Cellular markers in the gastric precancerous process

Moss, Steven F.

doi:10.1111/j.1365-2036.1998.00002.x

Cited by 61 publications

(58 citation statements)

References 67 publications

(83 reference statements)

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“…However, the remarkable technical advances in molecular biology seen in recent years have enhanced the understanding of carcinogenesis and the progression of cancer. Normal growth and differentiation of cells in the gastrointestinal tract are regulated by autocrine and paracrine secretion of peptide growth factors which are responsible for controlling maturation, differentiation and apoptosis (Moss, 1998;Park et al, 2005). In gastric cancer, where there is unrestricted growth, it is likely that there are abnormalities of secretion or response to those peptides.…”

Section: Discussionmentioning

confidence: 99%

PTEN/MMAC1 enhances the growth inhibition by anticancer drugs with downregulation of IGF-II expression in gastric cancer cells

Hwang

Kim²,

Lee³

et al. 2005

Exp Mol Med

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Section: Discussionmentioning

confidence: 99%

PTEN/MMAC1 enhances the growth inhibition by anticancer drugs with downregulation of IGF-II expression in gastric cancer cells

Hwang

Kim²,

Lee³

et al. 2005

Exp Mol Med

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“…The dynamic balance between cell proliferation and apoptosis is essential for maintaining normal mucosal integrity. Moss (48) described an increased rate of cell proliferation of epithelial cells and a decrease in the apoptotic index in H. pylori infection, with an increase in ROS and NO (48).…”

Section: Discussionmentioning

confidence: 99%

Implications of antioxidant enzymes in human gastric neoplasms

Monari¹

2009

Int J Mol Med

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Abstract. The present study is the first to evaluate the expression and activity of MnSOD, Cu/ZnSOD and catalase in human gastric samples, since ROS play a significant role in the pathogenesis of different forms of malignancy inducing mutations and various diseases such as gastric cancer. Biopsies and surgical samples from 53 patients (male/female 22/31, mean age 56.5±15.8 years) consisted of 15 healthy, 12 autoimmune atrophic gastritis, 10 Helicobacter pylori (HP) infection, 8 HP-negative chronic gastritis (CG) and 8 adenocarcinoma cases. Enzyme activity and expression were evaluated by spectrophotometry and immunoblotting after specific extraction in phosphate buffer. We found that MnSOD activity was increased in adenocarcinoma, CG and HP tissues (p<0.05-0.001), while Cu/ZnSOD was significantly lower in adenocarcinoma and HP tissues (p<0.001) when compared to the healthy control. MnSOD and Cu/ZnSOD were expressed to a significantly higher degree in adenocarcinoma and HP tissues (p<0.05 and <0.001 respectively) and to a significantly lower degree in CG tissues with respect to the healthy patients (p<0.05 and <0.001). A significant decrease in CAT activity in adenocarcinoma and HP tissues was observed (p<0.01 and <0.05). Gastric human neoplasms showed significant changes in antioxidant enzymes, that represent the first line in antioxidant protection against radical attack. The difficulties in correlating the antioxidant enzyme with the neoplasms was related to the complexity of the biochemical pathways that regulate the cellular redox balance. Our results are important in enhancing the understanding of the role that these enzymes play in the promotion/ suppression of the carcinogenesis cascade in human gastric mucosa.

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“…These genetic changes include the inactivation of p53, mutations in K-ras, decreased expression of p21, ampli®cation of c-met and c-ErbB-2, and microsatellite instability (reviewed in Kinzler and Vogelstein, 1996;Moss, 1998;Tahara, 1995). In an attempt to further characterize tumor progression, we performed PCR and SSCP analysis on genes commonly mutated in gastrointestinal cancers.…”

Section: Loh Of Smad4 Wild-type Allele Occurs Late In Gastric Tumorigmentioning

confidence: 99%

“…As in many tumor types, gastric carcinogenesis re¯ects a multistep process of morphologic abnormalities associated with the accumulation of genetic alterations, including activation of oncogenes and/or inactivation of tumor suppressor genes (reviewed in Correa, 1992;Kinzler and Vogelstein, 1996;Moss, 1998). It was recently demonstrated that one mechanism of gastric cancer progression is the inactivation of the TGF-b signaling pathway (Markowitz and Roberts, 1996;Yang et al, 1999a), where SMAD4/DPC4 is the central mediator (Heldin et al, 1997;Massague, 1998).…”

Section: Introductionmentioning

confidence: 99%

Haploid loss of the tumor suppressor Smad4/Dpc4 initiates gastric polyposis and cancer in mice

et al. 2000

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The tumor suppressor SMAD4, also known as DPC4, deleted in pancreatic cancer, is a central mediator of TGF-b signaling. It was previously shown that mice homozygous for a null mutation of Smad4 (Smad4 7/7 ) died prior to gastrulation displaying impaired extraembryonic membrane formation and endoderm dierentiation. Here we show that Smad4 +/7 mice began to develop polyposis in the fundus and antrum when they were over 6 ± 12 months old, and in the duodenum and cecum in older animals at a lower frequency. With increasing age, polyps in the antrum show sequential changes from hyperplasia, to dysplasia, in-situ carcinoma, and ®nally invasion. These alterations are initiated by a dramatic expansion of the gastric epithelium where Smad4 is expressed. However, loss of the remaining Smad4 wild-type allele was detected only in later stages of tumor progression, suggesting that haploinsuciency of Smad4 is sucient for tumor initiation. Our data also showed that overexpression of TGF-b1 and Cyclin D1 was associated with increased proliferation of gastric polyps and tumors. These studies demonstrate that Smad4 functions as a tumor suppressor in the gastrointestinal tract and also provide a valuable model for screening factors that promote or prevent gastric tumorigenesis.

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Cellular markers in the gastric precancerous process

Cited by 61 publications

References 67 publications

PTEN/MMAC1 enhances the growth inhibition by anticancer drugs with downregulation of IGF-II expression in gastric cancer cells

PTEN/MMAC1 enhances the growth inhibition by anticancer drugs with downregulation of IGF-II expression in gastric cancer cells

Implications of antioxidant enzymes in human gastric neoplasms

Haploid loss of the tumor suppressor Smad4/Dpc4 initiates gastric polyposis and cancer in mice

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