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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic inflammation of the colon and the rectum was induced by intracolonic administration of 25 mg trinitrobenzoic sulfonic acid (TNB) in 0.25 ml 30% ethanol. Three weeks after TNB administration the colon and the rectum showed transmural, granulomatous inflammation which had many similarities to Crohn's disease and furthermore to the morphological and functional changes which occur in early phases of postischemic intestinal damage. In the colon of TNB-treated animals the ATP and GTP levels were markedly decreased. The accumulation of thiobarbituric acid-reactive substances (TBA-RS) demonstrated a free radical-mediated component of the tissue damage. Treatment with oxypurinol radical scavenger and xanthine oxidoreductase inhibitor diminished the morphological changes, the loss of energy-rich nucleotides and the TBA-RS accumulation.
Cell Mol Biol 1992 Apr
PMID:Protective influence of oxypurinol on the trinitrobenzene sulfonic acid(TNB) model of inflammatory bowel disease in rats. 157 48

Thirty colorectal carcinomas, 1 adenoma of the colon, 1 case of Crohn's disease and 13 specimens of non-neoplastic colorectal mucosa were examined for qualitative and quantitative expression of the c-myc and c-fos protooncogenes. These genes encode nuclear proteins, which are both believed to regulate gene transcription. Oncogene expression was evaluated at the mRNA level by in situ hybridization and Northern blot analysis. Densitometric analysis of the specific bands on Northern blots revealed a highly significant overexpression of c-myc mRNA in colorectal carcinomas compared with non-neoplastic tissue (p less than 0.001). Furthermore, increased expression of c-myc mRNA was found in moderately and poorly differentiated carcinomas compared with well differentiated ones. In contrast to c-myc, c-fos mRNA expression was significantly lower in carcinomas than in non neoplastic tissue (p less than 0.02). Neither, c-myc nor c-fos mRNA levels showed a clear-cut correlation with tumor stage. We conclude that c-myc mRNA overexpression plays an important role in the progression of colorectal carcinomas. In contrast enhanced c-fos mRNA expression may be related to cell differentiation, both in tumors and non-neoplastic tissue.
Virchows Arch B Cell Pathol Incl Mol Pathol 1990
PMID:Expression of c-myc and c-fos mRNA in colorectal carcinoma in man. 198 Jul 63

We investigated soluble interleukin-2 receptor (sIL-2R), soluble CD8 (sCD8) and soluble intercellular adhesion molecule-1 (sICAM-1) levels in the sera of patients with non-malignant diseases believed to have an autoimmune or immunosuppressive component, Crohn's disease, celiac disease, and systemic lupus erythematosus (SLE). Sera of healthy blood donors served as controls. All samples were analyzed by commercial ELISA kits for sIL-2R, sCD8, and sICAM-1. Our control level of sIL-2R (x +/- S.D) was 395 +/- 84 units/ml, sCD8 (x +/- S.D.) 263 +/- 90 units/ml and sICAM-1 405 +/- 118 ng/ml. The 8 Crohn's disease patients had an average sIL-2R level of 920 +/- 329 units/ml, and an average sCD8 level of 355 +/- 91 units/ml, and sICAM-1 952 +/- 329 ng/ml. The four celiac disease patients had an average sIL-2R concentration of 1740 +/- 1071 units/ml, a sCD8 level of 460 +/- 320 units/ml and sICAM-1 1221 +/- 720 ng/ml. The three systemic lupus erythematosus patients had an average sIL-2R of 1023 +/- 123 units/ml, and an average sCD8 of 395 +/- 69 units/ml, and sICAM-1 1153 +/- 219 ng/ml. Thus, sIL-2R and sICAM-1 were significantly elevated over control levels in all 3 patient groups, and sCD8 was mildly elevated. These results indicate enhanced immune activation which may be a common feature in the onset and/or progression of these idiopathic illnesses.
Res Commun Mol Pathol Pharmacol 1995 Jan
PMID:Serum soluble interleukin-2 receptor, soluble CD8 and soluble intercellular adhesion molecule-1 levels in Crohn's disease, celiac disease, and systemic lupus erythematosus. 773 26

In the Western world, chronic inflammatory bowel disease (IBD) presents as two major clinical forms, Crohn's disease (CD) and ulcerative colitis (UC) [Targan, S.R. and Shanahan, F. (1994). In Retford, D.C (ed.), Inflammatory Bowel Disease: From Bench to Bedside. Williams and Wilkins, Baltimore]. Genetic epidemiological studies, the occurrence of rare syndromes associated with IBD, and animal models suggest that inherited factors play significant roles in the susceptibility to both forms of IBD [Yang, H.-Y. and Rotter, J.I. (1995) In Kirsner, J.B. and Shorter, R.G. (eds). Genetic Aspects of Idiopathic Inflammatory Bowel Disease. Williams and Wilkins, Baltimore, pp.301-331]. Recently, a genome-wide search on European families with multiple affected members with CD identified a putative susceptibility locus in the centromeric region of chromosome 16 [Hugot, J.-P. et al. (1996) Nature, 379, 821-823]. We have now tested this region in an independent set of US families, confirmed that this region is likely to contain a gene predisposing to CD, and further refined the chromosomal location of this gene. Most importantly with respect to this locus, our data also seem to indicate that there is heterogeneity both within the CD group, and between the CD and UC groups with respect to this locus. The susceptibility locus appears to be involved only in non-Jewish CD sibpairs and not in our Ashkenazi Jewish CD sibpairs. Additionally, we have tested sibpairs having either only UC or both UC and CD for involvement of this locus, and have found no evidence that this region predisposes to IBD in these patients.
Hum Mol Genet 1996 Oct
PMID:Susceptibility locus for inflammatory bowel disease on chromosome 16 has a role in Crohn's disease, but not in ulcerative colitis. 889 7

Somatic mutations of the adenomatous polyposis coli (APC) gene have been frequently found in sporadic colorectal tumors, and the frequency of such mutations remain constant as tumors progress from benign adenomas to malignant cancers. Thus the mutations of the APC gene may have a major role in the early development of sporadic colorectal tumors. Whether inactivation of the APC gene accounts for other types of primary tumors is still being investigated. We investigated for APC mutations within the mutation cluster region (a 684-bp region containing most of the mutations found in colorectal tumors) in 317 samples from a wide variety of human malignant and premalignant tissues, including 40 lung cancers, 47 renal cell carcinomas, 41 osteosarcomas and 21 other types of sarcomas, 45 acute lymphoid leukemias/lymphomas, 33 acute myeloid leukemias, 27 myelodysplastic syndrome samples, and 20 chronic colitis (ulcerative colitis and Crohn's disease) associated cancers and dysplasias, and 43 human malignant cell lines. We used single-strand conformation polymorphism assay following polymerase chain reaction. Samples with abnormal assay results were reamplified and analyzed by the direct DNA sequencing method. We detected a total of two cases with a base substitution. A silent mutation was detected in a case of myelodysplastic syndrome, and a novel nonsense mutation was discovered in a colorectal cancer cell line, SW837. In summary, we did not detect any functional mutations of the APC gene in a wide variety of tumors except for a colon cancer cell line, suggesting that alterations of the APC gene do not have a major role in the development of lung and renal cancers, various types of sarcomas, or hematological malignancies.
J Mol Med (Berl) 1997 Feb
PMID:Molecular analysis of the adenomatous polyposis coli gene in sarcomas, hematological malignancies and noncolonic, neoplastic tissues. 908 31

In a 12.5 cM genome-wide scan for psoriasis susceptibility loci, recombination-based tests revealed linkage to the HLA region (Zmax = 3.52), as well as suggestive linkage to two novel regions: chromosome 16q (60-83.1 cM from pter, Zmax = 2.50), and chromosome 20p (7.5-25 cM from pter, Zmax = 2.62). All three regions yielded P values < or = 0.01 by non-parametric analysis. Recombination-based and allele sharing methods also confirmed a previous report of a dominant susceptibility locus on distal chromosome 17q (108.2 cM from pter, Zmax = 2.09, GENEHUNTER P = 0.0056). We could not confirm a previously reported locus on distal chromosome 4q; however, a broad region of unclear significance was identified proximal to this proposed locus (153.6-178.4 cM from pter, Zmax = 1.01). Taken together with our recent results demonstrating linkage to HLA-B and -C, this genome-wide scan identifies a psoriasis susceptibility locus at HLA, confirms linkage to 17q, and recommends two novel genomic regions for further scrutiny. One of these regions (16q) overlaps with a recently-identified susceptibility locus for Crohn's disease. Psoriasis is much more common in patients with Crohn's disease than in controls, suggesting that an immunomodulatory locus capable of influencing both diseases may reside in this region.
Hum Mol Genet 1997 Aug
PMID:Evidence for two psoriasis susceptibility loci (HLA and 17q) and two novel candidate regions (16q and 20p) by genome-wide scan. 925 83

Crohn's disease is an idiopathic chronic panenteric intestinal inflammatory disease. Data concerning the pathogenesis of, and the immune responses occurring in, Crohn's disease are often conflicting. Current therapy is empirical and either non-specifically immunosuppressive or surgically ablative in nature. Although controversial, Crohn's disease may be thought of as having two different presentations, an aggressive fistulizing form and an indolent obstructive form. This is analogous to the tuberculoid and lepromatous manifestations of leprosy. If correct, this subclassification may provide key insights into the pathogenesis and differing host immune responses in Crohn's disease and also allow the development of more rational therapies.
Mol Med Today 1995 Oct
PMID:Is there clinical, epidemiological and molecular evidence for two forms of Crohn's disease? 941 75

The cause of the inflammatory bowel diseases Crohn's disease and ulcerative colitis is unknown, but epidemiological evidence suggests that it is multifactorial with a strong genetic component. Several genetic loci probably contribute to disease susceptibility, accounting for the complex pattern of inheritance and heterogeneous clinical manifestations. The combination of candidate gene studies and, more recently, genome-wide searches has resulted in the identification of a number of putative susceptibility loci. With large-scale, fine-mapping studies under way, and accelerating progress in the physical mapping of the human genome, rapid progress is now being made towards the identification of the genes responsible for inflammatory bowel disease.
Mol Med Today 1997 Dec
PMID:Mapping susceptibility loci in inflammatory bowel disease: why and how? 944 26

A subset of cytokine mediators belonging to the tumor necrosis factor (TNF) family cause apoptosis, acting through receptors and signaling pathways that have recently come to light. Further, at least one autoimmune disease results from a defined defect of apoptosis (mutations of the Fas ligand or its receptor). It is offered that many, and perhaps most autoimmune diseases may result from primary defects of apoptosis. Such defects may cause reflexive overproduction of TNF and other pro-apoptotic cytokines. The collateral damage produced by these mediators may be of pathogenetic importance in complex autoimmune disorders such as rheumatoid arthritis and Crohn disease, wherein TNF blockade is known to have ameliorative effects.
Blood Cells Mol Dis 1998 Jun
PMID:TNF, apoptosis and autoimmunity: a common thread? 964 22

Mast cells are traditionally known for mediating allergic reactions. In addition, these cells have been implicated in the pathogenesis of a variety of clinical conditions such as atopic and contact dermatitis, bullous pemphigoid, fibrotic lung disease, neurofibromatosis, psoriasis, scleroderma, rheumatoid arthritis, interstitial cystitis, ulcerative colitis, and Crohn's disease, but their role in host defense was an enigma until recently. Owing to the strategic location of mast cells at the host environment interface, their role in bacterial infections has been studied by a number of investigators. Latest reports show that mast cells have an ability to modulate the host's innate immune response to infectious agents. This review discusses the clinical implications of mast cell-bacteria interactions.
J Mol Med (Berl) 1998 Aug
PMID:Clinical implications of mast cell-bacteria interaction. 972 64


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