口腔健康相关生活质量的研究应用与进展

近20年来,口腔健康相关生活质量的测评越来越受到学者们的关注,它是反映口腔疾病及其防治对患者的身体机能、心理功能、社会功能等影响的多维综合评估体系.有关这方面的研究,国外在临床和基础科研领域都取得了一定的成果,而国内的报导却凤毛麟角,乏善可陈.本文旨在通过对口腔健康相关生活质量的测评体系的综述,以探讨我国口腔健康相关生活质量的未来发展方向.     

OVX1 and CEA in patients with colon carcinoma, colon polyps and benign colon disorders

The OVX1 tumor marker promises to complement CA125 for detection of early stage ovarian carcinoma. OVX1 has also been shown to be elevated in colon cancer patients. This study is designed to assess serum OVX1 levels in patients with specific stages of colon cancer, colon polyps or other GI disorders. Serum OVX1 and CEA were measured by radioimmunoassay or enzyme immunoassay for 206 patients at the time of colonoscopy or staging for colon carcinoma. In patients with stage I, II, III, or IV colon carcinoma, serum OVX1 was positive in 37%, 48%, 74% and 63%, respectively. Fifty-three percent of patients with colon polyps had elevated OVX1 levels, while OVX1 levels were positive in only 7% of healthy controls. If both OVX1 and CEA were considered, at least one of these markers was elevated in 36%, 60%, 79% or 89% of patients with stage I, II, III or IV colon carcinoma, respectively. The majority of patients with inflammatory bowel disease or diverticulosis also had elevated OVX1 levels. Both markers were positive in 27% of patients with colon carcinoma, and not in any patients with a normal colonoscopy or with a diagnosis of diverticulosis or hemorrhoids. In conclusion, serum OVX1 improves the sensitivity of CEA for detecting colon polyps and colon cancer; however, the use of OVX1 in this setting is hindered by its elevation in non-malignant colonic processes.     

The irritable colon

The irritable colon syndrome is a very common disorder with no serious sequelae. The cause is unknown but low dietary bulk and psychological factors are believed important. Sufferers may experience various combinations of diarrhea, constipation and abdominal pain. The mechanisms are obscure but abnormal colon motility has been amply demonstrated. Serious organic diseases such as colitis and carcinoma of the colon must be firmly excluded. Treatment consists of sympathetic explanation and reassurance, increased dietary bulk and occasional judicious use of antispasmodic agents.     

Normal human colon cells suppress malignancy when fused with colon cancer cells

Summary Normal human colon mucosa cells and cells obtained from histologically normal tissues near that cancer were fused with human colon cancer cells. Resultant hybrid populations of normal and malignant cell fusions behaved as nonmalignant cells in culture, were unable to grow in soft agar, did not express tumor-associated antigens, and were nontumorigenic in nude mice. Autofusion of the cancer cell population led to a phenotype intermediate between normal and malignant cells. That is, the cultures had a much lower plating efficiency in soft agar, and the tumors had a longer latency and slower growth rate in nude mice. This is the first cell culture system to demonstrate that normal epithelial cells can suppress malignancy of their autologous cancer cells, and is a prelude to more extensive studies of genetic events involved in malignant conversion of human colonic epithelium. This study was supported by The University of Texas Health Science Center at San Antonio Center for Human Cell Biotechnology and a graduate student stipend (T. J.) from the Department of Cellular and Structural Biology.     

Carcinoma of the colon

In a study of statistical data on 1,215 patients with carcinoma of the colon observed at a university hospital in a twenty-year period, it was noted that the overwhelming majority of patients who were living five years after operation had had no demonstrable extension to lymph nodes at the time of operation. In an increasing proportion of cases in the latter years of the period, diagnosis was made before the lesion was beyond an operable stage. What with today's better surgical techniques that make it possible to adapt operation to a variety of situations that may be encountered when the diseased area is visualized, and with better methods of preparing a patient and of sustaining him during operation, the wide excision so often necessary for cure may now be carried out deliberately and without hurry. The site of the lesion has great bearing on the prognosis, owing to the limits upon the extent of operation in some locations as against the possibility of wide excision of the original lesion and areas of metastasis in others.     

Polyamines and colon cancer

In colon cancer, the activities of polyamine-synthesizing enzymes and polyamine content are increased 3-4-fold over that found in the equivalent normal colonic mucosa, and polyamines have even been attributed as markers of neoplastic proliferation in the colon. Furthermore, and in contrast with all other cell systems in the body, normal and neoplastic cells in the colon are exposed to high concentrations of putrescine from the lumen, synthesized by colonic microflora. While such a high polyamine supply may be of benefit in non-neoplastic colonic mucosal growth, the role of luminal polyamines in colon cancer is a clear concern. Luminal polyamines are readily taken up by neoplastic colonocytes, they are utilized in full to support neoplastic growth, and their uptake is strongly up-regulated by the mitogens known to play an important role in colonic carcinogenesis. Inhibition of polyamine synthesis and their uptake, impaired utilization of exogenous polyamines, and enhanced catabolism of polyamines in neoplastic colonocytes are therefore logical approaches in the chemoprevention of colorectal cancer.     

Sphingolipids in colon cancer

Colorectal cancer is one of the major causes of death in the western world. Despite increasing knowledge of the molecular signaling pathways implicated in colon cancer, therapeutic outcomes are still only moderately successful. Sphingolipids, a family of N-acyl linked lipids, have not only structural functions but are also implicated in important biological functions. Ceramide, sphingosine and sphingosine-1-phosphate are the most important bioactive lipids, and they regulate several key cellular functions. Accumulating evidence suggests that many cancers present alterations in sphingolipids and their metabolizing enzymes. The aim of this review is to discuss the emerging roles of sphingolipids, both endogenous and dietary, in colon cancer and the interaction of sphingolipids with WNT/β-catenin pathway, one of the most important signaling cascades that regulate development and homeostasis in intestine. This article is part of a Special Issue entitled New Frontiers in Sphingolipid Biology.     

The potent colon carcinogen, 1,2-dimethylhydrazine induces mutations primarily in the colon

1,2-Dimethylhydrazine (DMH) is a potent colon carcinogen that is commonly used as an initiator in studies of the effects of diet on colon cancer. Previous studies have shown that although this compound produces multiple tumors in the colons in most individuals of every species tested, it is, at best, marginally mutagenic in the bone marrow (micronuclei) and small intestine (Dlb-1 mutations). Here we report its mutagenicity in the primary target tissue, the colonic epithelium, by means of the Mutatrade markMouse cII assay, an assay for intragenic mutations in a lambda shuttle vector that is integrated into the genome of these mice. Animals were treated with 0, 10, 20, or 30 mg/ml of DMH, either as a single injection or as multiple weekly injections, and mutations were measured in both the small intestine and colon. In the small intestine, there was an increase in mutant frequency following a single injection of DMH, but this was significant only at 30 mg/kg [induced mutant frequency (MF) = 18 x 10(-5) mutants/plaque]. In the colon, following a single treatment of DMH, there was a significant increase in mutant frequency at doses of 20 and 30 mg/kg (induced MF = 17 x 10(-5) and 23 x 10(-5) mutants/plaque, respectively). Following ten injections of 20 mg/kg of DMH, there was a greater than ten-fold increase in mutations in the colon (MF = 275 x 10(-5) mutants/plaque) than the small intestine (MF = 25 x 10(-5) mutants/plaque). These results show that DMH, under the conditions typically used for dietary studies, induces large numbers of mutations in the tissue in which it induces most cancers.     

左半结肠癌和右半结肠癌基因差异表达谱的建立

目的:初步探索左半结肠癌和右半结肠癌中基因表达的差异,为左右半结肠癌生物学特性上的差别提供分子遗传学依据。方法:以左右半结肠癌组织为研究对象,提取组织总RNA,依次进行样品RNA进行荧光标记,杂交和清洗,芯片扫描和芯片图像的采集和数据分析。结果:成功建立了左半结肠癌,左半结肠癌旁,右半结肠癌,右半结肠癌旁的基因表达谱,应用SAM软件分析比较得到左半结肠癌与右半结肠癌的差异基因共有11个,包括乳酸脱氢酶B链,泛素D,磷脂酰-4-3磷酸激酶C2-α,FAT,双特异性蛋白磷酸酶2,细胞周期蛋白依赖性激酶4抑制剂D,酪蛋白激酶-1结合蛋白,突触结合蛋白-13,锌指蛋白560,公认未定性蛋白,IgGFc结合蛋白。左半结肠癌旁与右半结肠癌旁的差异基因共有4个,包括金属蛋白酶7,早期生长反应蛋白1,左半结肠癌旁组织中下调的基因包括突触孔蛋白,膜相关磷脂酶A2基因。结论:左半结肠癌和右半结肠癌以及相应癌旁组织中存在差异表达基因,这些基因表达的差异可能是左右半结肠癌生物学性质差异的分子遗传学基础。     

miRNA expression in colon polyps provides evidence for a multihit model of colon cancer

Changes in miRNA expression are a common feature in colon cancer. Those changes occurring in the transition from normal to adenoma and from adenoma to carcinoma, however, have not been well defined. Additionally, miRNA changes among tumor subgroups of colon cancer have also not been adequately evaluated. In this study, we examined the global miRNA expression in 315 samples that included 52 normal colonic mucosa, 41 tubulovillous adenomas, 158 adenocarcinomas with proficient DNA mismatch repair (pMMR) selected for stage and age of onset, and 64 adenocarcinomas with defective DNA mismatch repair (dMMR) selected for sporadic (n = 53) and inherited colon cancer (n = 11). Sporadic dMMR tumors all had MLH1 inactivation due to promoter hypermethylation. Unsupervised PCA and cluster analysis demonstrated that normal colon tissue, adenomas, pMMR carcinomas and dMMR carcinomas were all clearly discernable. The majority of miRNAs that were differentially expressed between normal and polyp were also differentially expressed with a similar magnitude in the comparison of normal to both the pMMR and dMMR tumor groups, suggesting a stepwise progression for transformation from normal colon to carcinoma. Among the miRNAs demonstrating the largest fold up- or down-regulated changes (≥4), four novel (miR-31, miR-1, miR-9 and miR-99a) and two previously reported (miR-137 and miR-135b) miRNAs were identified in the normal/adenoma comparison. All but one of these (miR-99a) demonstrated similar expression differences in the two normal/carcinoma comparisons, suggesting that these early tumor changes are important in both the pMMR- and dMMR-derived cancers. The comparison between pMMR and dMMR tumors identified four miRNAs (miR-31, miR-552, miR-592 and miR-224) with statistically significant expression differences (≥2-fold change).