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PubMed2003

Differential gene expression profiles in colon epithelium of two rat strains with distinct susceptibility to colon carcinogenesis after exposure to PhIP in combination with dietary high fat.

Colon cancers develop through accumulation of multiple genetic and epigenetic alterations in colon epithelial cells, and the environment of the genetically altered epithelial cells may also have a substantial impact on their further development to cancer. In the present study, groups of 6-week-old F344 and ACI male rats, the former strain being susceptible to colon carcinogenesis induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and the latter being relatively resistant, were subjected to a long-term carcinogenesis experiment using our intermittent feeding protocol of PhIP in combination with a high-fat diet, which serves as a relevant risk factor that promotes the development of colon cancers. Animals were sacrificed at 60 weeks, and global gene expression analyses of normal parts of colon epithelial tissues were conducted using a high-density oligonucleotide microarray to elucidate the differential gene expression profile (environment) in normal colonic regions between F344 and ACI strains. Of 8799 entries on the RatU34A array, 74 genes exhibited 3-fold or greater variation. A subset of genes encoding ribosomal RNAs and proteins were highly preferentially expressed in the F344 strain. In addition, genes encoding fatty acid binding proteins and the peroxisome membrane protein 70 appeared up-regulated in the susceptible F344 strain. In the ACI strain, a mismatch repair gene, Msh2, was preferentially expressed, at approximately 20-fold the F344 level, along with a gene encoding a detoxification enzyme, catechol-O-methyltransferase. The combined effects of the repertoire of these differentially expressed genes in normal colon epithelial tissues may account for the distinct susceptibilities of F344 and ACI strains to colon carcinogenesis.

Animals↗
PubMed1993

The eae gene of Citrobacter freundii biotype 4280 is necessary for colonization in transmissible murine colonic hyperplasia.

Transmissible murine colonic hyperplasia is characterized by proliferation of anchored stem cells in the mucosa of the descending colon of laboratory mice and is caused by Citrobacter freundii biotype 4280. This bacterium produces attaching and effacing lesions in the descending colon prior to the onset of gross hyperplasia. By mutational analysis, the chromosomal eae gene of C. freundii biotype 4280 was shown to be necessary for colonic colonization. Conversely, bacteria cured of a 65-kb plasmid, which was identified in C. freundii biotype 4280, were not attenuated for colonic colonization or for the induction of colonic hyperplasia.

Adhesins, Bacterial↗
PubMed1993

Ileal and colonic epithelial metabolism in quiescent ulcerative colitis: increased glutamine metabolism in distal colon but no defect in butyrate metabolism.

Previous studies have shown that butyrate is an important energy source for the distal colon, and that its metabolism may be defective in ulcerative colitis (UC). A similar metabolic defect in the ileum might account for the occurrence of 'pouchitis' in UC patients after colectomy. A method has been developed that allows the measurement of metabolism in ileocolonoscopic biopsy specimens, and this has been used to assess butyrate and glutamine metabolism in quiescent UC and controls. Preliminary experiments showed optimal metabolism of butyrate at 1 mmol/l. In controls glutamine metabolism was greater in the ascending (mean (SD)) (4.9 (3.2) nmol/h/micrograms protein) than in the descending colon (1.4 0.7)) (p < 0.05, Mann-Whitney U test), but butyrate metabolism was similar in the two regions (ascending 62.6 (44.2), descending 51.5 (32.0)). Consequently ratios of butyrate/glutamine metabolism were higher in the descending colon (20.6 (14.3)) than in the ascending colon (14.3 (9.6)) (p < 0.05). In UC, rates of butyrate metabolism were similar in the ascending (92.5 (58.3) nmol/h/micrograms protein) and descending (93.3 (115)) colon, and these were not significantly different from controls. In UC, glutamine metabolism was similar in the ascending (6.2 (7.7) nmol/h/micrograms protein) and descending colon (7.8 (7.9)); the metabolism in the descending colon was significantly greater than in controls (p < 0.01). Butyrate (135 (56) nmol/h/microgram protein) and glutamine (24.1 (16.2)) metabolism in the ileum in UC, were not significantly different from control values (butyrate 111 (57), glutamine 15.5 (15.6)). These results confirm that there is regional variation of nutrient utilisation throughout the colon, but they do not support the hypothesis that UC is caused by a deficiency of butyrate metabolism.

Adolescent↗
PubMed2006

Beta-escin inhibits colonic aberrant crypt foci formation in rats and regulates the cell cycle growth by inducing p21(waf1/cip1) in colon cancer cells.

Extracts of Aesculus hippocastanum (horse chestnut) seed have been used in the treatment of chronic venous insufficiency, edema, and hemorrhoids. Most of the beneficial effects of horse chestnut are attributed to its principal component beta-escin or aescin. Recent studies suggest that beta-escin may possess anti-inflammatory, anti-hyaluronidase, and anti-histamine properties. We have evaluated the chemopreventive efficacy of dietary beta-escin on azoxymethane-induced colonic aberrant crypt foci (ACF). In addition, we analyzed the cell growth inhibitory effects and the induction of apoptosis in HT-29 human colon cancer cell line. To evaluate the inhibitory properties of beta-escin on colonic ACF, 7-week-old male F344 rats were fed experimental diets containing 0%, 0.025%, or 0.05% beta-escin. After 1 week, the rats received s.c. injections of azoxymethane (15 mg/kg body weight, once weekly for 2 weeks) or an equal volume of normal saline (vehicle). Rats were continued on respective experimental diets and sacrificed 8 weeks after the azoxymethane treatment. Colons were evaluated histopathologically for ACF. Administration of dietary 0.025% and 0.05% beta-escin significantly suppressed total colonic ACF formation up to approximately 40% (P < 0.001) and approximately 50% (P < 0.0001), respectively, when compared with control diet group. Importantly, rats fed beta-escin showed dose-dependent inhibition (approximately 49% to 65%, P < 0.0001) of foci containing four or more aberrant crypts. To understand the growth inhibitory effects, HT-29 human colon carcinoma cell lines were treated with various concentrations of beta-escin and analyzed by flow cytometry for apoptosis and cell cycle progression. Beta-escin treatment in HT-29 cells induced growth arrest at the G1-S phase, which was associated with the induction of the cyclin-dependent kinase inhibitor p21(WAF1/CIP1), and this correlated with reduced phosphorylation of retinoblastoma protein. Results also indicate that beta-escin inhibited growth of colon cancer cells with either wild-type or mutant p53. This novel feature of beta-escin, a triterpene saponin, may be a useful candidate agent for colon cancer chemoprevention and treatment.

Aesculus↗
PubMed1991

Mucin production by human colonic carcinoma cells correlates with their metastatic potential in animal models of colon cancer metastasis.

Patients with mucinous colorectal cancers characteristically present with advanced disease, however, the relationship between mucin production by colon cancer cells and their metastatic potential remains unclear. We therefore sought to define the relationship between mucin production by human colon cancer cells and metastatic ability by employing animal models of colon cancer metastasis. LS LiM 6, a colon carcinoma cell line with high liver metastasizing ability during cecal growth in nude mice produced twofold more metabolically labeled intracellular mucin and secreted four- to fivefold more mucin into the culture medium compared to poorly metastatic parental line LS174T. This was accompanied by a similar elevation in poly(A)+ RNA detected by blot hybridization with a human intestinal mucin cDNA probe, and increases in mucin core carbohydrate antigens determined immunohistochemically. Variants of LS174T selected for high (HM 7) or low (LM 12) mucin synthesizing capacity also yielded metastases after cecal growth and colonized the liver after splenic-portal injection in proportion to their ability to produce mucin. Inhibition of mucin glycosylation by the arylglycoside benzyl-alpha-N-acetyl-galactosamine greatly reduced liver colonization after splenic-portal injection of the tumor cells. These data suggest that mucin production by human colon cancer cells correlates with their metastatic potential and affects their ability to colonize the liver in experimental model systems.

Animals↗
PubMed2003

Associations of micronutrients with colon cancer risk in African Americans and whites: results from the North Carolina Colon Cancer Study.

African Americans have the highest incidence of colon cancer among United States racial/ethnic groups, but these disparities are largely unexplained. This report describes associations of micronutrients with colon cancer risk in African Americans and whites using data from a case-control study in North Carolina. Incident cases of histologically confirmed colon cancer, age 40-80 years (n = 613), and matched controls (n = 996) were interviewed in person to elicit information on potential colon cancer risk factors. A previously validated food frequency questionnaire adapted to include regional foods was used to assess diet over the year prior to diagnosis or interview date. Micronutrient exposure included food sources and dietary supplements. Multivariate logistic regression models estimated energy-adjusted and non-energy-adjusted odds ratios (ORs). African Americans reported lower mean micronutrient intakes than whites, primarily due to larger contributions from dietary supplements in whites. Controls generally reported higher micronutrient intakes than cases; however, these differences were only statistically significant for whites. In whites, high beta-carotene, vitamin C, and calcium intakes were associated with 40-60% reductions in colon cancer risk when contrasting highest to lowest quartiles in both energy-adjusted and non-energy-adjusted models, e.g., OR = 0.4 (95% confidence interval, 0.3-0.6) for the highest quartile of calcium in the energy-adjusted model. In African Americans, vitamins C and E were strongly inversely associated using both statistical approaches: high vitamin E intake was associated with a 70% reduced risk for colon cancer, and the OR comparing the highest to lowest quartiles of vitamin C was 0.5 (95% confidence interval, 0.3-0.8). Folate and lutein were not statistically significantly associated with colon cancer risk in either racial group. These results suggest that at high intakes, micronutrients commonly found in plant and other foods (in particular, beta-carotene, vitamin C, and calcium in whites and vitamins C and E in African Americans) exhibit independent associations consistent with 30-70% reductions in colon cancer risk.

Adult↗
PubMed1992

Changes in colonic mucins of germfree rats in response to the introduction of a "normal" rat microbial flora. Rat colonic mucin.

In order to determine the influence of bacterial colonization on amount and composition of colonic mucins, germfree male AS/Ztm rats were colonized with a rat specific intestinal flora for different times (2, 7, 14, 21, 28, 35, 120 days). The amount of colonic mucins was determined by gel filtration on Sepharose CL-4B; the relative amount of acidic mucins was calculated after ion exchange chromatography. In addition, cecal weight and dry matter of feces were monitored. While germfree and SPF rats revealed similar amounts of colonic mucins (7.0 vs. 7.2 mg mucin/300 g body weight), the initial phase of association was characterized by considerably decreasing values. After four weeks of association, the total amount of colonic mucins had almost equalized in the two groups. The amount of acidic mucins, having decreased during the first three weeks of colonization, rendered values comparable to the SPF mucins after four months of adaptation. Cecomegaly in germfree rats disappeared within the first two days, while solidification of the intestinal content occurred within four months. Mucin losses during initial phase of association are attributed 1. to the disappearance of the cecal mucin pool, and 2. to the mucin degrading activity of some bacterial strains known to be present in the intestinal flora. Further development is conducted by a stimulation of mucin secretion, described to follow the colonization. The initially increased secretion of neutral mucins is attributed to a pronounced release of immature mucin glycoproteins, while the shift to more acidic mucins is considered to result from stimulated secretion as well as from a selective bacterial degradation of neutral mucin components.

Animals↗
PubMed1992

Human colon adenocarcinoma cell lines display infrared spectroscopic features of malignant colon tissues.

Seven human colon cell lines were studied by infrared spectroscopy including study of several spectral parameters under high pressure (pressure tuning spectroscopy). The results were compared to those obtained from the study of normal and malignant colon tissues (B. Rigas et al., Proc. Natl. Acad. Sci. USA, 87: 8140-8144, 1990; P. T. T. Wong and B. Rigas., Appl. Spectrosc., 44: 1715, 1990). The seven adenocarcinoma cell lines displayed almost all of the important spectroscopic features of colon cancer tissues: (a) increased hydrogen-bonding of the phosphodiester groups of nucleic acids; (b) decreased hydrogen-bonding of the C--OH groups of carbohydrates and proteins; (c) a prominent band at 972 cm-1; and (d) a shift of the band normally appearing at 1082 cm-1 to 1086 cm-1. These cell lines differed spectroscopically from the colon cancer tissues in that: (a) they displayed a band at 991 cm-1, which is weak in colon tissues; and (b) the packing and degree of disorder of membrane lipids were close to those observed in normal colonic tissues. These findings (i) establish IR spectroscopy, used in combination with pressure tuning, as a useful method to address problems of tumor biology in cell culture systems, (ii) indicate that these cell lines offer a useful experimental model to explore the origin of the spectroscopic changes that we observed in colon cancer tissues, and (iii) support the idea that the malignant colonocyte is the likely source of all or most spectroscopic abnormalities of human colon cancer.

Adenocarcinoma↗
PubMed1989

[Validity of ano-rectal manometry in the diagnosis of cathartic colon as a cause of chronic pseudo-obstruction of the colon. Considerations on a case].

Cathartic colon is a rare pathology which hits old people and is radiologically characterized by dolichocolon and megarectum. It is nearly sure that the unusual length of the whole colon might be the first source of the cathartic disease. Rectal ampulla dilatation (megarectum) is due to the extended use of laxatives which induce changes in smooth muscle and in the myenteric nervous plexus. The anatomo-pathological changes of the rectum have been proved so far by histological examination of local and deep biopsy; now, in our opinion, they can be shown by manometry. The authors emphasize the possibility that cathartic colon might give episodes of diarrhoea and also recurrent bowel obstructions limited to the colon and so-called "chronic pseudo-obstruction" of the colon. They describe a case of this rare pathology admitted and treated in their ward. Gastric and esophageal motility in the patient was normal as was the motility of the upper rectum. Therefore they think that changes resulted from extended use of cathartics. In both cases patients show low manometric pressure, disordered peristalsis and in particular lack of internal anal sphincter relaxation in response to high balloon distension. As the occlusive status developed in an old patient (the patient was 81 years old), the authors think that the functional disorders were absent at birth. Cathartic colon is, in the authors experience, a cause of chronic pseudo-obstruction of the colon. Rectal manometry makes it possible to avoid surgical treatment. The therapy of pseudo-occlusion, if correctly diagnosed, consists in endoscopic intubation and decompression of the colon.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1988

Effect of activity-stress on experimental rat colon carcinogenesis: early histopathologic changes and colon tumor induction.

The effect of stress on experimental colon carcinogenesis was investigated in the rat by adapting the activity-stress ulcerogenesis model to the 1,2-dimethylhydrazine (DMH) rat colon carcinogenesis model. Activity-stress was applied intermittently (normal housing conditions alternated with activity-stress conditions on an equal time basis) to DMH-injected rats either throughout the experiment (AS-DMH) or following completion of DMH injections (DMH-AS). The AS-DMH treatment was associated with reduced colonic tumor induction compared with controls, as was to a lesser degree with DMH-AS condition. In a separate study, the early histopathologic effects on the colon of a single DMH injection, an activity-stress treatment, or the combination of both DMH and activity-stress treatments were compared with those of controls. Activity-stress moderated DMH-induced increases in colonic epithelial cell proliferation and nuclear hyperchromia when compared with DMH treatment alone. The findings of activity-stress-associated protection on colon tumor induction and the concordance of these results with quantitative early histopathologic alterations demonstrate that in the rat activity-stress exerts a protective influence in colon carcinogenesis. In addition, these results suggest further that risk modifiers of colon cancer can be assessed in short-term studies that quantify early histopathologic alterations.

Animals↗
PubMed1986

Colonic transit scintigraphy. A physiologic approach to the quantitative measurement of colonic transit in humans.

Colonic transit scintigraphy was developed to quantitatively evaluate colonic transit. Using this technique the progression of a radiolabeled marker from cecal instillation to defecation was studied in 7 normal male volunteers. An 8-ml bolus containing 50 mu Ci of indium 111-diethylene triamine pentaacetic acid was instilled into the cecum via a 2-mm tube, which was passed orally, and serial scintigrams were obtained over 48 h. By 48 h, 70.7% +/- 9.1% (mean +/- SEM) of the instilled activity had been defecated. The cecum and ascending colon emptied rapidly, with a half-emptying time of 87.6 +/- 27.0 min. Geometric center analysis showed an initial logarithmic progression of activity in the proximal colon and a linear progression distally. This study suggests that the transverse colon, not the cecum and ascending colon, may be the primary site for fecal storage. Colonic transit scintigraphy is a safe, physiologic, and quantitative method for evaluating the colonic transit of fecal material and may provide a useful tool for evaluating normal and abnormal large intestinal physiology.

Adult↗
PubMed1981

Colon epithelium. I. Light microscopic, histochemical, and ultrastructural features of normal colon epithelium of male Fischer 344 rats.

Although the colon of the inbred F344 rat is not distinctly demarcated into ascending, transverse, and descending segments as in the human colon, it can roughly be divided into ascending and descending portions that show distinct light microscopic, histochemical, and ultrastructural features. The ascending colon is characterized by a "herringbone" pattern of mucosal folds and test-tube-shaped uniform crypts that contain mucous cells (MC) with abundant mucin (acidic mucopolysaccharide--mostly sialomucin) in the lower one-third of the crypt, whereas the upper one-third contains two putative cell populations: 1) MC containing large globules of neutral mucopolysaccharide or sulfomucin and 2) columnar cells (CC), the full capabilities of which are unknown. The descending colon has longitudinal folds and contains sparse MC with small mucous granules at the lower one-third of the crypt, whereas the upper one-third contains numerous goblet cells. Neutral mucopolysaccharide is sparse and the acidic mucin is exclusively sulfated. Histochemically, the descending segment of the rat colon resembles the human descending colon in that the predominant type of mucus is sulfomucin. Ultrastructurally, the cell types observed in both the ascending colon and the descending colon are: a) MC, b) CC, c) endocrine cells, and d) undifferentiated cells.

Animals↗
PubMed1978

Synchronous cancer of the colon: a case for more definitive resection in colon cancer.

Carcinoma of the colon is reported to be the most common visceral cancer today in the United States, second only to cancer of the lung as a cause of cancer-related mortality. Three consecutive cases of multiple primary colon cancers-synchronous carcinoma, two of which were additionally associated with colonic polyps, prompted a review of the literature as it related to synchronous colon cancer. The incidence of this phenomenon seems to be in the range of three percent of colon cancers. These patients tend to have a higher than usual incidence of associated polyps and of metachronous colon cancer. Inasmuch as the colons of these patients have a clear proclivity to neoplastic transformation and recurrence, subtotal colectomy as the initial curative colon procedure is practiced. This diagnosis is more often made in retrospect. It would seem that subtotal colectomy should be the initial curative procedure for any cancer of the large bowel proximal to the rectum in otherwise healthy patients less than 60 years of age.

Aged↗
PubMed1995

Systemic and colonic venous hemostatic alterations in horses during low-flow ischemia and reperfusion of the large colon.

Twenty-four horses were randomly allocated to 3 groups. All horses underwent a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls, group-2 horses underwent 6 hours of colonic ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline blood samples were collected, then low-flow colonic ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. All horses were monitored for 6 hours. Citrated systemic venous (SV) blood samples were collected from the main pulmonary artery, and colonic venous (CV) samples were collected from the colonic vein draining the ventral colon. Samples were collected at 0, and 2, 3, 3.25, 4, and 6 hours for determination of one-stage prothrombin time, activated partial thromboplastin time, antithrombin III activity, and fibrinogen concentration. Data were analyzed statistically, using two-way ANOVA for repeated measures, and post-hoc comparisons were made by use of Student Newman Keul's test. Statistical significance was set at P < 0.05. There were significant decreases in all hemostatic variables by 2 hours in SV and CV samples from horses of all 3 groups, but there were no differences among the 3 groups for any of these variables. These hemostatic alterations could have been secondary to a hypercoagulable state or to fluid therapy-induced hemodilution. Colonic ischemia-reperfusion was not the cause of these alterations because these alterations also were observed in the sham-operated control horses. Significant temporal alterations existed even after accounting for the hemodilution.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1993

Failure of tripeptide colon mitosis inhibitor to suppress the cell proliferation of dimethylhydrazine-induced colonic cancers in rats.

The effects of tripeptide colon mitosis inhibitor (CMI, pGlu-His-Gly-OH) on the proliferation of tumoral cells of dimethylhydrazine (DMH)-induced colonic cancers in rats were studied. Additionally, the effects of CMI on hyperplastic colonic crypts in DMH-treated rats and on normal colonic crypts in carcinogen-untreated rats were estimated. As an index of the cell proliferation the incorporation of bromodeoxyuridine (BrDU) into cell nuclei was used. It was found that the tripeptide significantly suppressed the proliferation of the colonic crypts in normal, carcinogen-untreated rats. However, it failed to suppress the cell proliferation of DMH-induced colonic adenocarcinomas or adenomas and produced only a slight, statistically insignificant decrease of the BrDU labelling index in hyperplastic colonic mucosa of DMH-treated rats. These findings suggest that the process of carcinogenesis might 'switch off' the local negative control of the colonic cell proliferation exerted by endogenous CMI.

Adenocarcinoma↗
PubMed1997

Dietary fat and colon cancer: modulation of cyclooxygenase-2 by types and amount of dietary fat during the postinitiation stage of colon carcinogenesis.

Several epidemiological and experimental studies have indicated a strong relationship between different types of dietary fats and risk of colon cancer. However, the modulating effects of these nutritional factors at the molecular level are not fully elucidated. It has been documented that the modulation of tumorigenesis is associated with changes in the levels of prostaglandins production. To provide an understanding of the mechanism(s) of dietary fat-induced modulation of colon tumor development, we have analyzed the expression of cyclooxygenase (COX), an enzyme that catalyzes the metabolism of omega-3 and omega-6 polyunsaturated fatty acids in a critical step in prostaglandin biosynthesis. Male F344 rats were fed the semipurified AIN-76A diet containing low-fat corn oil and were s.c. injected azoxymethane (AOM) dissolved in normal saline at a dose rate of 15 mg/kg of body weight, once weekly, for 2 weeks. Vehicle controls received s.c. equal volumes of normal saline. One day after the second AOM or saline injection, rats intended to receive experimental diets were provided high-fat corn oil (HFCO) or high-fat fish oil (HFFO) mixed in semipurified AIN-76A diet, and the remaining rats continued to receive the low-fat corn oil diet. Animals were sacrificed 1, 12, or 36 weeks after the last AOM or saline injection, and their colonic mucosa, as well as the grossly visible colon tumors from rats sacrificed 36 weeks after the last AOM injection, were analyzed for the expression levels of COX-1 and COX-2. The results indicate that AOM induced increasingly high levels of COX-2 expression with advancing stages of colon tumorigenesis. HFCO further enhanced the AOM-induced COX-2 expression. In contrast, HFFO ingestion resulted in a significant decrease in COX-2 expression both in the colonic mucosa and in tumors. These results correlate with increased incidence and multiplicity of grossly visible colon tumors in AOM-treated animals that were fed the HFCO diet versus decreased tumor incidence and lower tumor multiplicity in animals that were fed the HFFO diet. No significant differences were observed in expression levels of COX-1. The data suggest that HFCO may promote colon tumorigenesis by up-regulating the COX-2 expression, whereas HFFO may exert its antitumor effect by inhibiting the COX-2 expression.

Animals↗
PubMed2000

The sss colonization gene of the tomato-Fusarium oxysporum f. sp. radicis-lycopersici biocontrol strain Pseudomonas fluorescens WCS365 can improve root colonization of other wild-type pseudomonas spp.bacteria.

We show that the disease tomato foot and root rot caused by the pathogenic fungus Fusarium oxysporum f. sp. radicis-lycopersici can be controlled by inoculation of seeds with cells of the efficient root colonizer Pseudomonas fluorescens WCS365, indicating that strain WCS365 is a biocontrol strain. The mechanism for disease suppression most likely is induced systemic resistance. P. fluorescens strain WCS365 and P. chlororaphis strain PCL1391, which acts through the production of the antibiotic phenazine-1-carboxamide, were differentially labeled using genes encoding autofluorescent proteins. Inoculation of seeds with a 1:1 mixture of these strains showed that, at the upper part of the root, the two cell types were present as microcolonies of either one or both cell types. Microcolonies at the lower root part were predominantly of one cell type. Mixed inoculation tended to improve biocontrol in comparison with single inoculations. In contrast to what was observed previously for strain PCL1391, mutations in various colonization genes, including sss, did not consistently decrease the biocontrol ability of strain WCS365. Multiple copies of the sss colonization gene in WCS365 improved neither colonization nor biocontrol by this strain. However, introduction of the sss-containing DNA fragment into the poor colonizer P. fluorescens WCS307 and into the good colonizer P. fluorescens F113 increased the competitive tomato root tip colonization ability of the latter strains 16- to 40-fold and 8- to 16-fold, respectively. These results show that improvement of the colonization ability of wild-type Pseudomonas strains by genetic engineering is a realistic goal.

Endoribonucleases↗
PubMed2005

Colonic Paneth cell metaplasia is pre-neoplastic condition of colonic cancer or not?

ABSTRACTS: BACKGROUND: The carcinogenesis of colorectal cancer has been accepted by a model for a cascade of genetic alterations, named the adenoma-carcinoma sequence. In order to elucidate the carcinogenesis of the colorectal cancer more clearly, the genetic abnormalies of the non-neoplastic mucosal epithelium of the colon and rectum should be investigated. It has been speculated that colonic Paneth cell metaplasia (PaM) is one of the pre-neoplastic mucosa of colonic cancer. Therefore, we studied the propria mucosa of the right colon with PaM from the standpoints of the frequency of the K-ras codon 12 mutations (K-ras), which is initial genetic abnormality in colorectal cancer, and the loss of heterozygosity of microsatellite markers (LOH-MS), which has a relationship to development of colorectal cancer. METHODS: Fifty-two regions with PaM histopathologically from 12 surgically resected right colon specimens were studied. DNA extraction of the colonic mucosa with PaM was obtained using a microdissection method, and the frequency of the K-ras of PaM was investigated by enriched polymerase chain reaction-enzyme linked mini-sequence assay, and the frequency of the LOH-MS (D2S123, D17S250 and D5S346) of PaM was examined by high resolution fluorescenced labeled PCR primers. RESULTS: K-ras mutation was detected in fifteen regions among 52 PaM (28.9%). All mutations were a single mutation and GGT changed to AGT in eleven and GAT in four. LOH-MS were detected in twenty-one regions among 52 PaM (40.4%) (D2S123: 35.4%, 17/48 regions, D17S250: 13.7%, 7/51 regions, and D5S346: 0%, 0/52 regions). No K-ras mutations and LOH-MS were detected in the controls (Colorectal mucosa with no PaM). CONCLUSIONS: Colonic mucosa with Paneth cell metaplasia may be one of the pre-neoplastic mucosa in the development of the colonic epithelial neoplasia.

Journal Article↗