Background and purpose:Tumor budding is a poor prognostic factor in colorectal cancer. In this study, we studied the tumor budding by counting the actual number in 10 high power fields and evaluated itsclinical application in predicting lymph node metastasis of T1 colorectal cancer.Methods:Tissue specimens from 307 patients with histologically conifrmed T1 colorectal cancer were enrolled. The clinicopathological characteristics including tumor budding were evaluated for their predictive value in lymph node metastasis. A formula was created to calculate the risk score for prediction of lymph node metastasis which was validated by 14 new cases.Results:In the multivariate analysis, it showed that tumor grade, lymphovascular invasion and the number of tumor budding were signiifcantly associated with lymph node metastasis. The probability of lymph node metastasis was calculated using the following equations:Z=1.571×(lymphovascular state: invasion, 1; no invasion, 0)+2.661×(tumor grade: high grade, 1; low grade, 0)+0.024×(budding counts)-3.885; Probability=1/1+e-Z. The high scores were correlated with the lymph node metastasis in the validations.Conclusion:We can accurately assess the risk of lymph node metastasis by counting the number of tumor budding in 10 high power fields. Therefore tumor budding could potentially assist treatment decision making in T1 colorectal cancer patients with high-risk lymph node metastasis.

Objective In this study, we aimed to translate and revise the Summary of Diabetes Self-Care Activities( SDSCA) and the Confidence In Diabetes Self-care( CIDS) scales, to test the reliability and validity of the two scales in Chinese adult type 1 diabetes( T1D) patients. Methods In the first step, Chinese versions( C-SDSCA and C-CIDS) were developed conceptually equivalent to the English versions. And the investigation was conducted in 100 patients from Guangdong T1D Translational Medicine Study. 15 of them were randomly chosen to be retested 4 weeks later. Cronbach's α were used to assess reliability, and factor analysis to its validity. The relationship between scores of C-SDSCA and C-CIDS were analyzed using Spearman correlation analysis. Results The overall Cronbach's α of C-SDSCA was 0.72 and the retest reliability was 0.95( sub-scale:0.67-1.00) . 4 common factors were extracted by factor analysis, and the cumulative contribution was 87.39％. As for C-CIDS, the general Cronbach's α was 0.84 and the retest reliability was 0. 70 ( sub-scale: 0. 49-0. 86 ) . 6 common factors were extracted and the cumulative contribution was 75.41％. The score of the two scales was positively related(r=0.61, P<0.01). Conclusion The revised C-CIDS and C-SDSCA scales turn out to have good reliability and validity, and can be used as instruments to assess diabetes self-management efficacy and self-care activities of Chinese adult T1D patients.

OBJECTIVE: To investigate the differential expression of the sensitive and resistant relative proteins in human breast cancer tissue. METHODS: A drug sensitive group and a drug resistant group for chemotherapy in patients with breast cancer were selected through neoadjuvant. The differential protein expression in 2 groups was detected by proteomics techniques, and parts of differential proteins were identified by Western blot. RESULTS: There were 13 differential proteins in the 2 groups, in which the expression of 3 proteins was up-regulated and 10 down-regulated. Seven proteins were identified by Western blot. The expression of keratin type I cytoskeletal 19 (KIC19), thymidine phosphorylase (TYPH) was upregulated, and the expression of heat shock protein 27 (HSP27), keratin type I cytoskeletal 9 (KIC9), collagen alpha-2(VI) (CO6A2), vimentin (VIME), and actin cytoplasmic 1 (ACTB) was down-regulated in the drug resistant group. There was significant difference between the 2 groups (P<0.01). CONCLUSION The expression of KIC19 and TYPH may be correlated with drug resistance in patients with breast cancer, and HSP27, KIC9, CO6A2, VIME, and ACTB may be correlated with drug sensitivity.
Adult ; Aged ; Breast Neoplasms ; drug therapy ; genetics ; metabolism ; Carcinoma, Ductal, Breast ; drug therapy ; genetics ; metabolism ; Drug Resistance, Neoplasm ; genetics ; Female ; Gene Expression Profiling ; HSP27 Heat-Shock Proteins ; metabolism ; Humans ; Keratin-19 ; metabolism ; Keratin-9 ; metabolism ; Middle Aged ; Neoadjuvant Therapy ; Neoplasm Proteins ; metabolism ; Proteome ; metabolism ; Proteomics ; Thymidine Phosphorylase ; metabolism

Objective:To investigate the clinicopathological characteristics of gastrointestinal tumors with SWI/SNF complex deficiency and to perform a prognostic analysis of the patients.Methods:Gastrointestinal tumor cases with SWI/SNF complex deficiency expression diagnosed at the Department of Pathology, Zhongshan Hospital, Fudan University, Shanghai, China from August 2021 to May 2023 were collected. Hematoxylin and eosin (HE) stained slides were reviewed, and immunohistochemical results were analyzed. Clinical and pathological information was recorded, and relevant literature was reviewed.Results:A total of 36 cases of gastrointestinal tumor with loss of SWI/SNF complex expression were identified, including 28 males (77.8%) and 8 females (22.2%). The average age at diagnosis was 70 years (range 48-85 years). Clinical staging showed 3 cases in stage Ⅰ (8.3%), 12 cases in stage Ⅱ (33.3%), 19 cases in stage Ⅲ (52.8%), and 2 cases in stage Ⅳ (5.6%). Complete or partial loss of ARID1A expression was observed in 20 cases (55.6%); complete or partial loss of SMARCA2 expression was observed in 24 cases (66.7%). SMARCA4 exhibited complete loss of expression in 4 cases (11.1%). Eleven cases (30.6%) showed concurrent complete or partial losses of both ARID1A and SMARCA2 expression. Twelve cases (33.3%) had mismatch repair protein deficiency, all of which were characterized by MLH1/PMS2 absence. Mismatch repair protein deficiency was associated with loss of ARID1A expression ( P<0.01). Patients with mismatch repair protein deficiency were also associated with earlier clinical stage and a lower risk of lymph node metastasis compared to the ones with intact mismatch repair proteins ( P<0.05). Conclusions:SWI/SNF complex deficiency in gastrointestinal tumors is associated with dedifferentiation and often accompanied by mismatch repair protein deficiency. Compared to the cases with intact mismatch repair proteins, the cases with defective mismatch repair protein have an earlier clinical stage and a lower risk of lymph node metastasis.

Objective:To compare the histologic features of immune-mediated hepatitis (IMH) due to immune checkpoint inhibitors (ICIs) monotherapy and combined ICIs anti-angiogenesis tyrosine kinases (TKIs) targeted therapy.Methods:Twenty-one IMH patients who had liver biopsy during ICIs treatment in Zhongshan Hospital of Fudan University from 2015 to 2019 were included. Among them, ten were treated with ICIs monotherapy, and 11 were treated with combined ICIs and anti-angiogenesis targeted therapy. The histologic features of IMH were assessed by HE staining and PD-L1/2 was evaluated by immunohistochemical staining.Results:Patients treated with monotherapy ICIs presented with different levels of lobular hepatitis and portal inflammation. Besides, there were also cholangitis, endothelialitis, Kupffer cells activation and peliosisi hepatitis. Eight cases (8/10) showed mild and two cases (2/10) showed moderate hepatic injury. As for patients receiving combined ICIs and TKIs therapy, the extent of IMH was more severe, with four cases (4/11) showing moderate-severe liver injury, with confluent or bridging necrosis, portal inflammation, cholangitis, interface hepatitis. Among these, one patient developed acute severe hepatitis with massive hepatocyte necrosis and died of multisystem dysfunction. In those cases with severe liver injury, many CD8 positive lymphocytes aggregated in the portal area and hepatic sinusoid, and PD-L1 was expressed in many endothelial cells. There were both 2 cases of death in ICIs monotherapy and combination therapy group. Among the latter group, 1 patient developed acute severe hepatitis with massive hepatocyte necrosis and died of multisystem dysfunction.Conclusion:Compared with ICIs monotherapy, combined ICIs and anti-angiogenesis targeted TKIs therapy may cause overlapping hepatic injury, leading to severe IMH.