[Error in an article on rectal cancer].
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Humans↗
Biomedical subjects
Steffen Bülow
Publications and source records attributed to Steffen Bülow.
VEGF concentrations in tumour arteries and veins from patients with rectal cancer.
This pilot study investigated the hypothesis that the tumour itself is the source of the elevated vascular endothelial growth factor (VEGF) concentrations which are often observed in peripheral blood from patients with rectal cancer. Twenty-four consecutive patients with primary rectal cancer were included. Blood samples were drawn preoperatively from peripheral veins (I) and intraoperatively from peripheral veins (II), tumour arteries (III), and tumour veins (IV). In the four compartments, VEGF concentrations were measured in serum, EDTA plasma, and supernatants from lysed whole blood. Additionally, automated complete white cell and platelet counts were performed. In serum and EDTA plasma, no significant differences in VEGF concentrations were observed (p = 0.1 and p = 0.5), respectively) between tumour arteries and tumour veins. However, in supernatants from lysed blood, VEGF concentrations were significantly (p = 0.03) lower in venous blood than in arterial blood. Unexpectedly, a 16% reduction (p < 0.0001) in the number of neutrophils was observed during transit of the arterial blood through the rectal tumours, while none of the other types of leukocytes or platelets was significantly reduced in numbers during the same passage. These findings indicate that the tumour itself is not the only source of elevated VEGF concentrations in peripheral blood from patients with rectal cancer. A consistent finding was that a large number of neutrophils disappeared from the blood during passage through the rectal tumour. However, the significance and fate of the migrating neutrophils cells are unknown and should be investigated further.
Adult↗
De novo mutations in familial adenomatous polyposis (FAP).
Familial Adenomatous Polyposis (FAP) results from a germline mutation in the APC gene. A new mutation rate of 4-9 x 10(-6) mutations/gametes/generation has been reported. In other familial cancer syndromes a bias for paternal origin of new mutations has been described. This bias is probably due to a larger number of cell divisions during spermatogenesis compared to oogenesis; giving a larger susceptibility for mutagenesis. We report here a molecular genetic analysis of 26 FAP patients with putative de novo APC mutations. In 15 families the novel origin of the mutations was confirmed by haplotyping and sequencing. Analysis of 10 of these mutations, in which the parental origin could be established, gave a 6 : 4 distribution in favour of maternal origin. This is in agreement with a 1 : 1 distribution and does not indicate an expected paternal bias. Moreover, no parental age effect was identified. We propose that APC germline mutations are not premeiotic events but more likely arise during the meiosis. This would give an equal susceptibility for mutagenesis during spermatogenesis and oogenesis, respectively. The model is in concordance with the previously established difference between APC somatic mutations, as being a mitotic event and APC germline mutations, as being a meiotic event. The confirmation of 15 de novo mutations by a molecular genetic approach is in fine agreement with previous results based on clinical records.
Adenomatous Polyposis Coli↗