Excessive collagen turnover products are released during colorectal cancer progression and elevated in serum from metastatic colorectal cancer patients

During cancer progression, the homeostasis of the extracellular matrix becomes imbalanced with an excessive collagen remodeling by matrix metalloproteinases. As a consequence, small protein fragments of degraded collagens are released into the circulation. We have investigated the potential of protein fragments of collagen type I, III and IV as novel biomarkers for colorectal cancer. Specific fragments of degraded type I, III and IV collagen (C1M, C3M, C4M) and type III collagen formation (Pro-C3) were assessed in serum from colorectal cancer patients, subjects with adenomas and matched healthy controls using well-characterized and validated ELISAs. Serum levels of the biomarkers were significantly elevated in colorectal cancer patients compared to subjects with adenomas (C1M, Pro-C3, C3M) and controls (C1M, Pro-C3). When patients were stratified according to their tumour stage, all four biomarkers were able to differentiate stage IV metastatic patients from all other stages. Combination of all markers with age and gender in a logistic regression model discriminated between metastatic and non-metastatic patients with an AUROC of 0.80. The data suggest that the levels of these collagen remodeling biomarkers may be a measure of tumour activity and invasiveness and may provide new clinical tools for monitoring of patients with advanced stage colorectal cancer

Intrinsic quadrupole moment of the nucleon

We address the question of the intrinsic quadrupole moment Q_0 of the nucleon in various models. All models give a positive intrinsic quadrupole moment for the proton. This corresponds to a prolate deformation. We also calculate the intrinsic quadrupole moment of the Delta(1232). All our models lead to a negative intrinsic quadrupole moment of the Delta corresponding to an oblate deformation.Comment: 17 pages, 5 figure

Genetic diversity in three invasive clonal aquatic species in New Zealand

<p>Abstract</p> <p>Background</p> <p><it>Elodea canadensis, Egeria densa </it>and <it>Lagarosiphon major </it>are dioecious clonal species which are invasive in New Zealand and other regions. Unlike many other invasive species, the genetic variation in New Zealand is very limited. Clonal reproduction is often considered an evolutionary dead end, even though a certain amount of genetic divergence may arise due to somatic mutations. The successful growth and establishment of invasive clonal species may be explained not by adaptability but by pre-existing ecological traits that prove advantageous in the new environment. We studied the genetic diversity and population structure in the North Island of New Zealand using AFLPs and related the findings to the number of introductions and the evolution that has occurred in the introduced area.</p> <p>Results</p> <p>Low levels of genetic diversity were found in all three species and appeared to be due to highly homogeneous founding gene pools. <it>Elodea canadensis </it>was introduced in 1868, and its populations showed more genetic structure than those of the more recently introduced of <it>E. densa </it>(1946) and <it>L. major </it>(1950). <it>Elodea canadensis </it>and <it>L. major</it>, however, had similar phylogeographic patterns, in spite of the difference in time since introduction.</p> <p>Conclusions</p> <p>The presence of a certain level of geographically correlated genetic structure in the absence of sexual reproduction, and in spite of random human dispersal of vegetative propagules, can be reasonably attributed to post-dispersal somatic mutations. Direct evidence of such evolutionary events is, however, still insufficient.</p