Lymphatic metastasis is an important prognostic factor for pancreatic cancer.However,lymphatic metastatic status (N0 or N1) can not reflect the degree of lymphatic metastasis.Lymph node ratio,which is defined as the number of positive lymph nodes divided by total examined lymph nodes,can reflect the degree of lymph metastatic metastasis and give consideration to examined lymph nodes.Lymph node ratio is superior to lymph metastatic status in staging,guiding treatment,and predicting prognosis.However,currently,lymph node ratio cannot replace lymph metastatic status for the undetermined minimum number of examined lymph nodes and cut-off value.Further evidence is needed to prove its clinical value.

] Objective To explore the role and mechanisms of FGF2 in chemo?resistance in breast cancer. Methods The inhibitors for different signal pathway were used to treat two drug?resistant breast cancer cell lines MCF?7/5?Fu and T47D/5?Fu established in our lab. MTS assay was used to determine chemo?sensitivity and Hoechst stain was used to measure apoptosis. Protein activation and FGF2 protein level in cell culture medium were detected by western blot and ELISA respectively. Results Akt inhibitor MK?2206 (20 nM) and mTOR inhibitor AZD8055 (2 nM) significantly reversed the chemo?resistance of MCF?7/5?Fu and T47D/5?Fu cell lines to 5?Fu and paclitaxel, but ERK1/2 inhibitor SCH772984 showed no significant effect. Compared to parent cell lines MCF?7 and T47D, p?Akt and p?S6K (represented as mTORactivity) levels were obviously up?regulated in MCF?7/5?Fu and T47D/5?Fu cell lines, and so do the FGF2 mRNA level and FGF2 protein level from culture medium. Moreover, FGFR inhibitor AZD4547 (4 nM) markedly reversed the chemo?resistance of MCF?7/5?Fu and T47D/5?Fu cell lines to 5?Fu and paclitaxel and down?regulated activation of FGFR?Akt?mTOR signal pathway. In agreement, FGF2 protein (10ng/ml) enhanced the chemo?resistance of MCF?7 and T47D cell lines to 5?Fu and paclitaxel and up?regulated activation of FGFR?Akt?mTOR signal pathway. Conclusion Activation of FGF2?FGFR?Akt?mTOR signal pathway promoted chemo?resistance of breast cancer cells.

Objective To explore the role of insulin-like growth factor-2/insulin-like growth factor1 receptor/insulin receptor substrate-1 (IGF2/IGF1R/IRS1) signal pathway inducing the chemoresistance of epidermal growth factor receptor 2 (ErbB2) positive breast cancer cells to Herceptin.Methods Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay were used to determine the expression levels of IGF2,IGF1 R,and IRS1.The direct targets of miR-126 were validated by dual-luciferase reporter gene assay.In SKBR3/pool2 cells,IGF1 R activity was reduced by an inhibitor of IGF1 R,and IRS1 was knocked-down by shRNAs.Furthermore,3-(4,5-dimenthylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay was performed to evaluate the sensitivity of these treated cells to Herceptin.Results IGF2,IGF1 R,and IRS1 were significantly higher expressed in SKBR3/pool2 cell compared to that in SKBR3 cell.Western blot assay showed that IGF2/IGF1R/IRS1 was activated in SKBR3/pool2 cells.Bioinformatics analysis combined with luciferase activity suggested that miR-126 directly targeted IRS1.MTS results demonstrated that the chemosensitivity to Herceptin of SKBR3/ pool2 cells with inhibitor of IGF1R or shRNAs targeting IRS1 or overexpressing miR-126 was significantly reduced.Conclusions IGF2/IGF1R/IRS1 signal pathway confers to the chemoresistance of ErbB2 positive breast cancer cells to Herceptin.

Objective To study the role of preoperative CA19-9 level in predicting resectability of pancreatic cancer.Methods Preoperative CA19-9 levels were determined by radioimmunoassay.The receiver operating characteristic curve was used to determine the cut-off point.The clinical value of the level of CA19-9 as a predictive marker of resectability was evaluated by the area under curve.Results The preoperative CA19-9 levels in the resectahle group was (313.6±515.5) kU/L,which was significantly lower than (852.1± 865.1)kU/L in the unresectable group (P＜0.001).The cut-off point of CA19-9 for predicting pancreatic cancer resectability was 312.1 kU/L,which had a sensitivity of 56.6％ and a specificity of 73.3％.The area under curve was 0.67.Conclusions The preoperative CA19-9 level may be used to predict resectability of pancreatic cancer.

Pancreatic neuroendocrine tumor is a common pancreatic tumor with high heterogeneity and multiple management modalities. A standard and practical staging system for pancreatic neuroendocrine tumors will be beneficial to clinical management and research. At present, there are two staging systems (ENETS and AJCC). Both of them have shortcomings which limit their clinical application. In addition, the coexistence of two staging systems is confusing to clinicians. We proposed a modified ENETS staging system by keeping the ENETS TNM definition and adopting the AJCC staging definition. The modified staging system can successfully distinguish patients with different prognosis and is helpful in establishing clinical standard. This study has been published in Journal of Clinical Oncology (JCO) and was selected as 2017 Best of JCO: Gastrointestinal edition. This paper was aimed to interpret the modified staging system in clinical practice.

Lymph metastasis has great impact on the prognosis of pancreatic cancer patients, which can relfect the biological and invasive potential of pancreatic cancer. However, currently, there is no standard in the clinical management of the lymph metastasis in pancreatic cancer. In this report, we will discuss and summarize the followings:lymph metastatic rate and its impact on prognosis, the rule of lymph metastasis, sentinel lymph node, intra-operative lymph nodes mapping, TNM staging, regional lymph nodes resection, number of lymph nodes examined, lymph node ratio, guiding adjuvant treatments, lymphatic targeted therapy.

Background and purpose:Ultrasound is a regular screening method of solid pseudopapillary tumor of the pancreas (SPTP). This study was to summarize the diagnostic value of ultrasound to SPTP.Methods:Clinical and ultrasound data of 62 SPTP cases in Fudan University Shanghai Cancer Center were retrospectively collected and analyzed.Results:Five cases of SPTP were undetected by ultrasound in the group. The features of ultrasound including: large mass located at the body and tail of the pancreas, clear boundary and regular shape, low ultrasound with uneven signal, or low signal mixed with no signal. A few cases have calciifcation and blood signal. Most of the cases presented no dilation of main pancreatic duct and bile duct and regional lymph nodes enlargement. Conclusion:Ultrasound can be used to detect SPTP which has special ultrasound signal features.

Non-small cell lung cancer (NSCLC) is the histological subtype with highest proportion of lung cancer. Since the discovery of NSCLC driver gene mutations, the drug treatment of NSCLC had evolved from conventional chemotherapy to molecular targeted therapy. Epidermal growth factor receptor (EGFR) was one of the most important driver genes of NSCLC. Three generations of tyrosine kinase inhibitors (TKIs) targeting mutant EGFR had been developed and applied to the clinic, and EGFR-tKIs Targeted therapy had significantly improved the progression-free survival(PFS) and overall survival(OS) of patients with NSCLC. However, most NSCLC patients inevitably developed drug resistance within 10-18 months after receiving targeted therapy with EGFR-TKIs. Great progress had been made on the research of EGFR-TKIs resistance mechanism in recent years. This article intended to briefly review the resistance mechanism of EGFR-TKIs targeted therapy in terms of EGFR secondary mutation, signal bypass activation, cell lineage switching and tumor microenvironment, etc.

Objective To explore the role and mechanism of long non-coding RNA (lncRNA)RP11-316M1.12 in breast cancer cells.Methods Bioinformatics analysis was performed to varify RP11-316M1.12 expression pattern in breast cancer tissues and normal tissues.Quantitative real time polymerase chain reaction (qRT-PCR) assay was used to check the expression level of RP11-316M1.12 in breast cancer cells and tissues.Further,the correlationship between RP11-316M1.12 expression and clinical paremeters of breast cancer was analysed according to RP11-316M1.12 level.RP11-316M1.12 was overexpressed in MCF-7 cells,and RP11-316M1.12 was knocked down in MDA-MB-231 cells.Transwell method was used to detect the invasive ability of these cells.Western blot was used to detect the expression of epithelialmesenchymal transition (EMT) markers in these cells.Results Gene Expression Profiling Interactive Analysis (GEPIA) database suggested that RP11-316M1.12 was highly expressed in breast cancer tissues than that in normal tissues.The similar results were got in 65 cases of breast cancer tissues and 23 cases of normal tissues by qRT-PCR assay.Meanwhile,we found that RP11-316M1.12 was enhanced in breast cancer cells than that in normal epithelial cell and RP11-316M1.12 expression is related to TNM stage and distant metastasis in breast cancer.Transwell assay demonstrated that RP11-316M1.12 significantly enhanced breast cancer cells invasion.Mechanismly,over expression of RP11-316M1.12 can remakably downregulated E-cadherin,enhanced ZEB1 and Vimentin expression in these cells.Conclusions RP11-316M1.12 was enhanced in breast cancer,and RP1 1-316M1.12 could accelerate invasion of breast cancer cells.