred in the evolutionary history of teleost fish. In returning to a stable diploid state, the polyploid genome reorganized, and large portions are lost, while the fish lines evolved to numerous species. Large scale transposon movement has been postulated to play an important role in the genome reorganization process.

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Article Synopsis
  • The study investigates the effects of the mycotoxin aflatoxin-B(1) and its mutagenicity in rat liver, finding that adding 1% of the plant Scutellaria baicalensis (Huang-qin) to their diet significantly reduces mutation frequency.
  • Two different batches of Huang-qin were tested, showing a reduction of mutant frequency by approximately 60% to 77%, alongside increased expression of protective genes.
  • The study highlights the potential of using plant-based materials for cancer prevention and suggests that variability in plant composition can influence their effectiveness.
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Prevention of esophageal cancer may be possible through dietary modification or supplementation. In this study we have investigated the mutation preventive properties of ellagic acid, green tea, and diallyl sulfide (DAS) against the mutagenicity of the nitrosamine N-nitrosomethylbenzylamine (NMBA) in the esophagus of the rat. In addition, the effect of the consumption of ethanol on the mutagenicity of NMBA was examined.

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A reduction in dietary intake has been shown to significantly increase the lifespan of rodents, lower the incidence of tumors, and reduce DNA damage. The objective of this study was to determine whether dietary restriction (DR) reduced the frequency of mutation induced by two environmentally relevant metabolically activated mutagens and one direct-acting mutagen in the lacI transgene of male and female Big BlueR rats. Both male and female rats were maintained on either an ad libitum (AL) or a 40%-reduced diet for 22 wk.

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Amongst approximately 25,000 mutants recovered from tissues of the lacI mouse and rat transgenic mutation assay, we identified seven mutants that carry changes that are unlike the majority of mutations that are normally recovered in these systems. The recovered mutants feature replacements and insertions of sequences that originate in the animal's genome, in the bacteriophage lambda construct that harbors the lacI gene, and in the genome of the E. coli plating host.

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2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a potent mutagen and carcinogen formed at high temperature during the cooking of meat. PhIP induces tumors in the colon and prostate of male rats and in the mammary gland of female rats and has been associated with the etiology of human cancers. We have recently demonstrated that PhIP induces mutations in the prostate in Big Blue transgenic rats.

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The Msh2 DNA mismatch repair gene is one of five genes implicated in the pathogenesis of hereditary nonpolyposis colorectal cancer (HNPCC). To address the possible mechanisms of the site-specific occurrence of HNPCC, the effect of Msh2 deficiency on mutations in different parts of the colon was investigated using the BC-1(lacI)/Msh2 double transgenic mouse. Compared to the Msh2(+/+) mice, Msh2(-/-) mice had an 8-9-fold increase of mutation frequency (MF) in the lacI gene from the cecum and the proximal and distal colon.

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The repair of damage to DNA is critical to the survival of a cell. However, not all organisms nor all individuals express a similar response to challenges to their genetic material. Numerous polymorphisms in genes involved in DNA repair have been found in individuals with DNA repair-related disease as well as in the general population.

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The heterocyclic amine 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a recognized mutagen and carcinogen in the colon and prostate of male rats and in the mammary gland of female rats. In the current study, we examined the mutagenicity of PhIP in the kidney of male and female lacI transgenic rats and its modulation by a dietary chemopreventive agent, conjugated linoleic acid (CLA). Sex-specific changes in mutation were observed following PhIP and CLA treatment.

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Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of linoleic acid, has been reported to inhibit chemically induced mammary and colon carcinogenesis in rodents. In a preliminary experiment, we found that CLA significantly reduced the induction of mutations by the dietary carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in the distal colon in male rats. Here, the chemopreventive properties of CLA were further evaluated by assessing its effect on PhIP-induced mutation and aberrant crypt foci (ACF) in both male and female rats.

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Mismatch repair (MMR) genes, such as Msh2, are classified as "mutator" genes, responsible for the microsatellite instability identified in many tumors. In the current study, the mutation frequency and mutational spectrum in thymic lymphoma arising in Msh2 deficient mice are investigated. Thymic lymphoma developed in Msh2-/- background displayed an eight to nine-fold increase in mutation frequency compared to the normal thymi in Msh2 deficient animals.

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