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  • 1
    ISSN: 1436-2813
    Keywords: superficial esophageal carcinoma ; p53 protein ; human papillomavirus (HPV) ; DNA ploidy ; cytofluorometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the p53 protein and human papilloma virus (HPV) by immunohistochemistry and DNA ploidy by cytofluorometry in paraffin-embedded esophageal carcinoma tissue specimens. Sixty-one patients with superficial esophageal carcinoma were operated on between 1983 and 1991 without any prior treatment. Immunostaining of the anti-p53 protein antibody (CM1) was positive in 32 carcinomas (52%). Patients with p53-positive tumors had a poorer outcome than those with p53-negative tumors (P〈0.05). In addition, patients with p53-positive tumors did not have any characteristic site of relapse. Only 5 of the 61 patients (8.2%) had HPV-positive tumors. One of these 5 carcinomas expressed both p53 protein and HPV. Three patients with HPV-positive tumors which had invaded the submucosal layer died of relapse. A determination of DNA ploidy revealed 30 patients with aneuploid tumors, 13 with polyploid tumors and 18 with diploid tumors. The outcome of the patients with aneuploid tumors was worse than that of the patients with diploid tumor (P〈0.05). p53 protein expression was not associated with DNA ploidy; however, the 16 patients who had both p53-positive and aneuploid tumors had a worse prognosis than patients with p53-negative and aneuploid tumors (P〈0.01). These findings suggest that p53 protein expression in conjunction with DNA ploidy may be a useful indicator in evaluating the prognosis of patients with superficial esophageal carcinoma.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2568
    Keywords: DCC GENE ; POLYMORPHISM ; CODON 201 ; FLAT-TYPE COLORECTAL TUMOR ; GENETIC MARKER
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Recent studies have identified the distinctexistence of flat-type colorectal tumors. The lowincidence of ras gene mutations in these tumors suggeststhat their genetic pathways of tumor progression may be different from those of the polypoid type.To elucidate further genetic alterations in flat-typecolorectal tumors, codon 201Arg/Glypolymorphism in the DCC (deleted in colorectalcarcinoma) gene was analyzed in normal tissue (normal colonicmucosa or peripheral lymphocytes) and in tumor tissuefrom 191 patients with colorectal tumors (36 patientswith flat-type colorectal tumors, 81 patients withpolypoid-type colorectal tumors, and 74 patients withadvanced carcinomas). For normal controls, 30 samplesobtained from patients who had neither colorectal tumors(confirmed by total colonoscopy) nor a family history of colorectal carcinoma were analyzed. DCC genecodon 201Arg/Gly polymorphism wasinvestigated by polymerase chain reaction-basedrestriction fragment length polymorphism analysis,fluorescence-based dideoxy sequencing, or both. For the flat type, thefrequency of codon 201Gly of the DCC gene was64% and 54% in the normal tissue of patients withadenoma with high-grade dysplasia and submucosalcarcinoma, respectively. It was 49%, 52%, and 49% in the normal tissueof patients with polypoid-type adenoma with high-gradedysplasia, submucosal carcinoma, and advanced carcinoma,respectively. In the normal tissue, codon 201Gly of the DCC gene was more frequentlyobserved in patients with flat-type adenoma withlow-grade dysplasia (67%) than in those withpolypoid-type adenoma with low-grade dysplasia (18%) orin normal controls (17%, P 〈 0.05, χ2test). Codon 201Arg/Gly polymorphism in tumortissues did not differ from that in the correspondingnormal tissues, except for 10 cases of carcinoma withloss of heterozygosity (LOH). In carcinomas with LOH, preferentialloss of the codon 201Arg allele was noted(9/10 cases). These results suggest that codon201Gly of the DCC gene is not only associatedwith flat-type colorectal tumors, but that it may serve as a usefulgenetic marker for identifying groups at higher risk forcolorectal cancer.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-5922
    Keywords: gastric mucous cell ; FGF ; EGF ; insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Almost completely homogenous gastric mucous epithelial cells of guinea pigs were grown to confluence in the presence of 10% fetal calf serum (FCS). FCS, epidermal growth factor (EGF), and insulin significantly increased 5-bromo-2′-deoxyuridine (BrdU) uptake by the cells and EGF together with insulin increased the cells' [3H] thymidine uptake. Basic fibroblast growth factor (bFGF) enhanced EGF-induced DNA synthesis by the cells, but vasoactive intestinal peptide (VIP), secretin, prostaglandin E2 (PGE2), and dibutyryl cyclic AMP (dbcAMP) neither induced DNA synthesis nor enhanced the effect of EGF on DNA synthesis by the cells. Gastrin, cholecystokinin-octapeptide (CCK8), and carbamylcholine chloride (CCh) also did not enhance the effect of EGF on DNA synthesis.125I-EGF,125I-bFGF, and125I-gastrin binding to the gastric mucous cells revealed the presence of high-affinity receptors for EGF and bFGF, but not for gastrin. Northern blot analysis showed the expression of EGF receptor mRNA, but not gastrin receptor mRNA. These results suggest that EGF, insulin, and bFGF may cooperatively regulate gastric mucous cell growth, but that gastrin and other gastrointestinal hormones do not have a direct stimulatory effect on mucous cell growth in the guinea pig.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1435-5922
    Keywords: Key words: colorectal cancer ; tumor evolution ; genetic change
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1435-5922
    Keywords: Key words: COX-2 ; p53 ; Ki-67 ; colorectal cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: The tumor-suppressive effects of nonsteroidal antiinflammatory drugs (NSAIDs) have been suggested to be due to a reduction in cyclooxygenase (COX)-2 activity, although the effects of COX-2 in the colonic mucosa and in colorectal cancer have not been determined. Ki-67 immunoreactivity in cancers is also attracting attention, as Ki-67 reflects cell proliferation, while p53 immunoreactivity is also of interest, as it reflects the malignancy of colorectal lesions. Accordingly, to determine these correlation, we investigated the distribution and intensity of COX-2, p53 and Ki-67 expression in both cancerous and non-cancerous tissues from patients with sporadic and ulcerative colitis (UC)-associated colorectal cancer. We selected 21 colorectal cancer specimens, obtained by surgical resection or colonoscopic biopsy, from 21 patients, including 3 with UC (13 men and 8 women; aged 42–78 years). Histological examination of hematoxylin and eosin-stained specimens revealed that 9 were well differentiated; 11, moderately differentiated; and 1 was a poorly differentiated adenocarcinoma. We used anti-COX-2, p53, and Ki-67 antisera to perform immunohistochemical staining by the labelled streptavidin biotin method and then assessed and graded the staining intensity and distribution. COX-2 staining was more intense in cancer tissue than in non-cancerous areas. Colorectal cancers associated with UC were not stained intensely. COX-2, p53, and Ki-67 positivity rates in were 38.1%, 38.1%, and 47.6%, respectively. There were no relationships among the distributions or intensities of COX-2, p53, and Ki-67 expression. Our results indicate that colorectal cancer tissues overexpress COX-2, but that there are no relationships between COX-2, p53, and Ki-67 expression, suggesting that COX-2 expression may not be related to cell proliferation or to the grade of malignancy. However, it is necessary to determine whether COX-2 in cancer tissue is involved in carcinogenesis or whether it is simply a product of cancer.
    Type of Medium: Electronic Resource
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