PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 1511368

Colon cancer overview.

P Greenwald
View original source ↗Export metadata ↓

Abstract

The scope of current prevention research support by the National Cancer Institute includes the clinical assessment of dietary modifications and cancer screening trials, epidemiologic studies, development of new chemopreventive therapies, and the use of advanced molecular biologic technologies to probe the genetic determinants of colorectal adenomas. Colorectal cancer frequently has been associated with high-fat low-fiber diets in epidemiologic and experimental studies. A recently initiated Phase III Dietary Intervention Study of Recurrence of Large Bowel Adenomatous Polyps will investigate the potential benefits of a low-fat high-fiber fruit-and-vegetable-enriched eating pattern to decrease the polyp recurrence rate. The Chemoprevention Program currently is supporting four Phase III controlled clinical intervention trials investigating the cancer-inhibiting effects on colorectal cancer of beta-carotene, piroxicam, calcium, and calcium plus fiber in persons with previous adenomas. A proposed early detection trial will screen for colorectal, prostate, lung, and ovarian cancers. A comparison of incidence and mortality trends indicates progress in colorectal cancer detection and therapy.

Explore related subjects

Anticarcinogenic AgentsClinical Trials as TopicColonic NeoplasmsDietFemaleHumansIncidenceMaleJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P Greenwald. 1992-09-01. Colon cancer overview.. https://doi.org/10.1002/1097-0142(19920901)70%3A3%2B%3C1206%3A%3Aaid-cncr2820701504%3E3.0.co%3B2-j

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1992

Inhibition of cell attachment by selenite.

Brief pre-exposure of HeLa cells to micromolar concentrations of selenite resulted in a dose-dependent decrease in the rate of their subsequent attachment to a solid matrix (tissue culture dish). Similar low concentrations of selenite also inhibited colony formation, but only when the cells were exposed prior to their attaching to the dish, not when they were exposed after attachment. This indicates that inhibition of cell proliferation by selenite requires exposure to higher concentrations for longer periods of time. In contrast, selenate, selenomethionine, selenocystine, and sulfite did not affect cell attachment, even at significantly higher concentrations. Thus, the inhibition of cell attachment is a specific effect of selenite. Selenite also inhibited the attachment of cells to bacteriological dishes coated with fibronectin, laminin, or collagen, proteins that are components of the extracellular matrix. There was no inhibition when the tissue culture dishes or the protein-coated dishes were pre-exposed to selenite. There was also no inhibition when the cells were exposed to selenite during the attachment process. Thus, pre-exposure of the cells to selenite was necessary for inhibition of attachment. Since cell attachment has been shown to be an important early step in tumor cell invasion and metastasis, these results suggest a novel mechanism of the anticarcinogenic effect of selenite: inhibition of the attachment of tumor cells to the extracellular matrix.

Anticarcinogenic Agents↗