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Biomedical subjects

Kai Xu

Publications and source records attributed to Kai Xu.

23 records · Page 2Linked to original sources
PubMed2003

[Effect of combination of syndrome differentiation depending treatment and chemotherapy on prognostic factors in treating mid-late patients with non-small call lung cancer].

OBJECTIVE: To observe the effect of combination of Syndrome Differentiation (SD) depending treatment and chemotherapy on prognostic factors in patients with non-small cell lung cancer (NSCLC). METHODS: One hundred and twenty patients with NSCLC were randomly divided into the TCM group, the western medicine (WM) group and the combined TCM and WM (TCM-WM) group. Besides the conventional supporting and symptomatic treatment given to all the 3 groups, to the TCM group, Chinese drug medication according to patients' SD (intravenons injection, decoction or Xiaoji Decoction) was given, to the WM group chemorherapy was given, and to the TCM-WM group, all the treatment used in both TCM and WM group were given. The long-term efficacy was analyzed by Kaplan-Meier method, the 24 prognostic factors that influencing survival rate were analyzed by COX regression model multiple factors analysis to screen the risk factor and protective factor. RESULTS: The median survival period in the TCM group was 285.00 +/- 17.92 days, in the WM group was 265.00 +/- 1.80 days, insignificant difference was found between them (P > 0.05), that in the TCM-WM group was 359.00 +/- 7.00 days, which was longer than that in the above two groups with significance (P < 0.05). The half-year and 1-year survival rates in the TCM group were 84.4% and 18.1%, in the WM group 82.5% and 20.6%, and in the TCM-WM group 92.5% and 42.7%. The 1-year survival rate in the TCM-WM group was higher than that in the TCM and WM group with significant difference (P < 0.05). Analysis on 24 prognostic factors indicated that there was significant difference (P < 0.05) in influence of such factors on survival rate as clinical stage, lymph node invasion, complications, TCM Syndrome typing, lactate dehydrogenase, carcinoembryonic antigen (CEA), CA199, Karnofsky scoring before treatment, therapeutic method, total scores of quality of life, stability of treatment, CD3+, etc. The former seven were the risk factors for prognosis of midlate NSCLC patients, and the latter 5 the protective factors. CONCLUSION: TCM-WM treatment could prolong patients' survival period, elevate the long-term survival rate, it could be taken as one of the best comprehensive therapies for mid-late NSCLC patients who have missed the opportunity of surgical resection.

Adolescent↗
PubMed2002

SARA, a FYVE domain protein, affects Rab5-mediated endocytosis.

Rab5, a member of the small GTPase family of proteins, is primarily localized on early endosomes and has been proposed to participate in the regulation of early endosome trafficking. It has been reported that phosphatidylinositol 3-kinases and FYVE domain proteins, such as EEA1, can be recruited onto early endosomes and act as Rab5 effectors. SARA (Smad anchor for receptor activation), also a FYVE domain protein, was initially isolated as a participant in signal transduction from the transforming growth factor beta receptor. Overexpressed SARA has been found on EEA1-positive early endosomes. In this report, we show that endogenous SARA is present on early endosomes and overexpression of SARA causes endosomal enlargement. Functionally, SARA overexpression significantly delays the recycling of transferrin. The transferrin receptor distributed on the cell surfaces was also greatly reduced in cells overexpressing SARA. However, the internalization rate of transferrin is not affected by SARA overexpression. The morphological and functional alterations caused by SARA overexpression resemble those caused by overexpression of Rab5:GTP mutant Rab5Q79L. Finally, all SARA-mediated phenotypic changes can be counteracted by overexpression Rab5:GDP mutant Rab5S34N. These results collectively suggested that SARA plays an important functional role downstream of Rab5-regulated endosomal trafficking.

Carrier Proteins↗
PubMed2002

A novel single tetracycline-regulative adenoviral vector for tumor-specific Bax gene expression and cell killing in vitro and in vivo.

Using a binary adenoviral system, we recently showed that the human telomerase reverse transcriptase (hTERT) promoter induces tumor-specific Bax gene expression. However, the strong cytotoxicity of Bax and other pro-apoptotic genes to packaging 293 cells has so far hindered construction of the desired single adenoviral vectors expressing toxic genes. We report here the construction of a single bicistronic adenoviral vector for tumor-specific Bax expression. The vector (Ad/gBax) utilizes the Tet-Off system and expresses a GFP/Bax fusion protein for easy detection. The hTERT promoter drives the expression of tTA, a transactivator capable of binding to TRE (tetracycline-responsive element) in the absence of tetracycline, which in turn induces expression of the GFP-Bax gene. The addition of tetracycline in 293 cells blocks the binding of tTA to TRE and substantially inhibits GFP-Bax expression and toxicity, thus allowing the packaging and production of Ad/gBax. Our data show that Ad/gBax could drive the high expression of GFP-Bax in tumor cells but not in normal cells and mouse tissues. Furthermore, the expression of GFP-Bax fusion protein elicited tumor-specific apoptosis in a variety of human cancer cells in vitro and in vivo at a level comparable to that induced by the binary system. Thus, Ad/gBax may become a potent therapeutic agent for the treatment of cancers.

Adenoviridae↗
PubMed2002

Expression of several genes in the human chromosome 3p21.3 homozygous deletion region by an adenovirus vector results in tumor suppressor activities in vitro and in vivo.

A group of candidate tumor suppressor genes (designated CACNA2D2, PL6, 101F6, NPRL2, BLU, RASSF1, FUS1, HYAL2, and HYAL1) has been identified in a 120-kb critical tumor homozygous deletion region (found in lung and breast cancers) of human chromosome 3p21.3. We studied the effects of six of these 3p21.3 genes (101F6, NPRL2, BLU, FUS1, HYAL2, and HYAL1) on tumor cell proliferation and apoptosis in human lung cancer cells by recombinant adenovirus-mediated gene transfer in vitro and in vivo. We found that forced expression of wild-type FUS1, 101F6, and NPRL2 genes significantly inhibited tumor cell growth by induction of apoptosis and alteration of cell cycle processes in 3p21.3 120-kb region-deficient (homozygous) H1299 and A549 cells but not in the 3p21.3 120-kb region-heterozygous H358 and the normal human bronchial epithelial cells. Intratumoral injection of Ad-101F6, Ad-FUS1, Ad-NPRL2, and Ad-HYAL2 vectors or systemic administration of protamine-complexed vectors significantly suppressed growth of H1299 and A549 tumor xenografts and inhibited A549 experimental lung metastases in nu/nu mice. Together, our results, coupled with other studies demonstrating a tumor suppressor role for the RASSSF1A isoform, suggest that multiple contiguous genes in the 3p21.3 120-kb chromosomal region may exhibit tumor suppressor activity in vitro and in vivo.

Adenoviridae↗