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PubMed1993

Modulation of oxidative DNA damage levels by dietary fat and calories.

Decreased dietary intake of fat and/or calories generally results in a lower incidence of mammary gland tumors in rodents. Feeding of either low-fat or calorie-restricted diets to rats also has been shown to result in decreased levels of oxidative DNA damage. Since oxidative DNA damage is suggested to have a role in carcinogenesis, this may be one mechanism by which dietary change can reduce cancer risk. The effects of calorie-restricted diets on both oxidative DNA damage levels and mammary gland tumor incidence are generally more pronounced than that of low-fat diets. There is, however, some difficulty in defining what amount of fat should be used to prepare 'low-fat' and 'high-fat' rodent diets as well as what a suitable fat intake for control diets should be in studies that examine the effects of dietary fat and/or calories on tumorigenesis. In particular, the promoting effects of dietary fat may be exerted only up to a certain level of fat, above which no further effect is observed. Another difficulty in the interpretation of the results is that there may be a time-dependent effect of high fat diets on oxidative damage, with increased damage resulting only when the diets are fed for longer periods of time. The appropriate experimental approach to model human dietary exposures therefore remains to be determined. Although the effects of caloric intake on mammary gland tumorigenesis appear to be more pronounced than that of fat intake, low-fat diets still may be useful as a preventive measure in human populations to reduce breast cancer risk for individuals who cannot safely reduce their caloric intake.

Animals↗

PubMed2005

Effects of nonylphenol on hepatic testosterone metabolism and the expression of acute phase proteins in winter flounder (Pleuronectes americanus): comparison to the effects of Saint John's Wort.

4-Nonylphenol (4-NP), a major by-product of alkylphenol ethoxylates, is used in several industries and as a consequence is quite common in rivers, estuaries and other aquatic environments that receive sewage discharges or are near offshore oil platforms. 4-NP is an environmental estrogen that also binds human and rodent Pregnane X-receptor (PXR), the orphan nuclear receptor that controls the expression of several detoxication genes in mammals, including several CYP3A and CYP2B family members. These P450s preferentially hydroxylate testosterone in the 6beta- and 16beta-positions, respectively. In this study, the effects of 4-NP on testosterone metabolism and hepatic CYP3A induction were compared to the effects of St. John's Wort (SJW), a well established mammalian PXR agonist, in winter flounder. Male winter flounder (Pleuronectes americanus) were injected with 100 mg/kg/day 4-NP or 500 mg/kg/day SJW or both (S and N) every 24 h. Forty-eight hours after the initial injections, flounder were euthanized. Western blots and testosterone 6beta-hydroxylation indicated that CYP3A was increased 50% by 4-NP, but was not affected by SJW. Testosterone 16beta-hydroxylase activity was also significantly increased in flounder treated with 4-NP (2.8 x), but not with SJW. This is not consistent with our hypothesis that both SJW and 4-NP would induce CYP3A. Subtractive hybridization was performed between control and 4-NP treated hepatic mRNA samples to isolate differentially expressed genes. Subtractive hybridization indicated that several acute phase proteins were altered by 4-NP. Quantitative real-time PCR (Q-PCR) confirmed 4-NP altered the expression of complement components C8b, cathepsin L, C-type lectin domain, FK506 binding protein 2 precursor (FKBP2) and an EST (expressed sequence tag). SJW and 4-NP treated flounder demonstrated similar induction profiles for the EST, cathepsin L and FKBP2, suggesting that SJW was at a sufficient dose to alter gene expression but not induce P450s. In conclusion, testosterone hydroxylase activity and Western blots indicate that SJW did not activate detoxication pathways in a similar manner to 4-NP.

Acute-Phase Proteins↗

PubMed2004

The use of nutraceuticals in cancer therapy.

The high prevalence of nutraceutical use among human patients with cancer suggests that the use of nutraceuticals in pet animals with cancer is probably common. Dogs with a wide variety of malignant diseases have significant alterations in carbohydrate, protein, and fat metabolism. These metabolic alterations may be ameliorated by using functional foods relatively low in soluble carbohydrate, moderate amounts of protein that includes sources of arginine, and moderate amounts of fat supplemented with omega-3 long-chain polyunsaturated fatty acids. Well-controlled clinical studies in a variety of species with cancer, including rodents, people, and dogs, have documented that increased dietary and serum levels of omega-3 fatty acids are associated with a number of health benefits, including improved disease-free interval, survival time, and quality of life. Other nutraceuticals of interest in patients with cancer include antioxidant vitamins, trace minerals, glutamine, protease inhibitors, garlic, tea polyphenols, vitamin A, and shark cartilage.

Animal Diseases↗

PubMed2005

Rodents as receptor species at a tritium disposal site.

New methods are being employed on the Department of Energy's Savannah River Site to deal with the disposal of tritium, including the irrigation of a hardwood/pine forest with tritiated water from an intercepted contaminant plume to reduce concentrations of tritium outcropping into Fourmile Branch, a tributary of the Savannah River. The use of this system has proven to be an effective means of tritium disposal. To evaluate the impact of this activity on terrestrial biota, rodent species were captured on the tritium disposal site and a control site during two trapping seasons in order to assess tritium exposure resulting from the forest irrigation. Control site mice had background levels of tritium, 0.02 Bq/mL, with disposal site mice having significantly higher tritium concentrations, mean=34.86 Bq/mL. Whole body tritium concentrations of the mice captured at the disposal site were positively correlated with tritium application and negatively correlated with precipitation at the site.

Animals↗

PubMed2004

Behavioral analysis of male rat sexual motivation and performance following acute ethanol treatment.

To characterize the effects of acute ethanol treatment on sexual motivation and performance, 30 male Long-Evans rats were assigned to one of three treatment conditions: saline (n=9), 0.25 g/kg ethanol (n=10), or 1.0 g/kg ethanol (n=11). Males were injected intraperitoneally 30 min before behavioral testing. Male rats were placed in a multilevel testing chamber 5 min prior to the introduction of a receptive female rat and level changes were recorded as an index of sexual motivation. After the female rat was placed in the chamber, standard measures of sexual performance were recorded over three weekly tests. Results indicated that the highest dose of ethanol (1.0 g/kg) increased male rat level-changing behavior compared to the saline group. Although ethanol treatment failed to affect most measures of sexual performance, males administered 1.0 g/kg ethanol had fewer anogenital investigations and had longer postejaculatory intervals (PEIs) compared to control animals. The data from this experiment suggest that ethanol increases rodent sexual motivation but impairs specific parameters of sexual performance.

Animals↗

PubMed2005

Altered diaphragm muscle action potentials in Zucker diabetic fatty (ZDF) rats.

The Zucker diabetic fatty (ZDF) rat is a model of type 2 diabetes, being characterized by obesity, diabetes, and dyslipidemia. In vitro studies tested the hypothesis that diaphragm muscle from ZDF rats has abnormal resting membrane potential and action potentials, similar to type 1 diabetic rodents. Resting membrane potential was comparable for muscle from ZDF and control rats. Diaphragm from ZDF rats had augmented action potential peak height (92.1 mV versus 82.4 mV, P<0.00001), overshoot (15.6 mV versus 8.1 mV, P<0.001) and area (80.7 mV ms versus 68.6 mV ms, P<0.001) compared with that from controls. Action potential rate of depolarization and repolarization were not affected. The K(+) blocker, 3,4-diaminopyridine, augmented action potential duration and area of muscle from ZDF and controls, but without significant differences between animal groups. These findings in ZDF rats contrast with type 1 diabetic rats, suggesting that isolated hyperglycemia differs from hyperglycemia combined with other metabolic perturbations with respect to diaphragm electrophysiological derangements.

Action Potentials↗

PubMed2004

Effect of epigallocatechin gallate on renal function in cyclosporine-induced nephrotoxicity.

INTRODUCTION: Nephrotoxicity is a clinically important side effect of cyclosporine (CsA). CsA-induced nephrotoxicity results from increased production of free radical species in the kidney. Epigallocatechin gallate (EGCG) acts as an antioxidant, thus, EGCG may have a protective effect on the alteration of renal function resultant from oxygen free radicals. The purpose of the present study was to investigate the protective effect of EGCG in a rodent model. METHODS: Experiments were performed on 3 groups. The normal control group (group 1) received normal saline solution. The CsA-treated group (group 2; 15 mg/kg body weight/d for 14 days) received subcutaneous injections. The EGCG-treated group (group 3) in addition received 25 mg of EGCG/kg body weight by intraperitoneal injection. RESULTS: There were significant increases in levels of blood urea nitrogen (BUN)(42.8 +/- 8.2 mg/dL; P < .001), serum creatinine (1.18 +/- 0.60 mg/dL; P < .05), and serum malondialdehyde (3.09 +/- 0.20 nmol/mL; P < .001), and a significant decrease in CCr(0.07 +/- 0.02 mL/min; P < .001) in group 2 compared with group 1. Levels of BUN (30.2 +/- 0.7 mg/dL; P < .01)and CCr (0.12 +/- 0.08 mL/min) were lower in group 3 than in group 2. Serum creatinine (0.71 +/- 0.04 mg/dL) and serum malondialdehyde level (2.13 +/- 0.15; P < .001 nmol/mL) were lower in group 3 than in group 2. There was no significant difference in CsA levels between group 2 (6.86 +/- 1.48 mug/mL) and group 3 (6.69 +/- 0.62 mug/mL). CONCLUSIONS: EGCG treatment significantly protected renal function and free radical-mediated injury in the kidney from CsA-induced changes.

Antioxidants↗

PubMed2006

Arginase induction by sodium phenylbutyrate in mouse tissues and human cell lines.

Hyperargininemia is a urea cycle disorder caused by mutations in the gene for arginase I (AI) resulting in elevated blood arginine and ammonia levels. Sodium phenylacetate and a precursor, sodium phenylbutyrate (NaPB) have been used to lower ammonia, conjugating glutamine to produce phenylacetylglutamine which is excreted in urine. The elevated arginine levels induce the second arginase (AII) in patient kidney and kidney tissue culture. It has been shown that NaPB increases expression of some target genes and we tested its effect on arginase induction. Eight 9-week old male mice fed on chow containing 7.5 g NaPB/kg rodent chow and drank water with 10 g NaPB/L, and four control mice had a normal diet. After one week all mice were sacrificed. The arginase specific activities for control and NaPB mice, respectively, were 38.2 and 59.4 U/mg in liver, 0.33 and 0.42 U/mg in kidney, and 0.29 and 1.19 U/mg in brain. Immunoprecipitation of arginase in each tissue with AI and AII antibodies showed the activity induced by NaPB is mostly AI. AII may also be induced in kidney. AI accounts for the fourfold increased activity in brain. In some cell lines, NaPB increased arginase activity up to fivefold depending on dose (1-5 mM) and exposure time (2-5 days); control and NaPB activities, respectively, are: erythroleukemia, HEL, 0.06 and 0.31 U/mg, and K562, 0.46 and 1.74 U/mg; embryonic kidney, HEK293, 1.98 and 3.58 U/mg; breast adenocarcinoma, MDA-MB-468, 1.11 and 4.06 U/mg; and prostate adenocarcinoma, PC-3, 0.55 and 3.20 U/mg. In MDA-MB-468 and HEK most, but not all, of the induced activity is AI. These studies suggest that NaPB may induce AI when used to treat urea cycle disorders. It is relatively less useful in AI deficiency, although it could have some effect in those patients with missense mutations.

Animals↗

PubMed2003

Alien/CSN2 gene expression is regulated by thyroid hormone in rat brain.

Alien has been described as a corepressor for the thyroid hormone receptor (TR). Corepressors are coregulators that mediate gene silencing of DNA-bound transcriptional repressors. We describe here that Alien gene expression in vivo is regulated by thyroid hormone both in the rat brain and in cultured cells. In situ hybridization revealed that Alien is widely expressed in the mouse embryo and also throughout the rat brain. Hypothyroid animals exhibit lower expression of both Alien mRNAs and protein levels as compared with normal animals. Accordingly, we show that Alien gene is inducible after thyroid hormone treatment both in vivo and in cell culture. In cultured cells, the hormonal induction is mediated by either TRalpha or TRbeta, while cells lacking detectable amounts of functional TR lack hormonal induction of Alien. We have detected two Alien-specific mRNAs by Northern experiments and two Alien-specific proteins in vivo and in cell lines by Western analysis, one of the two forms representing the CSN2 subunit of the COP9 signalosome. Interestingly, both Alien mRNAs and both detected proteins are regulated by thyroid hormone in vivo and in cell lines. Furthermore, we provide evidence for the existence of at least two Alien genes in rodents. Taken together, we conclude that Alien gene expression is under control of TR and thyroid hormone. This suggests a negative feedback mechanism between TR and its own corepressor. Thus, the reduction of corepressor levels may represent a control mechanism of TR-mediated gene silencing.

Animals↗

PubMed2002

Molecular genetics and function of NAT1 and NAT2: role in aromatic amine metabolism and carcinogenesis.

Aromatic and heterocyclic amines require metabolic activation to electrophilic intermediates that initiate carcinogenesis. N-Acetyltransferase 1 (NAT1) and 2 (NAT2) are important enzymes in the biotransformation of these carcinogens and exhibit genetic polymorphism. Human NAT1 and NAT2 alleles are listed at: http://www.louisville.edu/medschool/pharmacology/NAT.html by an international gene nomenclature committee. The high frequency of the NAT1 and NAT2 acetylation polymorphisms in human populations together with ubiquitous exposure to aromatic and heterocyclic amines suggest that NAT1 and NAT2 acetylator genotypes are important modifiers of human cancer susceptibility. For cancers in which N-acetylation is a detoxification step such as aromatic amine-related urinary bladder cancer, NAT2 slow acetylator phenotype is at higher risk. Multiple studies have shown that the urinary bladder cancer risk is particularly high in the slowest NAT2 acetylator phenotype or genotype (NAT2(*)5). In contrast, for cancers in which N-acetylation is negligible and O-acetylation is an activation step such as for heterocyclic amine-related colon cancer, NAT2 rapid acetylator phenotype is at higher risk. Although studies have found associations between NAT1 genotype and various cancers, the findings are less consistent and are not well understood. Since cancer risk requires exposure to aromatic and/or heterocyclic amine carcinogens modified by NAT1 and/or NAT2 acetylator genotype, the results from human epidemiology studies are dependent upon the quality and accuracy of the exposure assessment and genotype determination. Conclusions require understanding the relationship between genotype and phenotype, as well as the role of genetic variation in carcinogen metabolism, DNA repair, and host susceptibility. Investigations have been carried out in rapid and slow acetylator rodent models in which both exposure and genetic variability are tightly controlled. Human NAT1 and NAT2 alleles have been characterized by recombinant expression to further understand the effects of nucleotide polymorphisms on function and phenotype.

Acetylation↗

PubMed2000

Growth factor-dependent induction of p21(CIP1) by the green tea polyphenol, epigallocatechin gallate.

Tea polyphenols inhibit tumorigenesis and cell proliferation in rodent models, but their effects on cell signaling and cell cycle control pathways are undefined. Here, we show that the major polyphenol in green tea, epigallocatechin gallate (EGCG), inhibits S phase entry in epidermal growth factor (EGF) - stimulated MCF10A breast epithelial cells when provided in G0 or mid G1, but not when provided after the late G1 restriction point. EGCG induced p21(CIP1/WAF1/SDI1), inhibited cyclin D1-associated pRB kinase activity, and impaired pRB phosphorylation. The ability of EGCG to induce p21 depended upon the addition of EGF, indicating that EGCG synergizes with growth factor-dependent signals to induce p21 and impair cell cycle progression.

Antineoplastic Agents↗

PubMed2002

Identification of a novel transcript of X25, the human gene involved in Friedreich ataxia.

Friedreich ataxia (FRDA) is caused by a GAA triplet expansion in the first intron of the X25 gene. The X25 gene encodes a 210-amino acid protein, frataxin (A isoform). Here, we report the identification of a new transcript of the X25 gene generated by alternative splicing by the use of a second donor splice site in the intron 4. Full-length cDNA transcript sequence revealed an insertion of 8 bp between 4 and 5a exon sequence. This event leads to a frameshift in the mRNA reading frame and introduces a new stop codon at position 589. Therefore, this X25 transcript variant may encode a 196-amino acid protein, the A1 isoform, that structurally differs from the main A isoform of 210 amino acids after residue 160. In all human tissues analyzed, reverse transcription-polymerase chain reaction experiments demonstrated that the A1 isoform was expressed at low levels compared with the predominant A isoform. No difference in A and A1 isoform expression rate was detected between FRDA patients and normal controls. We did not find an A1 like splice variant in rodents.

Alternative Splicing↗

PubMed2000

Functional independence of circadian clocks that regulate plant gene expression.

BACKGROUND: Circadian clocks regulate the gene expression, metabolism and behaviour of most eukaryotes, controlling an orderly succession of physiological processes that are synchronised with the environmental day/night cycle. Central circadian pacemakers that control animal behaviour are located in the brains of insects and rodents, but the location of such a pacemaker has not been determined in plants. Peripheral plant and animal tissues also maintain circadian rhythms when isolated in culture, indicating that these tissues contain circadian clocks. The degree of autonomy that the multiple, peripheral circadian clocks have in the intact organism is unclear. RESULTS: We used the bioluminescent luciferase reporter gene to monitor rhythmic expression from three promoters in transgenic Arabidopsis and tobacco plants. The rhythmic expression of a single gene could be set at up to three phases in different anatomical locations of a single plant, by applying light/dark treatments to restricted tissue areas. The initial phases were stably maintained after the entraining treatments ended, indicating that the circadian oscillators in intact plants are autonomous. This result held for all the vegetative plant organs and for promoters expressed in all major cell types. The rhythms of one organ were unaffected by entrainment of the rest of the plant, indicating that phase-resetting signals are also autonomous. CONCLUSIONS: Higher plants contain a spatial array of autonomous circadian clocks that regulate gene expression without a localised pacemaker. Circadian timing in plants might be less accurate but more flexible than the vertebrate circadian system.

Arabidopsis↗

PubMed2003

The endometrium as a cause of implantation failure.

One of the biggest obstacles to reproductive success is our inability to diagnose or treat effectively the non-receptive endometrium. The endometrium becomes receptive for a limited period of time under the influence of steroid hormones and paracrine signals from the developing embryo. It is likely that the receptive state is characterized by the expression of particular genes that allow the normally refractory endometrium to respond to the embryo and permit attachment. Recently, several molecules have been reported whose function is essential for uterine receptivity in rodents and primates. This article will review current models of the control of receptivity and early implantation and assess progress in defining markers for the receptive endometrium in women. Although some genes have been identified whose expression is altered in women with subfertility, none of these molecular markers have yet proven clinically useful in the assessment of functional receptivity. The use of high throughput techniques such as microarrays and proteomic methods to investigate gene expression in the endometrium provides a novel approach to defining receptivity at the molecular level. The potential impact of these tools on clinical practice will be discussed.

Animals↗

PubMed2002

Glucomannan minimizes the postprandial insulin surge: a potential adjuvant for hepatothermic therapy.

Glucomannan (GM) is differentiated from other soluble fibers by the extraordinarily high viscosity of GM solutions. Administration of 4-5g of GM with meals, blended into fluid or mixed with food, can slow carbohydrate absorption and dampen the postprandial insulin response by up to 50%. Controlled clinical studies document that GM can promote satiety and weight loss, lower LDL cholesterol, improve diabetic control, and correct constipation, with minimal if any side-effects. Rodent studies suggest that GM may have potential for decreasing cancer risk and possibly even slowing the ageing process. Hepatothermic therapy, a technique for achieving rapid loss of body fat by optimizing the liver's capacity for fat oxidation, can only achieve its optimal efficacy if diurnal insulin levels are kept low; ingestion of GM with meals will evidently be of benefit in this regard by moderating postprandial insulin surges.

Appetite↗

PubMed1996

Translation initiation of ornithine decarboxylase and nucleocytoplasmic transport of cyclin D1 mRNA are increased in cells overexpressing eukaryotic initiation factor 4E.

The structure of m7GpppN (where N is any nucleotide), termed cap, is present at the 5' end of all eukaryotic cellular mRNAs (except organellar). The eukaryotic initiation factor 4E (eIF-4E) binds to the cap and facilitates the formation of translation initiation complexes. eIF-4E is implicated in control of cell growth, as its overexpression causes malignant transformation of rodent cells and deregulates HeLa cell growth. It was suggested that overexpression of eIF-4E results in the enhanced translation of poorly translated mRNAs that encode growth-promoting proteins. Indeed, enhanced expression of several proteins, including cyclin D1 and ornithine decarboxylase (ODC), was documented in eIF-4E-overexpressing NTH 3T3 cells. However, the mechanism underlying this increase has not been elucidated. Here, we studied the mode by which eIF-4E increases the expression of cyclin D1 and ODC. We show that the increase in the amount of cyclin D1 and ODC is directly proportional to the degree of eIF-4E overexpression. Two mechanisms, which are not mutually exclusive, are responsible for the increase. In eIF-4E-overexpressing cells the rate of translation initiation of ODC mRNA was increased inasmuch as the mRNA sedimented with heavier polysomes. For cyclin D1 mRNA, translation initiation was not increased, but rather its amount in the cytoplasm increased, without a significant increase in total mRNA. Whereas, in the parental NIH 3T3 cell line, a large proportion of the cyclin D1 mRNA was confined to the nucleus, in eIF-4E-overexpressing cells the vast majority of the mRNA was present in the cytoplasm. These results indicate that eIF-4E affects directly or indirectly mRNA nucleocytoplasmic transport, in addition to its role in translation initiation.

3T3 Cells↗

PubMed1995

Role of the transcription factor C/EBP beta in expression of a rat pregnancy-specific glycoprotein gene.

Pregnancy-specific glycoproteins (PSGs), which are the major placental proteins, and the carcinoembryonic antigens comprise a subfamily within the immunoglobulin superfamily. To understand the molecular mechanisms underlying the control of PSG expression, we characterized the promoter elements of a rodent PSG gene, rnCGM3, and showed that DNA elements at nucleotides -326 to -185 (PI) relative to the translation start site of rnCGM3 function as a promoter. The rnCGM3 PI promoter contains two placental factor binding sites, PISI and PISII. Both are transcription activation elements. In the present report, we screened a placental expression cDNA library with a rnCGM3-PISII probe (nucleotides -263 to -233) encompassing two overlapping palindromes (TGTTGCTCAACATGTTG) and demonstrated that the PISII-binding factor is C/EBP beta, a leucine zipper family of transcription factor. Gel mobility-shift and transient expression analyses showed that C/EBP beta and C/EBP isoforms, C/EBP alpha and C/EBP delta, bind to the PISII element and trans-activate rnCGM3 gene expression. Deletion of PISII from the rnCGM3 PI promoter greatly reduced the basal as well as the C/EBP-activated rnCGM3 expression. Gel supershift assays demonstrated that C/EBP beta is the placental isoform that binds to the PISII site rnCGM3. Moreover, C/EBP beta is expressed in high levels in the placenta, ovary, liver, lung, heart, and spleen, in contrast to C/EBP alpha, which is expressed primarily in the liver and only low levels in the placenta. Our results demonstrate that C/EBP beta is one of the transcription factors that positively regulate rnCGM3 expression during pregnancy.

Animals↗

PubMed2001

Constitutive expression of growth-related oncogene and its receptor in oligodendrogliomas.

OBJECTIVE: Gliomas may result from transformation of glial precursor cells. In the developing rat central nervous system (CNS), a paracrine pathway involving the cytokines growth-related oncogene (GRO1) and platelet-derived growth factor (PDGF) A chain closely regulates oligodendrocyte precursor cell number. The purpose of the present study was to analyze whether abnormal expression and activity of the GRO1-PDGF pathway is present in human gliomas. METHODS: Tumor specimens were studied to compare the messenger ribonucleic acid with the protein expression of components of the GRO1-PDGF pathway. Neutralizing antibodies were used in vitro to analyze whether the pathway contributed to tumor cell proliferation. RESULTS: Immunohistochemistry demonstrated that all components of the GRO1-PDGF pathway (GRO1 protein, its receptor CXCR2, PDGF A chain, and its receptor PDGFalphaR) were expressed by tumor cells in 6 (86%) of 7 of oligodendrogliomas as well as by 0 of 4 diffuse astrocytomas (World Health Organization Grades II and III) and 2 (18%) of 11 glioblastomas. Analysis by reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay showed CXCR2 messenger ribonucleic acid and GRO1 protein expression were present in oligodendrogliomas. Functional analyses with neutralizing antibodies limited bromodeoxyuridine incorporation in vitro by oligodendroglioma tumor cells, demonstrating a requirement for the GRO1-PDGF pathway in the proliferation of these cells. CONCLUSION: The GRO1-PDGF pathway was primarily expressed and functional in oligodendrogliomas. The tightly controlled paracrine pathway that regulates oligodendrocyte precursor proliferation in the developing rodent CNS was constitutively active in most oligodendrogliomas in the present study. The presence of this aberrantly functioning oncogenic pathway in a subset of primary CNS tumors opens new avenues to glioma treatment that are based directly on the biology of the proliferative glial cell type, a novel strategy for primary CNS tumor therapy.

Brain↗