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PubMed2002

DNA microarrays: a new diagnostic tool and its implications in colorectal cancer.

Effective treatment of colorectal cancer requires early detection and diagnostic and prognostic accuracy in characterizing patients of various risk groups. The development of DNA microarray makes it possible to analyze thousands of genes in a single tissue sample in one experiment and to characterize the biological behavior of colorectal cancer cells. Different cluster algorithms have been used to analyze large datasets on gene expression data, and initial results show significant differences between colorectal cancer and normal colon tissue. Although more than 6000 genes have been analyzed between colorectal cancer and normal tissue, different expression levels have been found in only 100-500 transcripts depending on the cluster algorithm. Most transcripts belong to genes involved in cell growth regulation, differentiation of cells, ribosomal proteins or metalloproteinase. A future goal in microarray technology will be the development of clustered gene chips which characterize each tumor type specifically and focus on gene expression that specifies cell identity.

Biomarkers, Tumor↗
PubMed2001

A United Kingdom coordinating committee on cancer research study of adjuvant chemotherapy for colorectal cancer: preliminary results.

Standard adjuvant chemotherapy for colorectal cancer consists of 5-fluorouracil with leucovorin or levamisole. The large, multicenter, randomized, double-blind QUASAR (Quick and Simple and Reliable) trial investigated whether treatment with a higher dose of leucovorin or the addition of levamisole to 5-fluorouracil and leucovorin improved survival. In the QUASAR study, 4,927 patients with colorectal cancer with no evidence of residual disease following resection, were randomized to receive fluorouracil (370 mg/m2) with high-dose (175 mg) or low-dose (25 mg) leucovorin and either levamisole (50 mg) or placebo. The fluorouracil and leucovorin regimen was given either monthly (as six 5-day courses with 4 weeks between the start of each course) or weekly (as 30 once-weekly doses). Levamisole or placebo was given three times daily for 3 days, repeated every 2 weeks for 12 courses. The primary endpoint was death from any cause. Survival was similar with both high- and low-dose leucovorin (70.1% v 71.0% at 3 years; P = .43) as well as recurrence rates (36.0% v 35.8%; P = .94), and with levamisole compared with placebo (69.4% v 71.5%; P = .06) as well as recurrence rates (37.0% v 34.9%; P = .16). Monthly and weekly treatments were equally effective (although this was a nonrandomized comparison), while weekly treatment was associated with significantly fewer toxic effects (neutropenia, mucositis, and diarrhea). High-dose leucovorin was not associated with a survival or recurrence benefit when compared with low-dose leucovorin. The ongoing QUASAR-1 trial aims to establish whether adjuvant chemotherapy has any worthwhile survival benefit in colorectal cancer patients with an uncertain indication following surgical resection.

Adjuvants, Immunologic↗
PubMed2003

Family history of colorectal cancer in a Sweden county.

Hereditary nonpolyposis colorectal cancer (HNPCC) and familial adenomatosis polyposis (FAP) are well-known high-risk cancer syndromes. Hereditary colorectal cancer (HCRC) with at least three relatives with colorectal cancer and a dominant pattern of inheritance but with no specifications for age at onset and two close relatives with colorectal cancer (TCR) are other forms of familial clustering known to carry an increased risk of the disease. The frequency of the total burden of familial colorectal cancer is not well known. We therefore investigated the family history of 400/411 (97%) eligible patients with recently diagnosed colorectal cancer in Västmanland county, Sweden, during a 3-year period. Records or death certificates confirmed the diagnoses of relatives. Five patients (1.2%, 95% CI 0.15-2.2) were diagnosed as having HNPCC, eight (1.9%, 95% CI 0.6-3.2) as having HCRC and thirty-four (8.3%, 95% CI 5.6-11.0) were identified as having TCR. In total, 47 patients (11.4%, 95% CI 8.3-14.5) were found to have a contributing familial background. The implication is thus that every ninth patient with colorectal cancer represents a highly or intermediately increased risk of the disease among relatives. We conclude that the low frequency of individuals identified by family history alone makes the establishment of surveillance programs feasible.

Adenomatous Polyposis Coli↗
PubMed2001

Polymorphic expression of decay-accelerating factor in human colorectal cancer.

BACKGROUND: We have previously shown that expression of decay-accelerating factor (DAF), a complement regulatory protein, is enhanced immunohistochemically on the luminal surface of cancer glands in human colorectal cancer and is detected in stool specimens of patients with colorectal cancer. The amount of DAF present in the stools might be influenced by the stability of DAF on the cell surface which is regulated by biochemical properties such as glycosylation of the protein. In the present study, to help elucidate the mechanism for the release of DAF from human colorectal cancers, we biochemically analyzed DAF expression by western and northern blotting by using surgically resected specimens of colorectal cancers. METHODS: Surgically resected colorectal cancer tissues were obtained from 10 patients. Expression of DAF was determined by western and northern blotting, and glycosylation of DAF protein was analyzed with glycosidase digestion. RESULTS: Northern blot analysis demonstrated that the expression of DAF mRNA in colorectal cancer was enhanced two- to threefold compared with normal tissues. In western blotting, expression of DAF protein in the cancer tissue was increased, and heterogeneity in the apparent molecular weight of DAF was observed among patients. When o-linked sugars were removed, this heterogeneity of DAF size diminished. CONCLUSIONS: The polymorphic expression of DAF in colorectal cancer is likely to reflect variability in the o-glycosylation of the protein. We speculate that this variability could affect the stability of DAF on the surfaces of cancer cells and, in turn, the amount of DAF shed into the stools of colorectal cancer patients.

Adult↗
PubMed1989

Colorectal cancer.

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Colorectal Neoplasms↗
PubMed1988

Colorectal cancer.

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Colorectal Neoplasms↗
PubMed1995

[Neoadjuvant chemotherapy with tegafur suppository for rectal cancer--effects of tegafur on nuclear DNA content of cancer cells--Tochigi Colorectal Cancer Study Group].

To assess the significance of neoadjuvant chemotherapy for large bowel cancer, we investigated an effect of tegafur on cancer cell kinetics by DNA content flow cytometric analysis. The pathologic specimens analyzed in this study were obtained from 28 patients with rectal cancer who had received tegafur suppositories prior to surgery. Mean cumulative doses administered were 13.4 g, and mean duration was 12.7 days. In 24 of the 28 specimens, the DNA ploidy and DNA index of the cancer cells were essentially unchanged after the chemotherapy, and DNA aneuploidy was present in 67%. The proportion of cells in S-phase in DNA aneuploid tumors was significantly higher than in DNA diploid tumors. The proportion of cells in G0G1-phase was inversely correlated to that in S-phase. After the chemotherapy, the proportions of cells in S-phase increased both in DNA diploid and aneuploid tumors, although a significantly higher mean value was found only for the latter (p < 0.05). In the DNA aneuploid tumors, there was a higher frequency of responders confirmed by histological evaluation (44%) as compared to the DNA diploid tumors (25%), and a tendency for increases in S-phase fraction of the responders to be greater than in non-responders. These results suggest that DNA flow cytometry-derived parameters may conceivably be useful in predicting the antitumor effect of 5-FU and its derivatives against large bowel cancer.

Aged↗