Construction and Analysis of a Mitochondrial Metabolism-Related Prognostic Model for Breast Cancer to Evaluate Survival and Immunotherapy.

As one of the most prevalent malignancies among women, breast cancer (BC) is tightly linked to metabolic dysfunction. However, the correlation between mitochondrial metabolism-related genes (MMRGs) and BC remains unclear. The training and validation datasets for BC were obtained from The Cancer Genome Atlas and Gene Expression Omnibus databases, respectively. MMRG-related data were obtained from the Molecular Signatures Database. A risk score prognostic model incorporating MMRGs was established based on univariate, LASSO, and multivariate Cox regression analyses. Independent factors affecting BC prognosis were identified through regression analysis and presented in a nomogram. Single-sample gene set enrichment analysis was employed to assess the immune levels of high-risk (HR) and low-risk (LR) groups. The sensitivity of BC patients in the two groups to common anti-tumor drugs was evaluated by utilizing the Genomics of Drug Sensitivity in Cancer database. 12 MMRGs significantly associated with survival were selected from 1234 MMRGs. A 12-gene risk score prognostic model was built. In the multivariate regression analysis incorporating classical clinical factors, the MMRG-related risk score remained an independent prognostic factor. As revealed by tumor immune microenvironment analysis, the LR group with higher survival rates had elevated immune levels. The drug sensitivity results unmasked that the LR group demonstrated higher sensitivity to Irinotecan, Nilotinib, and Oxaliplatin, while the HR group demonstrated higher sensitivity to Lapatinib. The development of MMRG characteristics provides a comprehensive understanding of mitochondrial metabolism in BC, aiding in the prediction of prognosis and tumor microenvironment, and offering promising therapeutic choices for BC patients with different MMRG risk scores.

Impact of ileostomy on postoperative wound complications in patients after laparoscopic rectal cancer surgery: A meta-analysis.

To prevent anastomotic leakage and other postoperative complications after laparoscopic rectal cancer surgery, a protective ileostomy is often used. However, the necessity of performing ileostomy after laparoscopic rectal cancer remains controversial. The aim of this meta-analysis was to assess the benefit of ileostomy on wound infection after laparoscopic rectal cancer. The Cochrane Library, EMBASE, Web of Science, and PubMed were used to retrieve all related documents up to September 2023. Completion of the trial literature was submitted once the eligibility and exclusion criteria were met and the literature quality assessment was evaluated. This study compared the post-operative post-operative complications of an ileostomy with that of non-ileostomy in a laparoscope. We used Reman 5.3 to analyse meta-data. Controlled studies were evaluated with ROBINS-I. The meta-analyses included 525 studies, and 5 publications were chosen to statistically analyse the data according to the classification criteria. There was no statistically significant difference in the rate of postoperative wound infections among ostomate and nonostomate (odds ratio [OR], 1.79; 95% confidence interval [CI], 0.66, 4.84; p = 0.25). In 5 trials, the incidence of anastomotic leak was increased after surgery in nonostomate patients (OR, 0.26; 95% CI, 0.12, 0.57; p = 0.0009). Two studies reported no significant difference in the length of operation time when nonstomal compared to stomal operations in patients with rectal cancer (mean difference, 0.87; 95% CI, -2.99, 4.74; p = 0.66). No significant difference was found in the rate of wound infection and operation time after operation among the two groups, but the incidence of anastomosis leak increased after operation. Protective ileostomy after laparoscopic rectal cancer was effective in reducing the risk of anastomotic leakage in patients, and we found no additional risk of infection. We cautiously conclude that protective ileostomy is active and necessary for patients with a high risk of anastomotic leakage after surgery, which needs to be further confirmed by high-quality studies with larger samples.

Effect of laparoscopic versus open surgery on postoperative wound complications in patients with low rectal cancer: A meta-analysis.

This meta-analysis was conducted to evaluate the effect of microinvasive and open operations on postoperative wound complications in low rectal carcinoma patients. Research on limited English has been conducted systematically in PubMed, Embase, Cochrane Library and Web of Science. The date up to the search was in August 2023. Following review of the classification and exclusion criteria for this research and the evaluation of its quality in the literature, there were a total of 266 related papers, which were reviewed for inclusion in the period from 2004 to 2017. A total of 1774 cases of low rectal cancer were enrolled. Of these 913 cases, the laparoscopic operation was performed on 913 cases, while 861 cases were operated on low rectal carcinoma. The overall sample was between 10 and 482. Five trials described the efficacy of laparoscopy have lower risk than open on postoperative wound infection in patients with low rectal cancer (OR, 0.72;95 % CI, 0.48,1.09 p = 0.12). Three studies results showed that the anastomotic leak was not significantly different between open and laparoscopy (OR, 0.86; 95% CI, 0.58,1.26 p = 0.44). Six surgical trials in low rectal cancer patients reported haemorrhage, and five cases of surgical time were reported, with laparoscopy having fewer bleeding compared with open surgery (MD, -188.89; 95% CI, -341.27, -36.51 p = 0.02). Compared with laparoscopy, the operation time was shorter for the open operation (MD, 33.06; 95% CI, 30.56, 35.57 p < 0.0001). Overall, there is no significant difference between laparoscopy and open surgery in terms of incidence of infection and anastomosis leak. However, the rate of haemorrhage in laparoscopy is lower，and operation time in open surgery is lower.

m6A-mediated upregulation of lncRNA RMRP boosts the progression of bladder cancer via epigenetically suppressing SCARA5.

Aim: This study aimed to elucidate the relationship between SCARA5 and RMRP in bladder cancer and their underlying mechanism. Methods: Biological functions were evaluated using cell-counting kit 8 assay, 5-ethynyl-2'-deoxyuridine incorporation, wound healing and Transwell assays. RNA immunoprecipitation, RNA pull-down and chromatin immunoprecipitation were employed. A xenograft tumor model in nude mice was also conducted. Results & conclusion: RMRP and SCARA5 exhibited an inverse correlation. Downregulation of RMRP significantly suppressed bladder cancer cell proliferation, migration and invasion, which was reversed by SCARA5 overexpression. RMRP recruited DNA methyltransferases to the promoter region of SCARA5, thereby triggering the methylation of the SCARA5 promoter to epigenetically suppress its expression. Our findings elucidate the machinery by which RMRP, stabilized by METTL3, exerts a promoter role in bladder cancer tumorigenesis by triggering SCARA5 methylation.

SCARA5 as a downstream factor of PCAT29, inhibits proliferation, migration, and invasion of bladder cancer.

Scavenger receptor class A, member 5 (SCARA5) has been identified a novel tumor suppressor in several cancers. However, the functional and underlying mechanism of SCARA5 in bladder cancer (BC) need investigation. Here, we found SCARA5 expression was downregulated in both BC tissues and cell lines. Low SCARA5 in BC tissues was associated with a shorter overall survival. Moreover, SCARA5 overexpression reduced BC cell viability, colony formation, invasion, and migration. Further investigation demonstrated that the expression of SCARA5 was negatively regulated by miR-141. Furthermore, the long non-coding RNA prostate cancer associated transcript 29 (PCAT29) inhibited the proliferation, invasion, and migration of BC cells by sponging miR-141. Luciferase activity assays revealed that PCAT29 targeted miR-141 and miR-141 targeted SCARA5. In conclusion, SCARA5, as a downstream factor of the PCAT29/miR-141 axis, inhibited the proliferation, migration, and invasion of BC cells. These findings provide novel insights into the detailed molecular mechanisms of BC development.

NEAT1 promotes the malignant development of bladder cancer by regulating the miR-101/VEGF-C pathway in vitro and in vivo.

BACKGROUND: NEAT1 has been shown to play an oncogenic role in many kinds of cancers. However, detailed roles of NEAT1 in bladder cancer are largely unknown. METHODS: In the present study, the expression of NEAT1, miR-101 and VEGF-C was detected in human bladder cancer samples. The relationship between NEAT1 and the prognosis of patients with bladder cancer was analysed. In vitro experiments explored the effects of NEAT1 on biological behaviours of bladder cancer T24 and 5637 cells. Bioinformatics prediction and luciferase assays were used to assay the regulatory mechanism of action of NEAT1 and miR-101. Loss and gain of the expression of miR-101 and VEGF-C were used to explore the effects of the NEAT1/miR-101/VEGF-C pathway on T24 and 5637 cells. The effect of NEAT1 on the growth of bladder cancer in vivo was explored using an orthotopic tumourigenesis model. RESULTS: NEAT1 and VEGF-C were significantly upregulated in bladder cancer samples, and miR-101 was significantly downregulated. NEAT1 upregulation was associated with poorer recurrence-free survival of patients with bladder cancer. Overexpression of NEAT1 promoted the proliferation, migration and invasion of bladder cancer cells. The results of the luciferase assay indicated that miR-101 was a target of NEAT1. The promoting effects of NEAT1 on bladder cancer cells were reversed by miR-101 upregulation, and inhibition of miR-101 enhanced the effects of NEAT1. Overexpression of VEGF-C had a clear synergistic effect with the action of NEAT1. Overexpression of NEAT1 increased tumour growth and induced the development of liver metastasis. CONCLUSIONS: In conclusion, our data indicated that NEAT1 was expressed at high levels in bladder cancer patients and correlated with unfavourable prognosis. NEAT1 promoted malignant development of bladder cancer in vitro and in vivo by regulating the miR-101/VEGF-C pathway.

BMSC-derived exosomal lncRNA PTENP1 suppresses the malignant phenotypes of bladder cancer by upregulating SCARA5 expression.

LncRNAs can be transported to tumor cells where they exert regulatory effects by bone marrow mesenchymal stem cells (BMSC)-derived exosomes. Here, we aimed to investigate the functional mechanism of BMSC-derived exosomal lncRNA PTENP1 in the progression of bladder cancer (BC). Methods of BMSC were identified by detecting surface markers through flow cytometry. Exosomes from BMSC were identified by transmission electron microscopy, nanoparticle tracking analysis (NTA), and western blot analysis of exosome markers. Cellular internalization of BMSC-derived exosomes (BMSC-Exo) into BC cells was detected by confocal microscopy. CCK-8, colony formation, flow cytometry, wound healing, and transwell assays were adopted to estimate cell proliferation, apoptosis, migration, and invasion abilities, respectively. Interplay between miR-17 and lncRNA PTENP1 or SCARA5 was verified by dual-luciferase reporter, RNA pull down, and/or RNA immunoprecipitation (RIP) assays. Tumor xenograft assay was conducted in nude mice to study the role of exosomal lncRNA PTENP1 in BC progression in vivo. We showed exosomal lncRNA PTENP1 can be delivered into and suppress the malignant phenotypes of BC cells. LncRNA PTENP1 was identified as a sponge of miR-17, and SCARA5 was identified as a target gene of miR-17. The exosomes derived from PTENP1-overexpressing BMSC (BMSCOE-PTENP1-Exo) abolished the promotive effects of miR-17 overexpression or SCARA5 knockdown on the malignant phenotypes of BC cells. Moreover, exosomal lncRNA PTENP1 was demonstrated to inhibit BC tumor growth in nude mice by miR-17/SCARA5 axis. In conclusion, BMSC-derived exosomal PTENP1 suppressed the BC progression by upregulating the expression of SCARA5 via sponging miR-17, offering a potential novel therapeutic target for BC therapy.

WITHDRAWN: SCARA5 regulated by MEG3/miR-141 axis attenuates proliferation, migration and invasion of bladder cancer.

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USP11 facilitates colorectal cancer proliferation and metastasis by regulating IGF2BP3 stability.

The abnormal expression of ubiquitin-specific protease 11 (USP11) is thought to be related to tumor development and progression; however, few studies have reported the biological function and clinical importance of USP11 in colorectal cancer (CRC). Therefore, it is necessary to further explore the role of USP11 in CRC. Immunohistochemical staining was used to explore the association between prognosis and USP11 expression in CRC. Cholecystokinin octapeptide (CCK-8), colony formation, transwell, and animal assays were used to study the abilities of proliferation, migration, and invasion in CRC cells. Co-immunoprecipitation assays, Western blotting, ubiquitination assays, and rescue experiments were performed to elucidate the interaction between USP11 and insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3). We verified that USP11 was overexpressed in CRC tissues and was associated with the depth of tumor invasion and metastasis. USP11 knockdown or overexpression could weaken or reinforce the abilities of proliferation, migration, and invasion in CRC cells in vivo or in vitro. IGF2BP3 was protected by USP11 from degradation via deubiquitination. The rescue experiments revealed that IGF2BP3 overexpression could effectively reverse the decrease in cell proliferation, migration, and invasion caused by USP11 knockdown. Therefore, USP11 might be involved in CRC tumorigenesis and development through a USP11-IGF2BP3 axis pathway, and USP11 overexpression might be a novel indicator for poor prognosis and a potential therapeutic target in CRC patients.

miR­204­5p promotes apoptosis and inhibits migration of gastric cancer cells by targeting HER­2.

Gastric cancer is one of the most common types of cancer worldwide, with a high incidence and mortality rate. MicroRNAs (miRs) play an important role in tumorigenesis, cell proliferation, migration, apoptosis and metastasis of cancer. The present study aimed to investigate the role and potential mechanism of miR­204­5p in gastric cancer. The mRNA expression levels of miR­204­5p in gastric cancer were determined by reverse transcription­quantitative PCR. Cell proliferation was determined using Cell Counting Kit­8 and colony formation assays. Flow cytometry analysis was performed to detect the cell apoptosis rate. Wound healing and Transwell assays were carried out to determine the cell migration and invasion rates, respectively. A putative binding site of miR­204­5p in the 3' untranslated region of human epidermal growth factor receptor 2 (HER­2) was predicted using a bioinformatics algorithm and confirmed using a dual­luciferase reporter assay. miR­204­5p levels were downregulated in gastric cancer cells. Overexpression of miR­204­5p significantly inhibited cell proliferation and decreased cell colony formation. Additionally, miR­204­5p decreased the migration and invasion rates of gastric cancer cells. Furthermore, an increased apoptotic rate was detected following overexpression of miR­204­5p, along with increased expression levels of Bax and decreased expression levels of Bcl­2. HER­2 was a direct target of miR­204­5p, and inhibition of HER­2 acted as a tumor suppressor by inhibiting cell proliferation, migration and invasion, and promoting cell apoptosis, which was reversed by the inhibition of miR­204­5p expression. These results suggested that miR­204­5p could exert its anti­tumor function by inhibiting cell proliferation, migration and invasion, and promoting cell apoptosis via regulation of HER­2, which may be a potential therapeutic target for gastric cancer.

miR­21 inhibits autophagy and promotes malignant development in the bladder cancer T24 cell line.

MicroRNA­21 (miR­21) is reported to exhibit cancer­promoting activity in various types of cancer. It has been previously demonstrated that miR­21 is overexpressed in bladder tumor tissue compared with normal mucosa. However, the functional mechanism of miR­21 in bladder cancer remains largely unknown. Thus, the current study aimed to determine the roles of miR­21 in autophagy and the malignant development of bladder cancer in T24 cells. Upregulation or downregulation of miR­21 was achieved following the transfection of miR­21 mimic or miR­21 inhibitor. An MTT assay was additionally performed to measure cell growth. Wound healing and transwell invasion assays were used to detect cell migration and invasion. The apoptotic potential and cell cycle were examined via flow cytometry and reverse transcription­quantitative PCR was performed to evaluate the expression of phosphatase and tensin homolog (PTEN), beclin 1, microtubule­associated protein l light chain 3B (LC3­II), cyclin D1, caspase­3, E­cadherin, matrix metallopeptidase­9 (MMP­9) and vimentin. The results revealed that the proliferation, migration and invasion of T24 cells was greatly increased in the miR­21 mimic group, while apoptosis was greatly inhibited. Additionally, T24 cells treated with miR­21 mimic exhibited G1­phase arrest. In the miR­21 mimic group, the expression of PTEN, beclin 1, LC3­II, caspase­3 and E­cadherin were decreased, while the expression of cyclin D1, MMP­9 and vimentin were increased. Opposite effects were observed in the miR­21 inhibitor group. The data of the current study may indicate that miR­21 overexpression inhibited autophagy and promoted the proliferation, migration, invasion and epithelial to mesenchymal transition of bladder cancer T24 cells. The results may further elucidate the molecular mechanism of miR­21 in the development of bladder cancer.

Differentiation of Intraspinal Tuberculosis and Metastatic Cancer Using Magnetic Resonance Imaging.

PURPOSE: This study aimed to explore the differences in the magnetic resonance imaging (MRI) findings between intraspinal tuberculosis and metastatic cancer, which may aid in making the correct diagnosis. PATIENTS AND METHODS: The clinical features and MRI findings of 15 patients with intraspinal tuberculosis and 11 patients with intraspinal metastatic cancers were retrospectively analyzed. RESULTS: The mean ages of the patients with intraspinal tuberculosis and metastatic cancer were 26.3 (15-42) and 52.1 (38-67) years, respectively. All intraspinal tuberculosis cases were secondary to primary extraspinal tuberculosis, including tuberculous meningitis (11/15), as well as pulmonary (9/15), vertebral (5/15), urinary tract (1/15), abdominal (1/15), cervical lymph node (1/15), and multisystem tuberculosis (9/15). The intraspinal metastases originated from the breast (5/11), lung (3/11), kidney (1/11), ovarian (1/11), and nasopharyngeal cancers (1/11). Both intraspinal tuberculosis and metastatic cancers presented with multiple intra- and extramedullary lesions throughout all regional segments of the spinal canal, accompanied by irregularly thickened meninges. Intraspinal tuberculous lesions had indistinct edges that integrated with each other, most of them exhibiting obvious enhancement on MRI. Conversely, intraspinal metastatic lesions were distinctly separated with clear edges and exhibited lesser enhanced MRI than intraspinal tuberculosis. CONCLUSION: A combined analysis of clinical features and MRI findings may be helpful in differentiating intraspinal tuberculosis from metastatic cancer.

Hypermethylation of the HIC1 promoter and aberrant expression of HIC1/SIRT1 contribute to the development of thyroid papillary carcinoma.

Hypermethylation leading to the loss of hypermethylated in cancer-1 (HIC1) gene expression occurs in many different types of human cancer. HIC1 is a transcriptional repressor that directly binds to the promoter region of NAD-dependent deacetylase sirtuin-1 (SIRT1). SIRT1 functions in cell growth, is anti-apoptotic, protect neurons, functions in senescence, and regulates energy restriction. Epigenetic modification and dysregulation affecting the HIC1/SIRT1 axis is potentially important for the development of malignancies. However, the importance of HIC1 expression in the development of papillary thyroid carcinoma, especially in Chinese patients, is uncertain. Therefore, we assessed the level of methylation in the HIC1 promoter and the mRNA and protein expression levels of HIC1 and SIRT1 in human thyroid papillary carcinoma and tumor adjacent control tissues. The demethylation reagent 5-aza-2'-deoxyctidine (5-aza-dc) and an HIC1 overexpression plasmid were used to manipulate the HIC1/SIRT1 pathway, and the effects on cell senescence, apoptosis, and cell cycle progression were assessed. Compared to normal thyroid tissue, thyroid tumors had lower expression of HIC1 and higher SIRT1 expression. The level of HIC1 methylation was also higher in thyroid carcinoma tissues than adjacent tissues. HIC1 expression was closely correlated with patient age and tumor progression. Restoration of HIC1 expression through an overexpression plasmid or 5-aza-dC treatment reduced SIRT1 expression and cell proliferation, and led to senescence, cell cycle arrest, and apoptosis. Aberrant expression of HIC1/SIRT1 and hypermethylation of the HIC1 promoter may be critical for the development and progression of papillary thyroid cancer.

Correlational research of Golgi phosphorylation protein 3 expression in colorectal cancer.

AIM: To investigate the effect of Golgi phosphorylation protein 3 (GOLPH3) expression on cell apoptosis, angiogenesis and prognosis in colorectal cancer (CRC). METHODS: The expression of GOLPH3 in CRC tissues and normal colorectal mucosae was determined by immunohistochemistry in 62 patients. In addition, immunohistochemistry was also carried out to detect the expression of vascular endothelial growth factor (VEGF), CD34 and microvessel density (MVD). Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay was used to determine the apoptotic index (AI). The Kaplan-Meier method was used to analyze the relationship between GOLPH3 expression and survival in another 123 CRC cases. RESULTS: Compared with normal colorectal mucosae, a notably higher level of GOLPH3 protein expression was identified in CRC tissues (53.2% vs 24.2%, P < 0.05). Positive GOLPH3 expression was significantly associated with tumor invasion depth, TNM stage, and lymph node metastasis (P = 0.001; P = 0.020; P = 0.020; P < 0.05, respectively), but not with tumor length, tumor site, and age (P = 0.363; P = 0.819; P = 0.599; P > 0.05, respectively). VEGF expression and MVD in GOLPH3-positive CRC was significantly higher than in GOLPH3-negative CRC (VEGF: 69.7% vs 31.0%; MVD: 21.45 ± 9.39 vs 14.24 ± 8.97; P < 0.05). GOLPH3 expression was negatively correlated with AI in CRC as shown by Spearman correlation analysis (r = -0.320, P < 0.05). The 5-year survival rate in GOLPH3-negative CRC (69.4%) was significantly higher than in GOLPH3-positive CRC (48.6%) (log-rank test, P < 0.05). CONCLUSION: High expression of GOLPH3 is found in CRC tissues. GOLPH3 expression may be a novel prognostic marker for CRC patients.

[Expression and significance of Clara cell secretory protein in injury lungs of Kunming mice after n-hexane long-term inhalation].

OBJECTIVE: To observe the expression of Clara cell secretory protein(CCSP) in the Kunming mouse model of n-hexane long-term inhalation, and to discuss the functions of Clara cell in injury lung induced by n-hexane. METHODS: 24 healthy mice were randomly divided into 4 groups: one control group and three n-hexane groups (4 w, 8 w and 12 w), 6 each group. Primary concentration of n-hexane was 17.6 g/m3, 8 hours per day, 6 d per week. After inhalation, n-hexane concentration of blood from celiac artery was detected. The lungs were embedded with paraffin and HE staining in the routine. The ratio of Clara cells with CCSP reaction in bronchiole and the number of macrophage cells with lysozyme reaction were determined by immuno-histochemistry. RESULTS: In the poisoning groups, the average n-hexane concentration of blood was significantly higher than that of the control group (P < 0.01). There were apparent pathologic damages in lungs of the poisoning mice. In poisoning 4 w, 8 w and 12 w groups, the ratio of Clara cells was significantly decreased [(73.33 +/- 4.21)%, (60.98 +/- 4.94)%, (34.04 +/- 2.33)% in terminal bronchiole, and (75.44 +/- 7.91)%, (58.54 +/- 4.86)%, (33.35 +/- 2.67)% in respiratory bronchiole] as compared with the control mice [(80.26 +/- 6.43)% and (81.74 +/- 7.75)%, P < 0.05 or P < 0.01], meanwhile the numbers of macrophage cells were gradually increased [(21.39 +/- 7.41), (28.54 +/- 10.73), (48.97 +/- 19.55) per microscopic field at 200x] in poisoning mice than those in control mice [(7.84 +/- 3.12) per microscopic field at 200x, P < 0.05 or P < 0.01]. CONCLUSION: In injury lungs after n-hexane inhalation, Clara cells are the target cells of n-hexane toxicity effect. Clara cells play an extensive protective role in lung inflammation.

Relationship between survivin expression and recurrence, and prognosis in hepatocellular carcinoma.

AIM: To study the expression of the inhibitor of apoptosis protein survivin in hepatocellular carcinoma (HCC), and its correlation with clinicopathological factors, cell proliferation, recurrence and prognosis after hepatectomy. METHODS: Immunohistochemical staining of survivin and Ki-67 was performed by the standard streptavidin-peroxidase technique on paraffin sections of 55 cases of HCC. RESULTS: The positive rate of survivin in HCC was 52.7% (29/55). Significant correlation was found between survivin expression with portal vein thrombi and intrahepatic matastasistic nodes (P < 0.05). The recurrent rate in survivin-positive HCC was significantly higher than that in survivin-negative HCC after hepatectomy, the 1- and 3-year survival rate in patients with survivin-positive tumors was significantly lower than that in patients with survivin-negative tumors (58.62 and 10.34% vs 76.92 and 30.77%, P < 0.05, log-rank test). The proliferation index (Ki-67) in survivin-positive HCC (33.83% +/- 18.90%) was significantly higher than that in survivin-negative HCC (19.60% +/- 19.35%) (P < 0.05). CONCLUSION: Survivin may play an important role in progression of HCC by promoting cell proliferation, and may be positively correlated with high risk of disease recurrence and poor prognosis in HCC. Its expression may serve as a prognostic factor for patients with HCC after hepatectomy.

Relationship between somatostatin receptor subtype expression and clinicopathology, Ki-67, Bcl-2 and p53 in colorectal cancer.

AIM: To study the SSTR1, 2, 3, 4, 5 expression and their relationships with clinico-pathological factors, cell proliferation, Bcl-2 and p53 expression in colorectal cancer cells. METHODS: Immunohistochemical staining of five SSTR subtypes, Ki-67, Bcl-2 and p53 was performed by the standard streptavidin-peroxidase (SP) technique for the paraffin sections of 127 colorectal cancers. and expression of five SSTR subtypes in 40 specimens of normal colorectal mucosae was detected with the same method. RESULTS: Positive staining for five SSTR subtypes was observed in colorectal cancer cells and normal colorectal mucosae. SSTR1 was the most predominant subtype in both colorectal cancer and normal colorectal mucosa, and the second was SSTR5 or SSTR2. As compared with normal colorectal mucosa, SSTR4 was more frequently expressed in colorectal cancer cells (2.5% vs 18.9%, P<0.05); the expression of SSTR2, 4, 5 in moderately to well differentiated colorectal adenocarcinoma was significantly higher than that in poorly differentiated ones (P<0.05), the SSTR1 expression in colorectal cancer with positive lymph node metastasis was significantly higher than that with negative lymph node metastasis (72.2% and 54.5%,P<0.05). In addition, in the ulcerative type of colorectal cancer, SSTR2 expression was obviously decreased (P<0.05); the correlation did not reach a statistical significance between the five SSTR subtypes expression and Dukes'stages (P>0.05), but the frequency of SSTR1 expression increased with Dukes'stage, while SSTR3 and SSTR5 expression decreased with Dukes' stage. Moreover, there was no correlation between expression of the five SSTR subtypes and other clinicopathological factors such as age, sex, tumor site, tumor depth, distant metastasis. The proliferative indexes in colorectal cancer cells with negative expression of SSTR2 and SSTR3 were significantly higher than that with positive expression (P<0.05). The Bcl-2 expression in colorectal cancer cells with positive expression of SSTR1, 2, 3, 5 was significantly lower than that with negative expression (P<0.05). There was no correlation between five SSTR subtypes and p53 expression. CONCLUSION: The most predominant SSTR subtype is SSTR1, and the second is SSTR2 or SSTR5. Five SSTR subtypes play different roles in the development of colorectal cancer. SSTR2 and SSTR3 can inhibit the proliferation and promote apoptosis of tumor cells.

[Expression and significance of Skp2 and p27kip1 protein in pathological scar].

OBJECTIVE: To study the expression of Skp2 gene (s-phase kinase associated protein 2) in the pathological scars and its relationship with p27kip1 level and to investigate its role and its probable mechanism in the pathogenesis of abnormal scars. METHODS: Immunohistochemical technique was performed to detect the expression and distribution of Skp2 and p27kip1 protein in hypertrophic scar (42 cases), keloid (18 cases), normal scar (40 cases) and normal skin (50 cases), statistics was used to analyze the data. RESULTS: The positive rate of Skp2 and p27kip1 protein expression was not statistically different between the hypertrophic scar and keloid (P > 0.05), while they were all remarkably significant in comparison between normal scar and abnormal scar (P < 0.05). In pathological scar the protein of Skp2 and p27kip1 showed a strong inverse correlation (P < 0.01). CONCLUSION: The result indicated that the expression of Skp2 was increased and it may lead to decrease p27kip1 level in the hypertrophic scar and keloid, Skp2 overexpression might play an important role in the proliferation of fibroblasts and in the pathogenesis of pathological scar by adjusting the regulation of cyclins such as p27kip1.

[Diagnostic accuracy of cell-block or tissue-fragment histology and cytology by fine needle lung aspiration].

OBJECTIVE: Study on the diagnostic accuracy and value of cell block and tissue fragment preparations collected from lung fine needle aspiration (FNA). METHODS: A total of 187 FNA (22G) samples from the lungs with matched histological diagnosis were studied. Among them, the diagnosis made by depending on 124 cell block and fragment preparations were analyzed in comparing retrospectively with the diagnosis of 187 cases by smear preparations. RESULTS: (1) Of the 124 cell blocks cases, 89 cases were true positives, 22 cases were true negatives, 13 cases were false negatives and no false positives. Of the 187 smears cases, the figure were 136, 30, 19 and 2 cases respectively. The diagnostic accuracy of cell blocks was 87.3% in sensitivity, 100% in specificity, 89.5% in overall accuracy. The figures for smears were 87.7%, 93.8% and 88.8% respectively. (2) For malignant tumours, the histological typing accuracy of cell blocks was 93.3% (83/89), and to be 67.9% (91/134) by diagnosis depending on the smears (P < 0.01). For the benign lesions, the figures were 86.4% (19/22) and 60% (18/30) respectively (P < 0.05). (3) It was possible to obtain many minisections for further studies from cell blocks. Immunoperoxidase staining on minisections was reliable and agreed with those on the surgical specimens. CONCLUSIONS: The diagnostic accuracy of cell block is high, particularly in histological typing which approaches to that of the diagnosis made depending on the postoperative specimens. A combined use of smears and cell block is recommended which may raise further the diagnostic accuracy.