Altered protein tyrosine kinase levels in human colon carcinoma

Article Abstract:

In an effort to better understand what events transform a normal, healthy cell into a malignant, cancerous cell, investigators are probing the molecular machinery working within every cell. Among the many biochemical events occurring in cells is the phosphorylation of proteins by protein kinases. Phosphorylation involves the addition of a phosphate group onto the molecular structure of a protein; the process changes the protein slightly and alters its function. Therefore, phosphorylation can serve as a means of regulating protein function within cells. Protein kinases are enzymes that transfer a phosphate group to proteins, and protein tyrosine kinases transfer a phosphate group specifically to a tyrosine residue within the protein's molecular structure. Protein tyrosine kinases became the subject of intense research when it was first found that the proteins coded for by some cancer-causing genes were, in fact, tyrosine kinases. Since that observation, it has become clear that tyrosine kinases are themselves regulated by phosphorylation, and so cell biologists now feel confronted by an exquisitely detailed network of regulatory enzymes controlling cell function. In an effort to determine if protein tyrosine kinases may play a role in the pathogenesis of colon cancer, the kinase activity was measured in both normal and cancerous tissues from 20 patients with colon cancer. Furthermore, the cells were fractionated (divided into component parts), so that the kinase activity associated with the soluble portion of the cells, the cytosol, could be measured separately from the kinase activity associated with the particulate, insoluble, fraction of cells. The results showed that the protein tyrosine kinase activity of the soluble part of cells was reduced in the cancerous tissues, but the tyrosine kinase activity expressed within the particulate fraction of the homogenized cells was greater in the cancerous specimens. The results suggest that abnormalities of cellular regulation are present in cancer cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Protein tyrosine kinase, Protein-tyrosine kinase, Carcinogenesis

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Protein kinase C activity in human colonic adenoma and colorectal carcinoma

Article Abstract:

It is generally thought that a cancer does not result from a single pathogenic event, but is rather the end result of a sequence of events. Little is known about the biochemical events which must occur along the sequence from normal tissue to cancer. However, in the case of colon cancer, it is clear that the majority of individual cancers arise from adenomas, tumors often called polyps, which have arisen from healthy colon tissues. One molecule that appears to play an important role in the sequence of events leading to cancer is protein kinase C (PKC). Interest in this enzyme was stimulated by the discovery that PKC activity is turned down in cells treated with phorbol esters, compounds that do not cause cancer but promote the development of tumors which have been initiated by some other cause. To learn more about the possible role of PKC in tumor progression, the level of PKC activity was measured in normal colon tissues, adenomatous polyps, and actual colon cancer. Measurements were also made to distinguish the portion of PKC that is associated with cell membranes from the portion that is freely dissolved in the cell cytoplasm. When the portion of PKC activity associated with the cell membranes was measured, it was found that the amount in the adenomas was less than the amount in normal tissues, and the amount in the cancerous tissue was lesser still. However, when the amount of PKC activity in the soluble cytosol fraction of the cells was measured, no differences were found between the normal, adenomatous, or cancerous tissues. It was also found that there was an inverse correlation between protein kinase C and adenoma size; the larger polyps tended to have the least PKC enzyme activity. (Consumer Summary produced by Reliance Medical Information, Inc.)

Protein kinases, Intestinal polyps, Colon (Anatomy), Colon, Polyps (Pathology), Polyps

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Investigations of the significance of the adenoma-carcinoma sequence in the small bowel

Article Abstract:

It is now well established that the appearance of cancers in some tissues is preceded by the development of dysplastic tissue, or tissue with an abnormal histological appearance. In the case of colorectal cancer, this dysplasia takes the form of an adenoma. The progression of adenoma to carcinoma has been well established in colorectal cancer, which is exceedingly common. However, both adenomas and cancers of the small intestine are exceedingly rare, and no single institution has accumulated enough case histories of small bowel cancer to determine reliably if the same adenoma-to-carcinoma sequence occurs in this tissue. Consequently, an extensive review of cases at many institutions as far back 1927 was conducted. It was found that the mean age for adenoma of the small intestine was lower than that for adenoma with carcinoma and carcinoma, and that the anatomical distributions of the three small bowel tumors were the same. Likewise, the sex ratios for adenomas and carcinomas of the small intestine were the same. The frequency of finding the residue of an adenoma in continuity with a carcinoma was the same as that found for carcinomas of the large intestine. These results suggest that, although the incidence is remarkably higher in the large intestine, the same adenoma-to-carcinoma sequence is at work in the small intestine as well. (Consumer Summary produced by Reliance Medical Information, Inc.)

Adenocarcinoma, Gastrointestinal cancer, Digestive system cancer

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