DNp73 exerts function in metastasis initiation by disconnecting the inhibitory role of EPLIN on IGF1R-AKT/STAT3 signaling.

Dissemination of cancer cells from primary tumors is the key event in metastasis, but specific determinants are widely unknown. Here, we show that DNp73, an inhibitor of the p53 tumor suppressor family, drives migration and invasion of nonmetastatic melanoma cells. Knockdown of endogenous DNp73 reduces this behavior in highly metastatic cell lines.

E2F1 in melanoma progression and metastasis.

Metastases are responsible for cancer deaths, but the molecular alterations leading to tumor progression are unclear. Overexpression of the E2F1 transcription factor is common in high-grade tumors that are associated with poor patient survival. To investigate the association of enhanced E2F1 activity with aggressive phenotype, we performed a gene-specific silencing approach in a metastatic melanoma model.

Spectrum and antibiotic resistance of uropathogens from hospitalised patients with urinary tract infections: 1994-2005.

From 1994-2005, all uropathogens cultured from the urine of hospitalised urological patients were identified and their sensitivity was tested against the most important antibiotics for the treatment of urinary tract infection (UTI). Duplicate isolates were eliminated. The following results were obtained: (i) there was no general trend of increase in resistance; (ii) certain uropathogens developed resistance to some antibiotics; (iii) vancomycin- or linezolid-resistant staphylococci or enterococci did not play a role; (iv) the lowest overall rates of resistance were found with piperacillin/tazobactam; and (v) ciprofloxacin and trimethoprim/sulfamethoxazole showed the next favourable overall activity.

Mutational analysis of Chk1, Chk2, Apaf1 and Rb1 in human malignant melanoma cell lines.

Four tumour suppressor genes (Chk1, Chk2, Apaf1 and Rb1) in nine human malignant melanoma cell lines were screened for a loss of gene expression, point mutations and small deletions/insertions by cDNA-based DGGE/SCCP analysis. In two cell lines alterations of the investigated genes could be demonstrated. This result confirms our assumption of the participation of dysfunctional p53 inducer/effector genes in human melanoma aetiology.

Adenovirus-mediated TA-p73beta gene transfer increases chemosensitivity of human malignant melanomas.

Malignant melanoma is the most aggressive form of skin cancer and has proven to be highly resistant to conventional chemotherapy. Intriguingly, the p53 tumor suppressor, a main mediator of chemoresistance in other tumor types, is rarely mutated in melanoma. However, we have previously shown that anti-apoptotic isoforms of p73 (deltaTA-p73), another member of the p53 family, are overexpressed in metastatic melanomas.