Objective To study the effect of gonadotropin releasing hormone agonist(GnRHa)against car-boplation-induced gonadotoxicity in rats. Methods Forty Wistar rats were divided into four groups which received carboplation, GnRHa + carboplation, GnRHa and normal saline respectively(n=10 for each group). Blood samples were collected from the abdominal aorta and the levels of blood follicle stimulation hormone (FSH) and estradiol (E<2>) were determined. Both ovaries and uterus of each rat were removed to measure the amount and the maturity of follicles. Body mass and morphological and pathological features of the rats were also observed. Results Compared with that in control group, the body mass of ovary and uterus decreased (P<0.05), and a significant reduction was observed in the number of ovarian follicles at each grade (P<0.05). The levels of E2 significantly lowered (P<0.05) and the level of FSH markedly ascended in group carboplation. Compared with that in group carboplation, the amount of primitive follicles significantly increased in group GnRHa + carboplation (P<0.05), and carboplation showed markedly protective effect on the ovarian and uterine morphological construction of rats. Conclusion Gn-Rha, appliying to preventing the rat reproduction damage in advance, has the certain protective function.

Serum levels of CXC chemokine ligand 10 (CXCL10) and chemokine receptor 3 (CXCR3) were determined in 50 patients with type 1 diabetes mellitus (T1 DM) and 30 normal control subjects by ELISA method.The results showed that serum levels of CXCL10 and CXCR3 in T1DM patients were significantly higher than those in normal subjects [(258.17 ± 39.12 vs 96.47 ± 26.91) ng/L,(851.87 ± 70.04 vs 441.82 ± 72.24) pg/ml,both P＜0.05].Serum level of CXCL10 in patients dropped sequentially with durations of diabetes ＜6 weeks,≥6 weeks or ＜3 years,and ≥ 3 years,being statistically significant between groups (P＜0.05).These results suggest that serum levels of CXC10 and CXCR3 may reflect the immune activity in T1DM.

Purpose To investigate the relationship between HPV infection and p53,p16,EGFR expression and prognosis in patients with salivary adenoid cystic carcinoma (ACC).Methods Totally 76 cases of adenoid cystic carcinoma specimens were selected,PCR-reverse dot blot hybridization was used to detect infection of HPV and SP immunohistochemical method was adopted to detect the expression of p53,p16,EGFR,Cdc2 in tumor tissues.Clinical data were collected and all the patients were followed up.The Kaplan-Meier method was used to estimate median overall survival and the Log-rank test to compare survival curves.Cox regression model was used for multivariate analyses.Results Infection rate of HPV in adenoid cystic carcinoma tissues was 0(0/76).The expression rate of p53,p16,EGFR,Cdc2 protein in adenoid cystic carcinoma tissues were 76.3％ (58/76),57.9％ (44/76),60.5％ (46/76) and 64.5％ (49/76)respectively.There was no correlation of the expression of p53,p16,EGFR and Cdc2 with gender,age,tumor location,TNM stage and histological type of patient.Kaplan-Meier survival analysis showed that EGFR-positive patients had shorter median overall survival rate (OS) than the negative ones (x2 =19.111,P ＜ 0.001).EGFR-positive patients had shorter median progression-free survival rate (PFS)than the negative ones (x2 =6.621,P ＜ O.01).Cdc2 positive patients had shorter median OS than the negative ones (x2 =3.870,P ＜ 0.05).Cdc2 positive patients had shorter median PFS than the negative ones (x2 =6.755,P ＜0.01).Cox regression analysis showed that expression of EGFR and Cdc2 was independent risk factors for the prognosis of patients with salivary gland ACC (relativerisk=13.417,13.075,P＜0.001).Conclusion There is no HPV infection detected in adenoid cystic carcinoma tissues.p53,p16,EGFR and Cdc2 are positively expressed in most salivary adenoid cystic carcinoma,p16 is unsuitable as a surrogate for HPV infection status of patient with ACC.Expression of EGFR and Cdc2 is independent risk factors in the prognosis of patients with salivary gland ACC.For the EGFR or Cdc2 positive patients should be followed up closely.

Objective: To evaluate the prognostic value of kinetic changes in minimal residual disease (MRD) status, as well as its relationship with risk stratification, therapeutic response and treatment in patients with newly-diagnosed multiple myeloma (MM) . Methods: A total of 135 patients with newly-diagnosed MM were screened, and 105 patients who achieved VGPR or more as the best responses were included into this study. The MRD status was determined by multiparameter flow cytometry (MFC) at multiple intervals after two cycles of treatment until clinical relapse, death, or last follow-up. The statistical methods included Kaplan-Meier analysis, Cox regression, etc. Results: ①In all 135 patients, 57.8% (78/135) patients achieved MRD negativity (MRD^-) after treatment. In 105 patients who achieved VGPR and thus included in this study, the MRD^- rate was 72.4% (76/105) , with a median interval of 3 months from starting treatment to achievement of MRD^- status. ②The 2-year PFS rate of patients with MRD^- status was significantly higher than that of MRD⁺ status (62.2% vs 41.3%, P=0.001) , while MRD persistence (MRD⁺) was an independent factor for poor prognosis (multivariate analysis for PFS: P=0.044, HR=3.039, 95%CI 1.029-8.974) . ③Loss of MRD^- status (i.e., MRD reappearance) showed inferior outcomes compared with MRD sustained negative ones, the PFS was 18 months versus not reach (P<0.001) and the OS was not reach for both (P=0.002) . ④The 2-year PFS and OS rates of patients with duration of MRD^-status≥12 months were significantly higher than those of the control group (PFS: 77.7% vs 36.7%, P<0.001; OS: 96.4% vs 57.9%, P<0.001 respectively) . Duration of MRD^- status was associated with a marked reduction in risk of relapse or death (univariate analysis for PFS: P<0.001, HR=0.865, 95%CI 0.815-0.918; for OS: P=0.001, HR=0.850, 95%CI 0.741-0.915 respectively) . ⑤Moreover, even in patients carrying high-risk cytogenetic abnormalities (CA) or ineligible for ASCT, MRD negativity remained its prognostic value to predict PFS (high-risk CA medianPFS: not reach vs 19 months, P=0.006; ineligible for ASCT medianPFS: not reach vs 25 months, P=0.052 respectively) . ⑥Last, treatment with the bortezomib-based regimens contributed to prolonged MRD^- duration (median MRD^- duratio: 25 months vs 10 months, P=0.034) . Conclusion Our findings supported MRD⁺ status as an independent poor prognostic factor in MM patients, which implicated that duration of MRD^- status also played a significant role in evaluation of prognosis, while loss of MRD^-status might serve as an early biomarker for relapse. Therefore, monitoring of MRD kinetics might more precisely predict prognosis, as well as guide treatment decision, especially for when to start retreatment in relapsed patients.

OBJECTIVETo investigate the association of neuroendocrine differentiation with progression and prognosis of gastric adenocarcinoma.

METHODSClinicopathological data of 240 patients with gastric adenocarcinomas were retrospectively analyzed. The expression of chromogranin A, synaptophysin and secrectagogin in cancer tissue was assessed by immunohistochemistry. The association of neuoroendocrine differentiation parameters with disease progression and survival of patients was analyzed.

RESULTSThe expression of synaptophysin was positively correlated with depth of invasion and secretagogin more often expressed in cases with lymph node metastasis. In Lauren diffuse type of cancer, expression of chromogranin A and secretagogin was unfavorable prognostic predictor. In TNM stage II adenocarcinoma, expression of chromogranin A and synaptophysin related to poor survival, and multivariate Cox proportional hazard model showed that synaptophysin was an independent predictor for poor survival.

CONCLUSIONNeuroendocrine differentiation predicts deeper depth of invasion, more possibility of lymph node metastasis and poor survival in gastric adenocarcinoma.

Adenocarcinoma ; diagnosis ; pathology ; Biomarkers, Tumor ; metabolism ; Chromogranin A ; metabolism ; Disease Progression ; Humans ; Immunohistochemistry ; Lymphatic Metastasis ; Neoplasm Staging ; Neuroendocrine Tumors ; diagnosis ; pathology ; Prognosis ; Proportional Hazards Models ; Retrospective Studies ; Secretagogins ; metabolism ; Stomach Neoplasms ; diagnosis ; pathology ; Synaptophysin ; metabolism