Pleistocene genetic legacy suggests incipient species of Sebastes mentella in the Irminger Sea.

To investigate a possible speciation event within the redfish (Sebastes mentella) complex in the Irminger Sea, we examined genetics, traditional morphology, geometric morphometrics and meristics of individuals sampled throughout the Sea. Tissue samples from 1901 fish were collected in 1995 and 1996 and from 1999 to 2002, and the fish were genotyped at nine microsatellite loci, two of which were developed for this study. Individual-based genetic analyses showed that two different gene pools exist in the Irminger Sea. Although these groups overlap extensively geographically, they segregate according to depth: those above and below 550 m. This signal of genotype distinction with depth was evident in both the earlier and later sampling. Historical imprints in the genetic data indicated that the redfish in the Irminger Sea are likely to represent a case of an incipient speciation event that began in allopatry during the Pleistocene glaciations followed by secondary contact. Although hybridization was observed between groups, an analysis of traditional and geometric morphometrics and of meristic variables suggested that restricted gene flow between the currently parapatric deep- and shallow-mesopelagic incipient species may be maintained by ecological isolation mechanisms.

TP53 mutations and abnormal p53 protein staining in breast carcinomas related to prognosis.

Abnormalities in the TP53 tumour suppressor gene were evaluated in 106 unselected breast carcinomas and compared to clinical outcome of the disease. Tumours were screened for p53 abnormalities using immunohistochemical staining and polymerase chain reaction-constant denaturant gel electrophoresis (PCR-CDGE) analysis, followed by PCR and direct sequencing. Allelic loss at the TP53 locus was determined with polymorphic markers by comparing normal and tumour DNA. For approximately half of the patients, abnormal p53 protein expression in serum was determined by an ELISA assay. p53 abnormalities, detected as mutations and/or nuclear staining, were found in 37.6 (38/101) of cases. Nuclear staining for p53 protein could be identified in 33.7% of the tumours. Mutations in exons 5-8 were detected in 18.9% of the tumours, and an association was found between mutations and nuclear staining. Allelic loss in the TP53 region on 17p was more frequent in tumours showing changes in the TP53 gene (72.7%) compared to tumours with no mutation (45.8%). Serum levels of p53 antibodies showed no association with either TP53 mutations or nuclear staining. Women with TP53 mutations in their tumours had an elevated risk of dying during the study period (RR (relative risk) = 3.4, P = 0.014). The effects of p53 positive staining were similar (RR = 3.2, P = 0.013). Considering all abnormalities, mutation and/or staining, the relative risk of dying from breast cancer was 3.5 (P = 0.008).