Renal cell carcinoma (RCC) comprises 3–4% of all malignant tumours among adults in Poland. Spontaneous regression of RCC is a rare but well-known phenomenon. Its frequency is estimated to be approximately 1% and a large part of the percentage is accounted for by the regression of pulmonary metastases in the course of clear type of RCC treatment. We searched PubMed, Embase and SciVerse Scopus databases, identifying 59 case reports of spontaneous regression of RCC. Those medical histories come from reports from around the world and date back up to 40 years. This review includes their analysis as well as description of possible explanations of this phenomenon postulated by different authors, including both misdiagnosis and immunological reactions. This study indicates that reliable diagnostics and reporting of all the cases of spontaneous regression play a key role, as this is the only method which enables a better perspective in understanding this issue.

The synchronous occurrence of GISTs and other gastrointestinal malignancies is more common than it has been considered. The development of gastrointestinal stromal tumors and other neoplasms may involve the same carcinogenic agents.

A soluble complement inhibitor factor H (FH) and its splice variant factor H-like protein (FHL) have been recently discovered to play a major role in malignant cell escape from complement-mediated cytotoxicity in lung-, ovarian-and glia-derived neoplasms. The role of FH in colon cancer has not yet been examined. Here, we studied immunocytochemically FH/FHL expression in tumor samples derived from 40 patients, with both primary colon adenocarcinoma and metastatic foci in the liver. FH/FHL immunoreactivity was present in stroma of both primary and metastatic tumors, in virtually all patients. The cellular immunoreactivity was observed infrequently. Importantly, when analyzed quantitatively, FH/FHL immunoreactivity was significantly increased in liver metastases when compared with the primary sites. In addition, we have analyzed FH and FHL expression in 5 colon cancer cell lines: SW480, SW620, HCT116, HT-29 and Lovo. FH mRNA and FH secretion were observed in SW620 and HT-29 cells, whereas FHL was produced only by HT-29 cell-line. By confocal and electron microscopy, FH immunoreactivity was associated with the plasma membrane and intracellular vesicular structures. Finally, we have analyzed the role of FH in the susceptibility of SW620 colon cancer cells to complement-mediated damage. When FH function was blocked, using specific antibody, the cells became more susceptible to lysis. Taken together, our results suggest an important role of FH/FHL in colon cancer cells defense against complement-mediated cytotoxicity, and in metastatic process. ' 2008 Wiley-Liss, Inc.Key words: factor H; colon cancer; metastasis; immunotherapy; complement Although recent years have brought many advances in clinical oncology, colon cancer is still a serious problem. Surgical resection remains as the most efficient treatment, but its results are often not satisfactory. Sixty percent of patients with colon cancer develop liver metastases, which, for a third of those, is the main and only metastatic site. About 25% of the patients have potentially resectable hepatic metastases, but at least half of them have recurrence after surgery. 1 Unfortunately, for a large group of patients, radical surgery is impossible. For about 60% of such patients, advanced chemo-and radiotherapy allows for a 5-year survival, however a major objection to this kind of treatment is severe side effects. 2 To improve disease-free survival, overall survival and to prevent formation of metastases, new strategies for effective treatment should be considered.

Osteosarcoma (OS) remains the most common malignancy among orthopaedic neoplasms. Despite advanced surgical techniques and attempts to use second-line chemotherapy, 5 year overall survival in OS patients is still reported to be as low as 60-70%. Progression to metastatic disease is the main cause of treatment failures. Broadening current knowledge on the pathogenesis and biology of metastatic OS tumors is a key element in improving treatment results, i.e. identifying potential therapeutic targets. Recent studies have brought new concepts into this field. This paper outlines the most important issues which may influence treatment methods in the near future. In a few sections, we discuss (1) a model of OS dissemination with special regard to proteins mediating the lysis of the extracellular matrix; (2) the mechanisms protecting circulating OS cells from programmed death; (3) the relationship between angiogenesis, its pathogenesis, and OS metastatic potential; (4) the role of cytokines in OS progression and site-specific metastasis formation; (5) an example of treatment resistance mechanism - the P glycoprotein efflux pump; and, finally, we theorize on (6) whether cancer stem cells may play a role in OS progression.

Abstract. The Deleted in Liver Cancer (DLC) protein family comprises proteins that exert their function mainly by the Rho GTPase-activating protein (GAP) domain and by regulation of the small GTPases. Since Rho GTPases are key factors in cell proliferation, polarity, cytoskeletal remodeling and migration, the aberrant function of their regulators may lead to cell transformation. One subgroup of these proteins is the DLC family. It was found that the first identified gene from this family, DLC1, is often lost in hepatocellular carcinoma and may be involved as a tumor suppressor in the liver. Subsequent studies evaluated the hypothesis that the DLC1 gene acts as a tumor suppressor, not only in liver cancer, but also in other types of cancer. Following DLC1, two other members of the DLC protein family, DLC2 and DLC3, were identified. However, limited published data are available concerning the role of these proteins in malignant transformation. This review focuses on the structure and the role of DLC1 and its relatives in physiological conditions and summarizes data published thus far regarding DLC function in the neoplastic process.