Artificial Downregulation of Ribosomal Protein L34 Restricts the Proliferation and Metastasis of Colorectal Cancer by Suppressing the JAK2/STAT3 Signaling Pathway.

The highly conserved ribosomal protein L34 (RPL34) has been reported to play an essential role in the progression of diverse malignancies. RPL34 is aberrantly expressed in multiple cancers, although its significant in colorectal cancer (CRC) is currently unclear. Here, we demonstrated that RPL34 expression was higher in CRC tissues than in normal tissues. Upon RPL34 overexpression, the ability of proliferation, migration, invasion, and metastasis of CRC cells were significantly enhanced in vitro and in vivo. Furthermore, high expression of RPL34 accelerated cell cycle progression, activated the JAK2/STAT3 signaling pathway, and induced the epithelial-to-mesenchymal transition (EMT) program. Conversely, RPL34 silencing inhibited the CRC malignant progression. Utilizing immunoprecipitation assays, we identified the RPL34 interactor, the cullin-associated NEDD8-dissociated protein 1 (CAND1), which is a negative regulator of cullin-RING ligases. CAND1 overexpression reduced the ubiquitin level of RPL34 and stabilized RPL34 protein. CAND1 silencing in CRC cells resulted in a decrease in the ability of proliferation, migration, and invasion. CAND1 overexpression promoted CRC malignant phenotypes and induced EMT, and RPL34 knockdown rescued CAND1-induced CRC progression. In summary, our study indicates that RPL34 acts as a mediator, is stabilized by CAND1, and promotes proliferation and metastasis, in part, through the activation of the JAK2/STAT3 signaling pathway and induction of EMT in CRC.

Where is the optimal plane to mobilize the anterior rectal wall in female patients undergoing total mesorectal excision?

BACKGROUND: Since Heald proposed the total mesorectal excision (TME) procedure, the prognosis of patients with rectal cancer has been significantly improved. But Heald did not specifically describe the anterior surgical plane in female patients. And the surgical plane for mobilizing the anterior rectal wall during TME surgery in female patients remains controversial. AIM: To investigate the anatomy of the female pelvis and identify the optimal plane for mobilizing the anterior rectal wall. METHODS: We retrospectively collected surgical procedure videos and clinical data of female patients diagnosed with middle or low rectal cancer who underwent the TME procedure between January 2020 and October 2022 across six hospitals. The patients were divided into two groups based on the surgical approach used to mobilize the anterior rectal wall: The experimental group was to open the peritoneum at the lowest point of the peritonea reflection and enter the plane for mobilizing, while the control group was cut at 0.5-1 cm above the peritoneal reflection and enter another plan. Then, we compared the preoperative and postoperative information between the two groups. We also dissected and observed ten adult female pelvises to analyze the anatomic structure and compare the entry plane between the two approaches. Finally, we researched the pathological structure between the rectum and the vagina. RESULTS: Finally, 77 cases that met the criteria were included in our study. Our observations revealed that the experimental group underwent a smooth procedure, entering the plane amidst the mesorectal fascia and adventitia of the vagina, whereas the control group entered the plane between the vaginal adventitia and muscle layers. Compared to the control group, the experimental group showed a significant decrease in intraoperative bleeding [22.5 (19.5-50) mL vs 17 (5-20) mL, P = 0.01], as well as a shorter duration of hospitalization [9 (7-11.25) d vs 7 (6-10) d, P = 0.03]. Through the examination of surgical videos and cadaveric studies, we discovered that Denonvilliers' fascia is absent in females. Additionally, pathological sections further revealed the absence of Denonvilliers' fascia in females, with only loose connective tissue present between the mesorectal fascia and adventitia of the vagina. CONCLUSION: The plane amidst the mesorectal fascia and vaginal adventitia is the optimal surgical plane to mobilize the anterior rectal wall for female patients undergoing the TME procedure.

MORC4 plays a tumor-promoting role in colorectal cancer via regulating PCGF1/CDKN1A axis in vitro and in vivo.

MORC family CW-type zinc finger 4 (MORC4) possessing nuclear matrix binding domains has been observed to be involved in multiple cancer development. By digging three gene expression omnibus (GEO) gene microarrays (GSE110223, GSE110224 and GSE24514), we found that MORC4 was overexpressed in colorectal cancer (CRC) samples (log2 Fold change >1, p < 0.05). We aimed to investigate the role of MORC4 in CRC malignant behaviors, with an emphasis on polycomb group ring finger 1 (PCGF1)/cyclin-dependent kinase inhibitor 1A (CDKN1A) axis. Firstly, we confirmed MORC4 as an upregulated gene in 60 pairs of frozen CRC and adjacent normal samples. MORC4 overexpression increased proliferation and metastasis, and decreased apoptosis in SW480 and HT29 cells, which was diminished by the knockdown of PCGF1, a transcriptional repressor of CDKN1A (a potent cyclin-dependent kinase inhibitor). MORC4 was further identified as a novel molecule that interacted with PCGF1 via coimmunoprecipitation. MORC4 itself did not substantially suppress CDKN1A transcriptional activity, but it augmented PCGF1's effect on CDKN1A. Additionally, MORC4 acted as the substrate of HECT, C2, and WW domain-containing E3 ubiquitin protein ligase 2 (HECW2) and was degraded through ubiquitin-proteasome system. Collectively, our work suggested that MORC4 accelerated CRC progression via governing PCGF1/CDKN1A signaling.

Ultrasound-guided Aspiration Combined with Medical Treatment for an Unexpected Rectal Endometriotic Cyst: A Case Report.

Most bowel endometriotic lesions are ill-defined serosal and subserosal nodules, and no case of cystic bowel endometriosis has been reported in the literature. This is the first report of an unexpected presentation of bowel endometriosis as a primary cyst located inside the posterior rectal wall. The patient was a 26-year-old nulliparous woman with progressive lower abdominal pain for 6 days and difficult defecation for 1 day. Colorectal surgeons recommended bowel resection owing to the giant rectal mass. However, the patient refused to undergo surgery. Ultrasound-guided aspiration of the rectal endometriotic cyst followed by gonadotropin-releasing hormone agonist injection was individually scheduled, which finally brought significant improvement both in symptoms and in the size of the rectal endometriotic lesion.

Cepharanthine suppresses proliferation and metastasis and enhances apoptosis by regulating JAK2/Stat3 pathway in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a familiar malignant tumor, and cepharanthine (CEP) was proven to prevent the malignant activity of multiple cancer cells, including HCC. However, there are few reports on the regulatory role of CEP in HCC. After treatment with CEP or/and JAK2/Stat3 inhibitor (AG490), the associative functions were assessed by MTT, wound healing, Trans well, and Hochest33342-PI double staining in HCC cells. Then the levels of CDK4, MMP-9, Bcl-2, p-JAK2/JAK2, and p-Stat3/Stat3 were monitored via western blot. Besides, the HCC xenograft model was constructed to verify the effects of CEP on tumor growth and the JAK/Stat3 pathway. CEP could restrain proliferation and metastasis and facilitate apoptosis in HCC cells. CEP also reduced Bcl-2 (anti-apoptosis), CDK4 (proliferation), and MMP-9 (invasion) expressions, and inhibited JAK2 and Stat3 phosphorylation. Besides, CEP suppressed HCC progression by JAK2/Stat3 pathway. Moreover, CEP inhibited the growth of subcutaneous HCC xenografts and reduced p-JAK2 and p-Stat3 in tumor tissues. CEP could suppress HCC progression by attenuating the JAK2/Stat3 pathway, indicating that CEP might be a therapeutic drug for HCC patients.

Short-term prognosis for hepatocellular carcinoma patients with lung metastasis: A retrospective cohort study based on the SEER database.

Our study aimed to develop a prediction model to predict the short-term mortality of hepatocellular carcinoma (HCC) patients with lung metastasis. The retrospective data of HCC patients with lung metastasis was from the Surveillance, Epidemiology, and End Results registration database between 2010 and 2015. 1905 patients were randomly divided into training set (n = 1333) and validation set (n = 572). There were 1092 patients extracted from the Surveillance, Epidemiology, and End Results database 2015 to 2019 as the validation set. The variable importance was calculated to screen predictors. The constructed prediction models of logistic regression, random forest, broad learning system, deep neural network, support vector machine, and naïve Bayes were compared through the predictive performance. The mortality of HCC patients with lung metastasis was 51.65% within 1 month. The screened prognostic factors (age, N stage, T stage, tumor size, surgery, grade, radiation, and chemotherapy) and gender were used to construct prediction models. The area under curve (0.853 vs. 0.771) of random forest model was more optimized than that of logistic regression model in the training set. But, there were no significant differences in testing and validation sets between random forest and logistic regression models. The value of area under curve in the logistic regression model was significantly higher than that of the broad learning system model (0.763 vs. 0.745), support vector machine model (0.763 vs. 0.689) in the validation set, and higher than that of the naïve Bayes model (0.775 vs. 0.744) in the testing model. We further chose the logistic regression prediction model and built the prognostic nomogram. We have developed a prediction model for predicting short-term mortality with 9 easily acquired predictors of HCC patients with lung metastasis, which performed well in the internal and external validation. It could assist clinicians to adjust treatment strategies in time to improve the prognosis.

Screening and Prognostic Analysis of Immune-Related Genes in Pancreatic Cancer.

Pancreatic cancer remains to have a high mortality, which is partly due to the lack of effective treatment strategies. In this study, genes with potential associations with immunophenotyping of pancreatic cancer were screened through bioinformatics analysis and the correlation between immune-related genes and the prognosis of pancreatic cancer patients was assessed. Firstly, differentially expressed immune genes were extracted from the pancreatic cancer-related datasets obtained for purposes of this study. The samples were processed by the "Consensus Cluster Plus" R package to determine the number of immune subtypes. Then, the pancreatic cancer immunophenotyping-related gene modules were determined. Differential analysis of immune gene modules was performed, and the function of genes related to pancreatic cancer immune subtypes was identified. The number of immune cells in the samples was calculated, followed by the differential expression analysis of immune cell numbers in each immune subtype of pancreatic cancer. The immune infiltration score was also estimated, and the correlation between the immune infiltration score and the patient prognosis with different immune subtypes was determined. Gene differences between each immune subtype were identified by differential expression analysis, and key immune genes affecting immunophenotyping were obtained. Following the analysis, 426 immune-related genes were identified to have potential involvement in the occurrence and development of pancreatic cancer, of which CD19 may be the most critical gene affecting the immunophenotyping of pancreatic cancer. CD19 played a significant role in the occurrence and development of IS2 and IS3 immune subtypes of pancreatic cancer through its action on B cells and T cells. Moreover, the expression of CD19 was increased in the collected pancreatic cancer tissues. Overall, our findings uncovered the critical role of CD19 in the prognosis of pancreatic cancer patients.

Centromere Protein A (CENPA) Regulates Metabolic Reprogramming in the Colon Cancer Cells by Transcriptionally Activating Karyopherin Subunit Alpha 2 (KPNA2).

The karyopherin α2 subunit gene (KPNA2), an oncogene, is involved in metabolic reprogramming in cancer. This study aimed to explore the function of KPNα2 in the growth and glycolysis in colon cancer (CC) cells. Genes from the Oncomine database that were differentially expressed in multiple CC types were screened. Bioinformatics analysis suggested that KPNA2 was highly expressed in CC, and consequently, high expression of KPNA2 was detected in the CC cell lines. Down-regulation of KPNA2 reduced viability and DNA-replication ability, and increased apoptosis of HCT116 and LoVo cells. It also reduced glucose consumption, extracellular acidification rate, and the ATP production in cells. Centromere protein A (CENPA) was confirmed as an upstream transcription activator of KPNA2. There was significant H3K27ac modification in the promoter region of KPNA2. CENPA primarily recruited histone acetyltransferase general control of amino acid synthesis (GCN)-5 to the promoter region of KPNA2 to induce transcription activation. Overexpression of either CENPA or GCN-5 blocked the role of short hairpin KPNα2 and restored growth and glycolysis in CC cells. To conclude, the findings from this study suggest that CENPA recruits GCN-5 to the promoter region of KPNA2 to induce KPNα2 activation, which strengthens growth and glycolysis in, and augments the development of, CC.

Identification and Validation of a Novel Inflammatory Response-Related Gene Signature for the Prognosis of Colon Cancer.

PURPOSE: The inflammatory response plays a crucial role in the occurrence and development of colon cancer. In this study, we aimed to explore a novel prognostic model for patients with colon cancer (COAD) based on inflammatory response-related genes. METHODS: Inflammatory response-related genes were obtained from Molecular Signatures database. Univariate and multivariate Cox regression analyses were used for model construction based on TCGA dataset. GSE39582 dataset and qRT-PCR dataset were used for validation. Gene set variation analysis and gene set enrichment analysis were performed to explore the potential regulatory pathways. The immune cell infiltration level was analyzed via CIBERSORT. Immunohistochemistry analysis and experiments were used to explore the function of genes in model. RESULTS: In this study, a novel prognostic signature was identified using stepwise Cox proportional hazards regression analysis based on TCGA dataset. The results were subsequently validated in 562 patients from GSE39582 and a qRT-PCR data set from 70 tumor samples. Functional analysis indicated that the tumor microenvironment and immune cell infiltrate were different between high- and low-risk groups. Additionally, IHC results showed that the protein levels of prognostic genes were significantly different between COAD tissues and adjacent non-tumorous tissues, and prognostic genes could regulate the malignant phenotype of COAD cells. CONCLUSION: Overall, the inflammation-related gene signature can be used for prognostic prediction in patients with COAD.

Analysis of the Clinicopathological Characteristics of Stage I-III Colorectal Cancer Patients Deficient in Mismatch Repair Proteins.

PURPOSE: To investigate the clinicopathological characteristics of stage I-III colorectal cancer (CRC) patients with deficient mismatch repair (dMMR) protein. PATIENTS AND METHODS: A retrospective analysis of 61 patients with stage I-III CRC confirmed by immunohistochemistry as dMMR after radical resection at Shenjing Hospital of China Medical University from May 2017 to June 2019 was performed. A total of 183 stage I-III CRC patients with proficient mismatch repair (pMMR) protein from the same period were randomly selected as a control group. The clinicopathological data of the two groups were investigated. RESULTS: There were significant differences between the two groups in age, sex, site of onset, maximum diameter of tumor, T stage, tumor differentiation, and histological type (P < 0.05). No significant difference was detected in nerve vessel invasion, cancer nodules, the N stage or the TNM stage. In the dMMR group, 41 patients (66.13%) showed PMS2/MLH1 deletion, and the number of MSH2/MSH6 deletion is 21 patients (33.87%). Among them, 34 patients (54.84%) had PMS2 and MLH1 deficiency. In total, 16 patients (25.81%) had MSH2 and MSH6 deficiency. A total of 5 patients (8.06%) showed simply PMS2 deletion and 5 patients (8.06%) showed simply MSH6 deletion. In total, 2 patients (3.23%) showed concurrent loss of PMS2, MLH1 and MSH2. No significant difference were found (P > 0.05) in the above factors among dMMR CRC patients with different MMR proteins deletions. CONCLUSION: Our results show that dMMR status may be more likely exist in female and younger (≤55 years) patients with a greater tumor burden (>5cm), right colon, T4 stage disease, poor differentiation and mucinous adenocarcinoma. Loss of PMS2 and MLH1 is the most common pattern of MMR protein expression deficiency, followed by concurrent deletion of MSH2 and MSH6.

Identification and Validation of a Novel Six-Gene Prognostic Signature of Stem Cell Characteristic in Colon Cancer.

Cancer stem cells play crucial roles in the development of colon cancer (COAD). This study tried to explore new markers for predicting the prognosis of colon cancer based on stem cell-related genes. In our study, 424 COAD samples from TCGA were divided into three subtypes based on 412 stem cell-related genes; there were significant differences in prognosis, clinical characteristics, and immune scores between these subtypes. 694 genes were screened between subgroups. Subsequently a six-gene signature (DYDC2, MS4A15, MAGEA1, WNT7A, APOD, and SERPINE1) was established. This model had strong robustness and stable predictive performance in cohorts of different platforms. Taken together, the six-gene signature constructed in this study could be used as a novel prognostic marker for COAD patients.

The function of BTG3 in colorectal cancer cells and its possible signaling pathway.

PURPOSE: B-cell translocation gene 3 (BTG3) has been identified as a candidate driver gene for various cancers, but its specific role in colorectal cancer (CRC) is poorly understood. We aimed to investigate the relationship between expression of BTG3 and clinicopathological features and prognosis, as well as to explore the effects and the role of a possible BTG3 molecular mechanism on aggressive colorectal cancer behavior. METHODS: BTG3 expression was assessed by immunohistochemistry (IHC) on specimens from 140 patients with CRC. The association of BTG3 expression with clinicopathological features was examined. To confirm the biological role of BTG3 in CRC, two CRC cell lines expressing BTG3 were used and BTG3 expression was knocked down by shRNA. CCK-8, cell cycle, apoptosis, migration, and invasion assays were performed. The influence of BTG3 knockdown was further investigated by genomic microarray to uncover the potential molecular mechanisms underlying BTG3-mediated CRC development and progression. RESULTS: BTG3 was downregulated in colorectal cancer tissues and positively correlated with pathological classification (p = 0.037), depth of invasion (p = 0.016), distant metastasis (p = 0.024), TNM stage (p = 0.007), and overall survival (OS) and disease-free survival (DFS). BTG3 knockdown promoted cell proliferation, migration, invasion, relieved G2 arrest, and inhibited apoptosis in HCT116 and LoVo cells. A genomic microarray analysis showed that numerous tumor-associated signaling pathways and oncogenes were altered by BTG3 knockdown. At the mRNA level, nine genes referred to the extracellular-regulated kinase/mitogen-activated protein kinase pathway were differentially expressed. Western blotting revealed that BTG3 knockdown upregulated PAK2, RPS6KA5, YWHAB, and signal transducer and activator of transcription (STAT)3 protein levels, but downregulated RAP1A, DUSP6, and STAT1 protein expression, which was consistent with the genomic microarray data. CONCLUSIONS: BTG3 expression might contribute to CRC carcinogenesis. BTG3 knockdown might strengthen the aggressive colorectal cancer behavior.

Naringenin induces laxative effects by upregulating the expression levels of c-Kit and SCF, as well as those of aquaporin 3 in mice with loperamide-induced constipation.

Constipation is a common affliction which causes discomfort and affects the quality of life of affected individuals. Naringenin (NAR), a natural flavonoid widely found in citrus fruits and tomatoes, has been reported to exhibit various pharmacological effects, such as anti-inflammatory, anti-atherogenic, anti-mutagenic, hepatoprotective and anticancer effects. Increasing evidence has indicated that NAR has potential for use in the treatment of constipation. Thus, the aim of this study was to evaluate the laxative effects of NAR in mice with loperamide-induced (Lop-induced) constipation. The data indicated that NAR relieved Lop-induced constipation in mice based on the changes of fecal parameters (numbers, weight and water content), the intestinal charcoal transit ratio and the histological alteration. ELISA revealed that NAR regulated the production levels of gastrointestinal metabolic components, such as motilin (MTL), gastrin (Gas), endothelin (ET), substance P (SP), acetylcholinesterase (AChE) and vasoactive intestinal peptide (VIP) in serum. The expression levels of enteric nerve-related factors, glial cell line-derived neurotrophic factor (GDNF), transient receptor potential vanilloid 1 (TRPV1), nitric oxide synthase (NOS), c-Kit, stem cell factor (SCF) and aquaporin 3 (AQP3) were examined by western blot analysis and RT-PCR analysis. The results of this study suggest that NAR relieves Lop-induced constipation by increasing the levels of interstitial cells of Cajal markers (c-Kit and SCF), as well as AQP3. Thus, NAR may be effective as a candidate in patients suffering from lifestyle-induced constipation.

Knockdown of protein phosphatase magnesium-dependent 1 (PPM1D) through lentivirus-mediated RNA silencing inhibits colorectal carcinoma cell proliferation.

Colorectal cancer is one of the most common cancers in the world. Protein phosphatase magnesium-dependent 1 d (PPM1D) is aberrantly upregulated in many human carcinoma cells, and recent research has suggested that it could be a potential therapeutic target of cancer. However, the function of PPM1D in colorectal carcinoma cells is not well studied. To investigate the function of PPM1D in colorectal carcinoma, we used lentivirus-based RNA silencing to knock down the expression of PPM1D in RKO cells. We found that the lentivirus-mediated RNAi system efficiently decreased the expression level of endogenous PPM1D. Inhibiting PPM1D expression efficiently inhibited the proliferation and colony formation of RKO cells. Moreover, we found that PPM1D silencing led to G0/G1 cell-cycle arrest and the accumulation of cells at the sub-G1 phase. Furthermore, we found that PPM1D knockdown reduced the expression level of cyclinB1, inhibited ERK phosphorylation and activated the AKT signaling pathway. We found that PPM1D plays a crucial role in colorectal carcinoma cell proliferation and colony formation. Our work provides strong evidence suggesting that PPM1D is a potential therapeutic target of human colorectal cancers. Lentivirus-mediated PPM1D silencing is a promising gene therapeutic method to treat colorectal cancers.

Mutation spectrum in human colorectal cancers and potential functional relevance.

BACKGROUND: Somatic variants, which occur in the genome of all cells, are well accepted to play a critical role in cancer development, as their accumulation in genes could affect cell proliferations and cell cycle. METHODS: In order to understand the role of somatic mutations in human colorectal cancers, we characterized the mutation spectrum in two colorectal tumor tissues and their matched normal tissues, by analyzing deep-sequenced transcriptome data. RESULTS: We found a higher mutation rate of somatic variants in tumor tissues in comparison with normal tissues, but no trend was observed for mutation properties. By applying a series of stringent filters, we identified 418 genes with tumor specific disruptive somatic variants. Of these genes, three genes in mucin protein family (MUC2, MUC4, and MU12) are of particular interests. It has been reported that the expression of mucin proteins was correlated with the progression of colorectal cancer therefore somatic variants within those genes can interrupt their normal expression and thus contribute to the tumorigenesis. CONCLUSIONS: Our findings provide evidence of the utility of RNA-Seq in mutation screening in cancer studies, and suggest a list of candidate genes for future colorectal cancer diagnosis and treatment.

Expression profile analyses of human HCT-116 colon cancer cell line before and after serum induction.

Multi-exon genes may generate distinct isoforms in different conditions and exhibit versatile properties. Here we investigated the isoform-specific gene expression and the gene expression changes of without and with serum-induced human HCT-116 colon cancer cell lines. For these analyses, 4 transcriptome sequencing datasets were used and 2 replicates for each condition. We observed that ~73% of those expressed genes in four samples generated only one isoform, while ~27% encoded at least two isoforms. Our results show that human gene expression can exhibit great flexibility in alternative splicing. Those expressed genes generated ~1.4 isoforms for each gene across four samples on average. In addition, most of these expressed genes were expressed at moderate or low levels. We found that these four samples have similar patterns of their gene expression distributions. Furthermore, we also conducted the differential expression analysis between without and with serum-induced two conditions of these four samples. We detected that 123 genes were differentially expressed and 110 of them were up-regulated. Among those differentially expressed genes, we found intriguing phenomena that a portion of them could be clustered into different functional groups and some oncogenes and proto-oncogenes are differentially expressed.

Laparoscopic versus open gastrectomy for early distal gastric cancer: a meta-analysis.

BACKGROUND: We performed a meta-analysis in an attempt to answer whether short-term outcomes and lymph nodes harvested after laparoscopy-assisted gastrectomy (LAG) are comparable to those reported after conventional open gastrectomy (COG). METHODS: Prospective randomized clinical trials were eligible if they included patients with distal gastric cancer treated by LAG versus COG. End points were operating time, intra-operative blood loss, size of wound, overall post-operative complications, time to first flatus, time to start oral intake, hospital stay and lymph nodes harvested. RESULTS: Six trials including 668 patients were included. For four of the 13 end points, the summary point estimates favoured LAG over COG; there was a significant reduction in intra-operative blood loss (weighted mean difference (WMD) −115.60, 95% confidence interval (CI) −159.16 to −72.04, P < 0.00001), size of wound (WMD −5.27, 95% CI −8.94 to −1.60, P= 0.005), overall post-operative complications (odds ratio 0.55, 95% CI 0.35 to 0.85, P = 0.008) and hospital stay (WMD −2.65, 95% CI −4.97 to −0.32, P= 0.03) for LAG. However, the combined results of the individual trials show significant longer operating time (WMD 112.98, 95% CI 60.32 to 165.64, P < 0.0001) and significant reduction in lymph nodes harvested (WMD −4.79, 95% CI −6.79 to −2.79, P < 0.00001) in the LAG group. There was no significant difference between the two groups in time to first flatus, time to start oral intake, wound infection, intra-abdominal fluid collection and abscess, anastomotic stenosis and leakage and pulmonary complications. CONCLUSION: The results of this meta-analysis suggest that LAG for early distal cancer is a feasible and safe alternative to COG, with better short-term outcomes.

[Laparoscopic versus conventional open resection for colorectal cancer: a meta-analysis on recurrence].

OBJECTIVE: To compare the recurrence between laparoscopic resection and conventional open resection for colorectal cancer with meta-analysis. METHODS: Eligible articles were identified by searches of MEDLINE, EMBASE and the Cochrane database between January 1991 and January 2007 using the terms (laparoscopy, surgery, minimal invasive, colon, intestine, large, colectomy, colonic neoplasms, rectal neoplasms and randomized controlled trial). Prospective randomized clinical trials were eligible if they included patients with colorectal cancer treated by laparoscopic surgery versus open surgery followed-up by recurrence. Data were extracted from these trials by three independent reviewers. RESULTS: Ten trials with recurrence information of 2474 patients were involved. In the combined results, no significant difference in the OR for overall recurrence between the laparoscopic surgery and open surgery group was found (OR 0.95, 95%CI 0.76 to 1.19, P=0.64). Stratified by recurrence type, the combined results of the individual reports showed no significant differences for local recurrence (OR 0.79, 95%CI 0.50 to 1.25,P=0.32), distant metastasis (OR 0.89, 95%CI 0.62 to 1.28, P=0.54) and port-site or wound-site recurrence (OR 1.04,95%CI 0.21 to 5.27,P=0.96) between the two surgical techniques. CONCLUSION: The recurrence rates for patients with colorectal cancer treated by laparoscopic surgery do not differ significantly from those by open surgery. Longer follow up studies will further define outcomes comparing the two techniques in the treatment of colorectal cancer.

[Total mesorectal excision versus conventional radical surgery for rectal cancer: a meta analysis].

OBJECTIVE: To compare treatment outcomes of total mesorectal excision (TME) with those of conventional radical surgery (CRS) for rectal cancer. METHODS: Literature reviews were performed with key words, such as rectal cancer, total mesorectal excision, TME on all studies reported on TME versus CRS for rectal cancer between January 1986 to May 2006. According to the same screening criteria, 17 clinical studies were included in our systematic reviews. Two of our co-authors drew the details of trial design, characteristics of participants, results and so on from the studies included. Data analyses were performed by using RevMan 4.2. RESULTS: Sample volume in this Meta analysis was 5267 rectal cancer cases. Quality and quantity analyses were performed within all included studies, prospective studies (prospective nonrandomized studies and multicenter prospective nonrandomized studies) and retrospective studies. The results showed that postoperative survival rate was significantly increased [OR 1.81 (95%CI 1.55-2.11, P<0.00001), OR 1.79 (95%CI 1.49-2.15, P<0.00001) and OR 1.84 (95%CI 1.39-2.45, P<0.00001)] and local recurrence rate was significantly reduced [OR 0.35 (95%CI 0.29-0.43, P<0.00001), OR 0.41 (95%CI 0.32-0.53, P<0.00001) and OR 0.29 (95%CI 0.22-0.39, P<0.00001)] after TME was used. The results of all study analyses agreed with those from prospective studies analyses, in which postoperative mortality was significantly reduced [OR 0.51 (95%CI 0.32-0.87, P=0.007) and OR 0.56 (95%CI 0.33-0.94, P=0.04)] after TME treatment, meanwhile the results of retrospective study analyses indicated that there was no significant difference between TME group and CRS group in postoperative mortality [OR 0.39 (95%CI 0.14-1.10, P=0.07)]. TME was a risk factor for postoperative anastomotic leak according to the results of all included studies and prospective study analyses, but no difference between TME group and CRS group had been found [OR 1.24 (95%CI 0.84-1.83, P=0.29) OR 1.98 (95%CI 0.85-4.61, P=0.11)]. CONCLUSIONS: TME is still the standard operative technique for rectal cancer. As compared with CRS, TME results in lower postoperative local recurrence rate and higher survival rate.