Somatic mutations in FAT cadherin family members constitute an underrecognized subtype of colorectal adenocarcinoma with unique clinicopathologic features.

Background: The FAT cadherin family members (FAT1, FAT2, FAT3 and FAT4) are conserved tumor suppressors that are recurrently mutated in several types of human cancers, including colorectal carcinoma (CRC).

Aim: To characterize the clinicopathologic features of CRC patients with somatic mutations in FAT cadherin family members.

Methods: We analyzed 526 CRC cases from The Cancer Genome Atlas PanCancer Atlas dataset.

In situ magnetic separation and immobilization of dibenzothiophene-desulfurizing bacteria.

In situ cell separation and immobilization of bacterial cells for biodesulfurization were developed by using superparamagnetic Fe(3)O(4) nanoparticles (NPs). The Fe(3)O(4) NPs were synthesized by coprecipitation followed by modification with ammonium oleate. The surface-modified NPs were monodispersed and the particle size was about 13 nm with 50.

pH neutralization while succinic acid adsorption onto anion-exchange resins.

Succinic acid is a useful chemical and its purification from fermentation broth by ion-exchange resins has widely drawn attention. In this study, pH neutralization in the process of adsorption of succinic acid from model solutions and fermentation broth by anion-exchange resin NERCB 04 has been tested. Adsorption capacity of NERCB 04 was about 0.

[Comparison of the desulfurization activity among several bacteria and analysis of the conservation of their desulfurization genes].

Several bacteria, Bacillus brevis R-6, Pseudomonas delafleldii R-8, Nocardia globerula R-9, Bacillus sphaericus R-16, Rhodococcus erythropolis LSSE8-1 and Gordonia nitida LSSEJ-1, which can convert dibenzothiophene into 2-hydroxybiphenyl and sulfate, were investigated. Desulfurization products were quantitively determined by HPLC. Result revealed that each of these bacteria desulfurize DBT at a different rate.

Study on blocking the leukemia immune escape after BMT by Fas-Fas ligand pathway.

Background: To investigate if bone marrow transplantation (BMT) with bone marrow mononuclear cells (BMMCs) transducted with murine soluble Fas gene (sFas) using adenovirus vector could block the immune escape of leukemia cells eliminate the residual leukemia cells and reduce their relapse.

Methods: The recombinant adenovirus vector with murine sFas, adsFas, and the control vector adEGFP were constructed using homologous recombination between two plasmids in Escherichia coli. BMT was carried out after the BMMCs were infected with Adenoviruses.

[Study on blocking the tumor immune escape by Fas ligand pathway].

The expression of Fas ligand (FasL) on the membrane of many kinds of leukemia or solid tumor cells played an important role in the immune escape of tumor cells. This study was aimed to know if the soluble Fas (sFas), expressed by adenovirus, could block the immune escape of tumor cells by FasL pathway. The two recombinant adenoviral vectors, AdsFas with murine soluble Fas gene and AdEGFP with enhanced GFP protein gene, were constructed by homologous recombination between two plasmids in Escherichia coli with the AdEasy adenovirus vector system.

[Retroviral vector-mediated in vitro expression of human soluble fas].

Leukemic cells from patients expressed high level FasL cause apoptosis of autologous activated T cells via the Fas/FasL pathway. To investigate the role of soluble Fas (sFas) in reversing this process, a retroviral-mediated expression vector pLXIN-sFas was established. A retroviral-mediated expression system of human sFas was established in vitro and the biological activity of the expression product sFas was observed.

[Study on expression and function of fas ligand in human myeloid leukemia cells].

To determine whether the Fas receptor-Fas ligand (FasR-FasL) system, which triggers apoptosis in sensitive cells, is an important mechanism of cytotoxicity in myeloid leukemia. FasL expression was investigated in myeloid leukemia cells and its upregulation by a combination of IL-2 and INF-gamma, +/- as well as its function of inducing Jurkat cells to apoptosis mainly by flow cytometry (FCM). Results showed that leukemia cells expressed more FasL (3.