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Objective To construct a Nomogram model that can accurately predict early death of metastatic colon cancer (mCC). Methods A total of 6 669 patients from the SEER database were identified using inclusion and exclusion criteria. Multivariate logistic regression was used to identify risk factors for early mortality and to construct a Nomogram. The predictive performance of the Nomogram was evaluated by C-index, calibration curve, and decision curve analysis (DCA). Results Primary tumor location, differentiation grade, T stage, M stage, bone metastases, brain metastases, CEA, tumor size, age and marital status were independent factors for early death in patients with mCC. A Nomogram was constructed based on these variables. The C-index and the calibration curve of the Nomogram showed the good predictive ability of the nomogram. DCA showed that the Nomogram had a superior clinical net benefit in predicting early death compared with TNM stage. Conclusion The developed Nomogram has good predictive ability and can help guide clinicians to identify patients with high-risk mCC for individualized diagnosis and treatment.
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Objective@#To explore the role of microtubule actin cross-linking factor 1(MACF1) in the metastasis of gastric cancer.@*Methods@#From 2009 to 2012, at The First Affiliated Hospital of Zhengzhou University, the paraffin blocks of gastric cancer and normal tissue adjacent to cancer of 107 patients who received radical gastrectomy were collected. The expression of MACF1 in tissues at protein level was detected by immunohistochemical staining. In 2017, at The First Affiliated Hospital of Zhengzhou University, fresh specimens samples of gastric cancer and normal tissue adjacent to cancer of 42 patients who received radical gastrectomy were also collected. The expression of MACF1 at mRNA level was determined by quantitative real-time polymerase chain reaction (PCR). MACF1 knockout gastric cell line was established. The effects of MACF1 on cell migration and invasion were verified by wound-healing test and Transwell assay. The effects of MACF1 on cell microtubule and actin were analyzed by filamentous actin (F-actin) staining. T-test, chi-square test and multivariate analysis were used for statistical analysis.@*Results@#The positive expression rate of MACF1 in gastric carcinoma tissues was 71.0%(76/107), which was significantly higher than that of the corresponding normal tissues adjacent to cancer (22.4%, 24/107), and the difference was significant (t=4.145, P=0.016). The expression of MACF1 at mRNA level in cancer tissues of 42 patients with gastric cancer was 6.463±0.672, which was significantly higher than that of corresponding normal tissue adjacent to cancer (1.727±0.331), and the difference was statistically significant (t=6.326, P<0.01). The differences in positive expression rate of MACF1 in different tumor infiltration depth, different TNM stage and lymph nodes metastasis were statistically significant (χ2=1.170, 7.959 and 5.288; all P<0.01). The five-year survival rate of patients with high expression of MACF1 was 32.9% (25/76), which was significantly lower than that of patients with normal MACF1 expression (64.5%, 20/31), and the difference was statistically significant (χ2=25.093, P=0.034). The high expression of MACF1 was an independent prognostic factor affecting overall survival rate in patients with gastric cancer after surgery(hazard ratio (HR)=0.513, 95%confidence interval (CI): 0.411 to 0.922, P=0.038). The results of wound-healing assay showed that at 24 hour after wound the migration ability of MACF1 knockout AGS- MACF1-/- cells was (18.77±3.82)%, which was lower than that of wild type AGS cells ((76.24±5.36)%), and the difference was statistically significant (t=6.249, P=0.014). The migration ability of MACF1 knockout HGC27-MACF1-/-cells was (42.48±7.37)%, which was lower than that of wild type HGC27 cells ((82.35±4.28)%), and the difference was statistically significant (t=5.938, P=0.017). The results of Transwell assay indicated that the number of migration cells of MACF1 knockout AGS-MACF1-/- cells was 87.0±11.0, which was less than that of wild type AGS cells (200.0±16.0), and the difference was statistically significant (t=5.820, P=0.028). The number of migration cells of MACF1 knockout HGC27-MACF1-/-cells was 151.0±13.0, which was less than that of wild type HGC27 cells (268.5±20.5), and the difference was statistically significant (t=4.840, P=0.040). The results of F-actin staining demonstrated that the number of actin filaments of MACF1 knockout AGS-MACF1-/- cells was 216.60±18.09, which was less than that of wild type AGS cells (491.30±5.02), and the difference was statistically significant (t=14.630, P=0.005).@*Conclusions@#The abnormally high expression of MACF1 in gastric cancer tissues may be correlated with the poor prognosis of patients with gastric cancer. MACF1 promotes the invasion and metastasis of gastric cancer cells by affecting the formation of F-actin and cell skeleton.
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Objective To explore the role of microtubule actin cross-linking factor 1 (MACF1) in the metastasis of gastric cancer.Methods From 2009 to 2012,at The First Affiliated Hospital of Zhengzhou University,the paraffin blocks of gastric cancer and normal tissue adjacent to cancer of 107 patients who received radical gastrectomy were collected.The expression of MACF1 in tissues at protein level was detected by immunohistochemical staining.In 2017,at The First Affiliated Hospital of Zhengzhou University,fresh specimens samples of gastric cancer and normal tissue adjacent to cancer of 42 patients who received radical gastrectomy were also collected.The expression of MACF1 at mRNA level was determined by quantitative real-time polymerase chain reaction (PCR).MACF1 knockout gastric cell line was established.The effects of MACF1 on cell migration and invasion were verified by wound-healing test and Transwell assay.The effects of MACF1 on cell microtubule and actin were analyzed by filamentous actin (F-actin) staining.T-test,chi-square test and multivariate analysis were used for statistical analysis.Results The positive expression rate of MACF1 in gastric carcinoma tissues was 71.0％ (76/107),which was significantly higher than that of the corresponding normal tissues adjacent to cancer (22.4％,24/107),and the difference was significant (t =4.145,P =0.016).The expression of MACF1 at mRNA level in cancer tissues of 42 patients with gastric cancer was 6.463 ±0.672,which was significantly higher than that of corresponding normal tissue adjacent to cancer (1.727 ± 0.331),and the difference was statistically significant (t =6.326,P ＜ 0.01).The differences in positive expression rate of MACF1 in different tumor infiltration depth,different TNM stage and lymph nodes metastasis were statistically significant (x2 =1.170,7.959 and 5.288;all P ＜ 0.01).The five-year survival rate of patients with high expression of MACF1 was 32.9％ (25/76),which was significantly lower than that ofpatients with normal MACF1 expression (64.5％,20/31),and the difference was statistically significant (x2 =25.093,P =0.034).The high expression of MACF1 was an independent prognostic factor affecting overall survival rate in patients with gastric cancer after surgery (hazard ratio (HR) =0.513,95％ confidence interval (CI):0.411 to 0.922,P =0.038).The results of wound-healing assay showed that at 24 hour after wound the migration ability of MACF1 knockout AGS-MACF1 / cells was (18.77 ± 3.82) ％,which was lower than that of wild type AGS cells ((76.24 ± 5.36) ％),and the difference was statistically significant (t =6.249,P =0.014).The migration ability of MACF1 knockout HGC27-MACF1-/-cells was (42.48 ± 7.37)％,which was lower than that of wild type HGC27 cells ((82.35-± 4.28) ％),and the difference was statistically significant (t =5.938,P =0.017).The results of Transwell assay indicated that the number of migration cells of MACF1 knockout AGS-MACF1-/-cells was 87.0 ± 11.0,which was less than that of wild type AGS cells (200.0 ± 16.0),and the difference was statistically significant (t =5.820,P =0.028).The number of migration cells of MACF1 knockout HGC27-MACF1-/-cells was 151.0 ± 13.0,which was less than that of wild type HGC27 cells (268.5 ± 20.5),and the difference was statistically significant (t =4.840,P =0.040).The results of F-actin staining demonstrated that the number of actin filaments of MACF1 knockout AGS-MACF1-/-cells was 216.60 ± 18.09,which was less than that of wild type AGS cells (491.30 ± 5.02),and the difference was statistically significant (t =14.630,P =0.005).Conclusions The abnormally high expression of MACF1 in gastric cancer tissues may be correlated with the poor prognosis of patients with gastric cancer.MACF1 promotes the invasion and metastasis of gastric cancer cells by affecting the formation of F-actin and cell skeleton.
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Objective: To investigate the expression of ALC1 protein during esophageal squamous cell carcinoma (ESCC) development and progression, so as to explore its association with clinicopathological characteristics and overall survival of ESCC patients, and the effect of ALC1 overexpression on malignant biological behavior of esophageal squamous cells. Methods: Immunohistochemistry (IHC) was used to detect ALC1 protein expression in 245 primary ESCC tissues and their paired normal esophageal mucous membranes, and to determine its correlation to gender, age, tumor cell differentiation, invasion, TNM stage, lymph nodes metastasis, and overall surviv-al rate of ESCC patients. MTT assay, colony formation assay, transwell invasion, and wound healing assay were used to observe the ef-fect of ALC1 on ESCC cell proliferation, invasion, and migration. Results: The expression ratio of ALC1 in esophageal squamous cell car-cinoma was higher compared with that in their paired normal esophageal mucous membranes (41.6% vs . 21.2% , P<0.05). Upregula-tion of ALC1 was associated with ESCC invasion, TNM stage, and lymph node metastasis (P<0.05). The overall survival of ESCC patients with ALC1 overexpression was significantly lower than that in patients with downregulated ALC1 expression (P=0.002). Therefore, ALC1 may promote the proliferation, invasion, and migration of ESCC cells. Conclusions: ALC1 upregulation may play an important role in the progression and development of ESCC. Upregulation of ALC1 leads to poorer disease prognosis, and could promote the prolifera-tion, invasion, and migration of the KYSE30 ESCC cells. Therefore, ALC1 may have potential prognostic value for ESCC patients.
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Objective To investigate the role of cell adhesion molecule L1 like (CALL) in the genesis and development of esophageal squamous cell carcinoma (ESCC).Methods From July 2007 to December 2010,a total of 100 patients with ESCC who received radical resection of esophageal cancer were enrolled.The ESCC tissues and corresponding tumor-adjacent normal tissues were obtained.The expression of CALl was determined by tissue microarray technology and immunohistochemical staining.The CALL over-expressed esophageal cancer cell line was established.The effects of CALL on cell migration and invasion were detected by wound-healing assay and Transwell assay,respectively.The effects of CALL on actin microfilament was analyzed by filamentous actin (F-actin) staining.Chi square test,Fisher's exact test,multivariate analysis and t test were performed for statistical analysis.Results The positive expression rate of CALL in ESCC tissues was 56 ％ (56/100),which was lower than that of tumor-adjacent normal tissues (95％,95/100),and the difference was statistically significant (x2=41.114,P＜0.01).There were statistically significant differences in CALL expression at protein level among patients with ESCC of different differentiation degree,different pathological T stage,lymph node metastasis and different TNM stage (x2=13.702,5.317,21.453,Fisher's exact test;all P＜ 0.05).The five year disease related survival rate of ESCC patients with down-regulated expression of CALL was 0(0/49),which was lower than those with normal CALL expression (25.5％,13/51),and the difference was statistically significant (x2 =43.338,P＜0.01).The median survival time of CALL expression down-regulated group was 17 months,and that of normal expressed group was 38 months.CALL expression was an independent risk factor of disease special survival rate (hazard ratio (HR) 0.353,95％ confidence interval (CI) 0.188 to 0.666,P=0.001).The results of wound-healing assay showed that the migration ability of CALL overexpressed CALL-k30 cells was lower than that of Vec-k30 cells in control group on 24 hours after wound.The results of Transwell invasion test showed the number of migrating cells penetrating CALL k30 cells attached to the inferior surface of the membrane was 44.000±13.748,which was less than that of the Vec k30 cells (154.333±25.007),and the difference was statistically significant (t=5.136,P=0.036).The results of F-actin staining demonstrated that actin filaments of CALL-k30 cells was 234.667 ± 65.118,which was lower than that of Vec-k30 cells (597.000± 119.929),and the difference was statistically significant (t=4.707,P=0.042).Conclusions CALL lowers the migration and invasion abilities of esophageal cancer cells by inhibiting F-actin microfilaments.Its abnormal expression may play an important role in the genesis,development and prognosis of ESCC.
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Background and purpose: Chemokines play an important role in cancer occurrence and development. However, little about the function of CCL26 in esophageal squamous cell carcinoma (ESCC) is reported. This study was designed to observe and study the expression of chemokine CCL26 in ESCC tissues and to analyze their association with pathological features of ESCC. Methods: Expressions of chemokine CCL26 in 197 ESCC tissues and their corresponding paraneoplastic normal esophageal tissues were determined by tissue array and immunohistochemistry (IHC) technique, and its correlations to age, gender, lymph nodes metastasis, TNM stage, general classification and 5-year survival rate of ESCC patients were further analyzed. Results: ①CCL26 was expressed in both ESCC and paraneoplastic normal esophageal tissues. The expression of CCL26 in ESCC tissues was signiifcantly higher than that in paraneoplastic normal esophageal tissues (61.8%vs 20.6%, P0.05).③Survival analysis showed that the abnormal expression of CCL26 was associated with 5-year survival rate of patients with ESCC. The 5-year survival rate of ESCC patients with CCL26 positive expression was obviously lower than that of ESCC patients with CCL26 negative expression. Conclusion: CCL26 upexpression might play an important role in the progression and development of ESCC patients. The high level of CCL26 expression is correlated with lymph node metastasis and poor survival. Detection of CCL26 expression may have important prognostic values in ESCC patients.
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<p><b>OBJECTIVE</b>To investigate the roll of bone sialoprotein (BSP), a secreted glycoprotein, found in mineralized tissues in the development and progression of human esophageal squamous cell carcimoma (ESCC), and explore its association with clinicopathological characteristics and five-year survival of the patients.</p><p><b>METHODS</b>The expression of BSP was determined in 211 primary ESCC tumors and their paired nontumorous tissues using tissue-array, RT-PCR and immunohistochemistry.</p><p><b>RESULTS</b>Primary ESCC tissues showed a significantly higher expression rate of BSP mRNA than their paired nontumorous tissues (93.8% vs. 16.6%, P < 0.001), the same with BSP protein (56.9% vs. 31.3%, P < 0.001). The expression rate of BSP protein was correlated to lymph node metastasis and TNM stage (P < 0.05). The 5-year survival rate of BSP protein-positive ESCC patients was significantly lower than that of BSP protein-negative ESCC patients (P < 0.05). Multivariate analysis showed that tumor differentiation, TNM staging and BSP protein expression were independent factors affecting the prognosis of ESCC patients (P < 0.05).</p><p><b>CONCLUSIONS</b>The abnormal expression of BSP may play a significant role in the malignant progression and prognosis of ESCC, and BSP might be a marker reflecting the biologial behavior of ESCC.</p>
Subject(s)
Humans , Blotting, Western , Carcinoma, Squamous Cell , Diagnosis , Metabolism , Esophageal Neoplasms , Diagnosis , Metabolism , Immunohistochemistry , Integrin-Binding Sialoprotein , Genetics , Metabolism , Lymphatic Metastasis , Neoplasm Staging , Prognosis , RNA, Messenger , Survival RateABSTRACT
Objective To evaluate the efficacy and safety of sorafenib in the treatment of advanced renal cell carcinoma.Methods The clinical date of 33 patients with advanced renal cell carcinoma from September 2007 to April 2012 was reviewed retrospectively.26 were males and 7 were females,with an average age of 69 years.Pathological diagnosis showed 30 clear cell RCCs,2 papillary RCCs,and 1 unclassified RCC.These patients were treated by sorafenib 400 mg twice a day until intolerable toxicity or disease progression.The primary end points were objective response rate,clinical benefit rate,median survival time,median progression-free survival and the incidence of adverse reaction.Results All patients were evaluable for response and toxicity,with 8 patients (24％) of partial remission,19 cases (58％) of stable disease,and 6 cases (18％) of disease progression.The disease control rate was 82％,the median progression-free survival was 10.2 months,while the median survival time was 16.5 months.The common adverse reactions included hand-foot skin reaction (61％),diarrhea (46％),hypertension (21％).Most adverse reactions occurred around the second week after drug therapy,with the duration unequal.The majority of adverse reactions could be released by symptomatic treatment,which did not affect the medication.Conclusion Sorafenib has good short term efficacy for patients with advanced renal cell carcinoma,and most adverse reactions were tolerable.