PubMed · 12072820
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Maureen J O'Sullivan, Louis P Dehner, Peter A Humphrey, John D Pfeifer. 2002. Transcripts, transcripts, everywhere.. https://doi.org/10.1097/00125480-200207000-00009
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Previous analysis of tumor-specific constitutional LOH had identified a putative tumor-suppressor gene (LOH18CR) active in osteosarcoma tumorigenesis, which mapped to a subregion of chromosome 18q linked to both familial Paget's disease and FEO. Using 9 new polymorphic loci within the previous minimal region of LOH, we have reduced the minimal region of LOH in osteosarcoma tumors to localize the LOH18CR locus to the distal end of chromosome 18q21.33. This new region is approximately 500 kb and contains at least 7 known genes; however, it excludes 2 previous candidate genes: TNFRSF11A (RANK) and BCL2.
OBJECTIVES: To call attention for necessity of the knowledge of the early symptoms of childhood cancer and for the responsibility of the parents, physicians and teachers rendering health supervision to the children and to alert that the early detection and prompt treatment is of paramount importance in achieving cures in childhood cancer. SOURCES: Literature review using Medline. SUMMARY: The diagnosis of childhood cancer is complex and many variables play an important role. Early detection and prompt therapy have the potential to reduce mortality and treatment morbidity. A better understanding of the relationship between symptoms and diagnosis is important for the development of effective public health strategies. CONCLUSIONS: There are several factors that may be associated with length of time between symptoms and diagnosis. Lag time to diagnosis depends on tumor type and age. To determine warning signs and symptoms that should alert to the possibility of malignant disease is still a challenge.
Signal transduction downstream HGF receptor (MET) activation involves multiple pathways that account for mitogenesis, motility and morphogenesis in a cell type-dependent fashion. MET receptor is aberrantly expressed in almost 100% of human osteosarcomas. We analyzed the effect of the MET receptor activation in five human osteosarcoma cell lines evaluating the levels of HGF-dependent activation of MAPK and PKB/AKT as biochemical readouts of mitogenic and invasive responses, respectively. All the cell lines tested expressed high levels of the MET proto-oncogene. Four cell lines showed activation of the MAPK cascade upon HGF stimulation, suggesting that this growth factor serves a common proliferative function in osteosarcomas. Two lines showed activation of PKB/AKT that is known to be involved in migration mediated by HGF receptor. Accordingly, cell lines where MAPK cascade was activated responded to HGF with increased proliferation, while induction and inhibition of PKB/AKT activity corresponded to acquisition or block of the invasive-motile response to HGF, respectively. Both the HGF dependent responses were reverted by the specific MET inhibitor K252a. These data show that HGF activates both the mitogen and motogen machinery in osteosarcoma cells and suggest that HGF might promote their malignant behavior by concomitant activation of different pathways and biological functions.