Literature DB >> 1707385

Expression of enzymatically active sucrase-isomaltase is a ubiquitous property of colon adenocarcinomas.

O Wiltz1, C J O'Hara, G D Steele, A M Mercurio.   

Abstract

Adenocarcinoma of the colon is one of the most prevalent and lethal of all human malignancies. The early diagnosis and management of this disease could be improved if biological markers, whose expression was restricted to malignant colon cells, were identified. Sucrase-isomaltase is a glycoprotein hydrolase expressed throughout the small intestine and fetal colon but not in the normal adult colon. This study shows that the expression of enzymatically active sucrase-isomaltase is a ubiquitous property of primary and metastatic colon adenocarcinoma. Significant sucrase enzyme activity (i.e., greater than 5 mU/mg protein) was observed in 16 colon carcinomas but not in adjacent normal colon mucosa. Sucrase-isomaltase messenger RNA was identified in all tumors using reverse transcriptase polymerase chain reaction. Using a quantitative polymerase chain reaction analysis, this study shows that the amount of sucrase-isomaltase messenger RNA in tumors examined (3.4 x 10(-8) to 3.19 x 10(-7) micrograms/micrograms total RNA) was greater than in adjacent mucosa (0 to 3.4 x 10(-8) micrograms/micrograms total RNA). This induction of sucrase-isomaltase messenger RNA and enzyme activity was corroborated by immunostaining. Of 30 colon adenocarcinomas examined, 80% were positive for sucrase-isomaltase. In addition, all colon carcinoma metastases examined were positive for sucrase-isomaltase. The staining pattern was distinct and demarcated tumor cells from the surrounding histologically normal tissue. No sucrase-isomaltase staining was seen in normal mucosa from the same patients. With the exception of lung, no sucrase-isomaltase immunostaining was observed in a variety of examined noncolonic adenocarcinomas. Thus, the specificity and ubiquity of sucrase-isomaltase expression in adenocarcinomas of the colon can be exploited to improve the clinical management of this disease. In addition, studies on the structure of the sucrase-isomaltase gene and its regulatory elements should contribute toward understanding the alteration of gene expression by oncogenic transformation of the colonic mucosa.

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Year:  1991        PMID: 1707385

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  5 in total

1.  Growth and propagation of normal rat intestinal epithelial cells.

Authors:  R M Odedra; C A Hart; J R Saunders; B Getty; S van de Wall; S H Sorensen; H Embaye; R M Batt
Journal:  In Vitro Cell Dev Biol Anim       Date:  1996-02       Impact factor: 2.416

2.  SSO Clinical Award Lecture. The surgical oncologist as a key translator of basic biology to patients with gastrointestinal cancer: asking the right questions.

Authors:  G Steele
Journal:  Ann Surg Oncol       Date:  1994-05       Impact factor: 5.344

3.  Is Barrett's esophagus the precursor of most adenocarcinomas of the esophagus and cardia? A biochemical study.

Authors:  J C Mendes de Almeida; P Chaves; A D Pereira; N K Altorki
Journal:  Ann Surg       Date:  1997-12       Impact factor: 12.969

4.  A novel colonic repressor element regulates intestinal gene expression by interacting with Cux/CDP.

Authors:  François Boudreau; Edmond H H M Rings; Gary P Swain; Angus M Sinclair; Eun Ran Suh; Debra G Silberg; Richard H Scheuermann; Peter G Traber
Journal:  Mol Cell Biol       Date:  2002-08       Impact factor: 4.272

5.  Novel DNA-binding proteins regulate intestine-specific transcription of the sucrase-isomaltase gene.

Authors:  P G Traber; G D Wu; W Wang
Journal:  Mol Cell Biol       Date:  1992-08       Impact factor: 4.272

  5 in total

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