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Letters to the Editor |
1 Department of Clinical Chemistry/564, UMC Nijmegen, PO Box 9101, 6500HB Nijmegen, The Netherlands, Fax 31-243541743, E-mail j.dekok{at}akc.umcn.nl
To the Editor:
I read with interest the reports by Klaassen et al. (1) and Boynton et al.(2) published in the July issue of Clinical Chemistry. The first study demonstrated increased amounts of human DNA in the feces of patients with colorectal tumors compared with healthy persons (1), and the second study showed that the majority of DNA isolated from the stools of patients with colorectal tumors was of high molecular weight, in contrast to the fragmented apoptotic DNA found in stools from colonoscopy-negative patients (2). The authors hypothesized that this intact DNA originated from tumor cells because physiologically shed healthy mucosa cells are apoptotic, leading to nucleosomal DNA fragmentation.
The authors of both studies, however, did not discuss a frequently occurring phenomenon in patients with colorectal cancer, i.e., bleeding from the tumor into the lumen of the gut. This bleeding is the basis of the fecal occult blood test, a very simple and inexpensive method used as an indirect (but not very specific) tumor marker. During bleeding, leukocytes with high-molecular-weight DNA are also introduced into the feces. This DNA may still be intact in stool, especially when the site of the bleeding is in the distal part of the colon. The sensitivities and specificities reported in both studies closely resembled those of the immunochemical fecal occult blood tests (50% and 95%, respectively) that were also performed in patients with adenomas >1 cm (3). Increased concentrations of stool DNA were detected in patients with tumors in the distal part of the colon, but not in patients with tumors in the proximal part (1). This supports the suggestion that the increased amounts of (intact) DNA in stool originate mainly from blood and not from nuclease-resistant tumor cells. Even in the one patient with a tumor in the ileum (2), the presence of other sites of bleeding as the origin of intact fecal DNA (e.g., hemorrhoids) cannot be excluded.
In my opinion, both studies present a complex and expensive method to demonstrate bleeding in colorectal cancer patients. Any bleeding in the distal part of the colon obscures the specificity of the presented methods, and the only specific method to detect the presence of malignant cells (i.e., DNA) in stool is the demonstration of tumor-derived DNA alterations, which was unfortunately not performed in these studies.
References
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