TIP27 has an important role in glucose homeostasis through the regulation of hepatic glucose metabolism and insulin sensitivity. Furthermore, this regulation requires activation of PI3-kinase.

HLA-haploidentical hematopoietic SCT (HSCT) is an option for severe aplastic anemia (SAA) patients. Here, we evaluated the outcomes of 26 adult-SAA patients who received HLA-haploidentical HSCT in five transplant centers in southwestern China. Most of the patients in this study failed prior therapy and were transfused heavily before the transplantation. The patients received fludarabine þ cyclophosphamide þ antithymocyte globulin as conditioning regimens and then unmanipulated peripheral blood plus marrow transplantation. Micafungin, i.v. Ig and recombinant human TPO were used for post-grafting infection prevention and supportive care. Of 26 patients, 25 achieved engraftment at a median of 13 days (range, 11-19 days) after HSCT. One of 25 patients experienced graft rejection and did not achieve sustained engraftment after second HSCT. Therefore, the final engraftment rate was 92.3%. Three of 25 (12%) patients developed acute GVHD, 10 of 25 (40%) patients developed chronic GVHD (9 with limited whereas the other with extensive). The OS rate was 84.6% and the average follow-up time was 1313.2 (738-2005) days for surviving patients. This encouraging result suggests that HLA-haploidentical HSCT is an effective therapeutic option for adults with acquired SAA if an HLA-identical donor is not available.

Glypican-5 (GPC5) is a member of the heparin sulfate proteoglycans. Previous studies of GPC5 in lung tumorigenesis showed conflicting results. In this study, we confirmed that GPC5 was downregulated in lung adenocarcinoma tissues compared with adjacent normal lung tissues. The low expression of GPC5 was significantly associated with poor outcome in lung adenocarcinoma. To understand the biological mechanism of the downregulation, we examined the promoter methylation status of GPC5 gene. We found that GPC5 was significantly hypermethylated in lung cancer tissues and lung cancer cell lines compared with normal lung tissues. The methylation level of GPC5 was negatively correlated with its transcriptional expression. De-methylation experiments further confirmed that the loss of GPC5 expression was regulated by its hypermethylation. Overexpression of GPC5 inhibited proliferation, migration and invasion of lung cancer cells in vitro, and repressed tumor growth in vivo, whereas knockdown of GPC5 was able to reverse the effect. Furthermore, we demonstrated that GPC5 could suppress the Wnt/β-catenin signaling by binding to Wnt3a at the cell surface, which mediated its function as a tumor suppressor. Overall, these findings demonstrate that GPC5 is a novel epigenetically silenced tumor suppressor, which inhibits tumor growth by suppressing Wnt/β-catenin signaling in lung adenocarcinoma. Our findings substantially expand our understanding about the role and the molecular mechanism of GPC5 in tumorigenesis of lung cancer.

a report of three cases. Haematologia (Budap) 1989; 22: 195-199 They used semiquantitative RT-PCR technique to study the expression levels of ASPP members in a panel of paired normal and tumor RNA samples derived from breast cancer patients. The results showed that the expression levels of ASPP1 and ASPP2 were downregulated in 60% of human breast tumors expressing wild-type p53. Eight tumors expressing wild-type p53 overexpressed iASPP relative to their normal paired controls, whereas seven of these tumors showed normal levels of ASPP1 and ASPP2.Wild-type p53 exists in 95% of leukemias. 5 How this kind of cancer arose despite its being in possession of intact, functional p53? The discovery of ASPP family might clear up this mystery. To understand the status of ASPP members in leukemia, we investigated the expression levels of ASPP members in three leukemia cancer cell lines HL-60, K562 and Jurkat (Table 1). The results showed that the level of ASPP1 is downregulated and that of the iASPP is upregulated. Our results suggest that abnormal ASPP expression could be an important step in the genesis of human hematopoietic neoplasms and might be a useful molecular marker for diagnosis of leukemia.These results, together with the research of Lu and coworkers in breast cancer, suggest that new ASPP family is not only important in breast cancer, but also in leukemia, and may be important in many other kinds of human cancers.