[Necessity of No.13 lymph node dissection in advanced gastric carcinoma].

OBJECTIVE: To investigate the feasibility and necessity of No.13 lymph node dissection for advanced gastric carcinoma. METHODS: Clinical data of 144 cases who were diagnosed as TNMII-III stage gastric carcinoma were collected from January 2007 to December 2009 in the Department of General Surgery at the First Affiliated Hospital of Nanchang University. Seventy-two cases who received D2 radical gastrectomy plus No.13 lymph node dissection were selected as the study group, and they were matched 1:1 to 72 cases who received D2 Radical gastrectomy (the control group) for TNMII-III stage gastric carcinoma. The differences in the intraoperative and postoperative parameters and survival time were compared, and the factors associated with No.13 lymph node metastasis were analyzed. RESULTS: There were no significant differences between the two groups in operative time [(2.8 ± 0.4) h vs. (2.7 ± 0.4) h], blood loss [(191.9 ± 81.5) ml vs. (186.0 ± 81.7) ml], the incidence of postoperative complications (18.1% vs. 15.3%), length of hospital stay [(12.3 ± 4.2) d vs. (11.9 ± 3.2) d] and 3-year survival rate (63% vs. 57%) (all P>0.05). In the study group, there were 15 patients (20.8%) with positive No.13 lymph nodes, and the 3-year survival rate was 13%, significantly lower compared to those with negative No.13 lymph node (73%, n=57) (P<0.05). Multivariate analysis showed that N stage (P<0.01) and histological type (P<0.05) were independently associated with No.13 lymph node metastasis. CONCLUSION: No.13 lymph node dissection for TNMII-III stage gastric cancer is feasible and necessary.

Isolation of a novel member of small G protein superfamily and its expression in colon cancer.

AIM: APMCF1 is a novel human gene whose transcripts are up-regulated in apoptotic MCF-7 cells. In order to learn more about this gene's function in other tumors, we cloned its full length cDNA and prepared its polyclonal antibody to investigate its expression in colon cancers with immunohistochemistry. METHODS: With the method of 5' rapid amplification of cDNA end (RACE) and EST assembled in GenBank, we extended the length of APMCF1 at 5' end. Then the sequence encoding the APMCF1 protein was amplified by RT-PCR from the total RNA of apoptotic MCF-7 cells and cloned into the prokaryotic expression vector pGEX-KG to construct recombinant expression vector pGEX-APMCF1. The GST-APMCF1 fusion protein was expressed in E. coli and used to immunize rabbits to get the rabbit anti-APMCF1 serum. The specificity of polyclonal anti-APMCF1 antibody was determined by Western blot. Then we investigated the expression of Apmcf1 in colon cancers and normal colonic mucosa with immunohistochemistry. RESULTS: A cDNA fragment with a length of 1 745 bp was obtained. APMCF1 was mapped to chromosome 3q22.2 and spanned at least 14.8 kb of genomic DNA with seven exons and six introns contained. Bioinformatic analysis showed the protein encoded by APMCF1 contained a small GTP-binding protein (G proteins) domain and was homologous to mouse signal recognition particle receptor beta(SRbeta). A coding region covering 816 bp was cloned and polyclonal anti-APMCF1 antibody was prepared successfully. The immunohistochemistry study showed that APMCF1 had a strong expression in colon cancer. CONCLUSION: APMCF1 may be the gene coding human signal recognition particle receptor beta and belongs to the small-G protein superfamily. Its strong expression pattern in colon cancer suggests it may play a role in colon cancer development.