We have confirmed the profound anti-tumour effect of imatinib in DFSP harbouring t(17;22) with long-term responses. Imatinib therapy may in some cases lead to tumour resectability of lesser disfiguration.

This analysis showed that melanoma patients ≥ 65 years of age are characterized by a higher primary tumor stage and worse prognosis in the presence of regional node metastases than younger patients. Additionally, the results indicate that the same radical surgical therapy is necessary for patients ≥ 65 years old as in younger patients.

Gastrointestinal stromal tumors (GISTs) comprise a recently defined entity of the most common mesenchymal neoplasms of the gastrointestinal tract. Advances in the understanding of the molecular mechanisms of GIST pathogenesis have resulted in the development of a treatment approach which has become a model of targeted therapy in oncology. The introduction of imatinib mesylate (inhibiting KIT/PDGFRA (platelet-derived growth factor receptor-alpha) and their downstream signaling cascade) has revolutionized the therapy of advanced (inoperable and/or metastatic) GISTs. Imatinib has now become the standard of care in the treatment of patients with advanced GIST. However, a majority of patients eventually develop clinical resistance to imatinib. Over the last few years major progress has been made in elucidating the mechanism of disease progression (as secondary mutations in KIT and/or PDGFRA kinase domains) and resistance to imatinib. Currently, the sole approved second-line drug is sunitinib--a multitargeted agent, an inhibitor of tyrosine kinase, of KIT and PDGFRA/B and of the vascular endothelial growth factor receptors (VEGFRs)-1, -2 and 3, FMS-like tyrosine kinase-3 (FLT3), colony stimulating factor 1 receptor (CSF-1R), and glial cell-line derived neurotrophic factor receptor (REarranged during Transfection; RET). However, a number of new generation tyrosine kinase inhibitors, alone or in combination, are being evaluated at present alongside treatment options alternative to inhibiting the KIT signaling pathway (as heat shock protein 90 or mammalian target of rapamycin). This article discusses the factors relating to imatinib resistance as well as upcoming potentially effective treatment options for patients with progressive disease available in 2008 and those under investigation with more individualized treatment methods, which has been recently patented. This review focuses on the current achievements in targeted therapy of advanced GISTs, and how the insight into the resistance mechanisms may allow in the near future to treat patients with advanced GISTs.

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The aim of the study was to analyse coagulation disorders in patients with locally advanced cancer of the head and neck (CHN)and with no other clinical cause for coagulation disorders treated with radiation therapy alone or concurrent chemoradiotherapy. We also assessed the duration of disorders in the course of therapy.The analysed group consisted of 33 patients with locally advanced CHN documented as stage T3 or T4 acc. to the TNM classification. Coagulology tests (activated partial thromboplastic time /APTT/, prothrombin time, fibrinogen concentration, euglobulin lysis time, C -reactive protein and anti-thrombin III concentration, d-dimer level, PAI-1, plasminogen level and plasmin-anti-plasmin assays) were performed before, during and after the completion of treatment.In all cases pre-tratment abnormal fibrinolysis was observed. We observed elevated PAI-1 levels in all blood tests regardless of the treatment stage, while elevated plasminogen concentration and euglobulin lysis time was observed in a majority of tests. Increased PAI-1 level persisted independently of tumor regression during treatment. Half of our patients also presented with a tendency towards shortened APTT. One patient had a significantly higher d-dimer level at the end of the treatment. Decreased APTT was the sole factor influencing overall survial (OS) confirmed in multivariate analysis (Cox's proportinal hazard model). Despite the occurence of abnormal fibrinolysis and decreased APTT, we did not observe an increased risk of coagulation disorders.We conclude that among caogulation tests only a decrease in APTT is, at present, a stasistically confirmed predective factor of shorter OS in CHN patients. Autothrombotic prophylactic treatment may be an effective option in this clinical setting. There is need for further studies on large patient groups.