Jinu-Huang Su

Correlations between umbilical and maternal serum adiponectin levels and neonatal birthweights

Objective.  To measure adiponectin levels in maternal serum and umbilical cord serum at delivery, and examine whether or not there are correlations between adiponectin levels and neonatal birthweights, maternal body weights and body mass indexes.

High Visfatin Expression in Breast Cancer Tissue Is Associated with Poor Survival

Background: Adipocytokines, adipocyte-secreted hormones, play a critical role in breast cancer development. The expression of visfatin, a newly discovered adipocytokine, in breast cancer tissues was determined and correlated with patient clinicopathologic variables. Methods: Visfatin expression in breast cancer tissues was analyzed by immunohistochemistry. Visfatin expression was correlated with clinicopathologic variables as well as recurrence rates, using the χ2 test. The prognostic value of visfatin for disease-free and overall survival was evaluated by Kaplan–Meier estimates, and the significance of differences between curves was evaluated by the log-rank test. Results: High visfatin expression in breast cancer tissues was significantly correlated with tumor size, estrogen receptor (ER) negativity, and progesterone receptor (PR) negativity. Hormone therapy, but not radiotherapy or chemotherapy, decreased the recurrence rate in patients with high visfatin expression. Whereas high visfatin expression alone was associated with poor disease-free and overall survival, worse disease-free and overall survival was observed when high visfatin expression was combined with ER- and PR-negative status. Cox regression analysis also revealed that visfatin is an independent predictor of disease-free and overall survival. Conclusion: High visfatin expression in breast cancer tissue is associated with more malignant cancer behavior as well as poor patient survival. Impact: Visfatin is an independent prognosis predictor for breast cancer. Cancer Epidemiol Biomarkers Prev; 20(9); 1892–901. ©2011 AACR.

STAT3 ser727 phosphorylation and its association with negative estrogen receptor status in breast infiltrating ductal carcinoma.

Although it is known that STAT3 transcriptional activity is modulated by phosphorylation at serine residue 727, the role of STAT3 serine phosphorylation in breast cancer remains mostly unexplored. In this study, we examined the expression patterns of serine residue 727‐phosphorylated STAT3 (p‐ser727‐STAT3) in breast infiltrating ductal carcinoma tissues and nearby noncancer tissues by using immunoblotting techniques, and correlated the expression profiles with clinicopathological characteristics. A significantly elevated p‐ser727‐STAT3 expression was observed in 61.8% (42/68) of breast cancer tissues as compared to corresponding noncancer tissues (p < 0.001). Further, immunohistochemical analysis also showed an increased nuclear p‐ser727‐STAT3 staining in cancer lesions. The increased p‐ser727‐STAT3 expression in breast infiltrating ductal carcinoma tissues correlated significantly with negative estrogen receptor (ER) status, increased stage of cancer and increased tumor size (p = 0.001, 0.024 and 0.014, individually). Intriguingly, we noticed that the expression levels of p‐ser727‐STAT3 in ER‐negative breast cancer cell lines were higher than those in ER‐positive breast cancer cell lines. In ER‐positive MCF7 cells, treatment with ERα‐specific siRNA increased, whereas treatment with anticancer drug tamoxifen decreased the expression of p‐ser727‐STAT3, phenomena not observed in ER‐negative MDA‐MB‐231 cells. In conclusion, our results suggest that p‐ser727‐STAT3 may be involved in the pathogenesis of breast cancer in an ER‐dependent manner.

Arsenic-induced Mre11 phosphorylation is cell cycle-dependent and defective in NBS cells.

Cancer-prone diseases ataxia-telangiectasia (AT), Nijmegen breakage syndrome (NBS) and ataxia-telangiectasia-like disorder (ATLD) are defective in the repair of DNA double-stranded break (DSB). On the other hand, arsenic (As) has been reported to cause DSB and to be involved in the occurrence of skin, lung and bladder cancers. To dissect the repair mechanism of As-induced DSB, wild type, AT and NBS cells were treated with sodium arsenite to study the complex formation and post-translational modification of Rad50/NBS1/Mre11 repair proteins. Our results showed that Mre11 went through cell cycle-dependent phosphorylation upon sodium arsenite treatment and this post-translational modification required NBS1 but not ATM. Defective As-induced Mre11 phosphorylation was rescued by reconstitution with full length NBS1 in NBS cells. Although As-induced Mre11 phosphorylation was not required for Rad50/NBS1/Mre11 complex formation, it might be required for the formation of Rad50/NBS1/Mre11 nuclear foci upon DNA damage.

Decreased expression of phosphorylated JNK in breast infiltrating ductal carcinoma is associated with a better overall survival

Phosphorylation/activation of c‐jun NH2‐terminal kinase (JNK) has an ambivalent role, pro‐proliferation or antiproliferation, in human cancers, which is determined by different cell types and by its crosstalk with other kinases. So far, the role of phosphorylated JNK (p‐JNK) in breast cancer is mostly undefined. In this study, we analyzed the expression of p‐JNK, as well as p‐ERK1/2 and p‐38, in the pair of cancer and noncancer breast tissues, by using immunoblotting techniques. These results were further correlated with the clinicopathological characteristics and overall survival. Decreased p‐JNK1/2 expression in cancer tissues was observed in 48.5% of breast infiltrating ductal carcinoma (IDC) cases and was correlated significantly with the increased tumor grade and the decreased age at diagnosis (p = 0.030 and 0.029). Interestingly, the Kaplan–Meier survival curve showed that the decreased p‐JNK1/2 expression was associated with a better overall survival of IDC (p = 0.004). The expression of p‐JNK1/2 was positively correlated with p‐p38 (p = 0.002), but not p‐ERK1/2. Furthermore, co‐expressed p‐JNK1/2 and p‐p38 was associated with a poor overall survival of IDC (p = 0.007). In conclusion, our results indicate that the aberrant p‐JNK1/2 expression and the co‐expressed p‐JNK1/2 and p‐p38 in breast tissues may play a role in the carcinogenesis of breast IDC.

Elevated amniotic fluid leptin levels in pregnant women who are destined to develop preeclampsia.

Objective. To analyze whether leptin levels of the amniotic fluid elevate during early pregnancy in women destined to develop preeclampsia and to evaluate the relationship between amniotic fluid leptin levels and gestational age, maternal body mass index, and fetal sex. Study design. Leptin levels of the amniotic fluid were compared in two groups of women, preeclamptic (n=20) and normotensive pregnant (n=40), matched for fetal sex, maternal body mass index at sampling, gravidity and fetal gestational age at sampling. Furthermore, amniotic leptin levels in 400 normotensive pregnant women were analyzed for their correlation with gestational age, maternal body mass index, and fetal sex. Results. Median leptin concentrations were significantly higher (p<0.001) in the women with preeclampsia (7.3±0.7 ng/ml) than in the normotensive pregnant women (4.1±0.3 ng/ml), independent of fetal sex. The leptin levels in the amniotic fluid decreased with advanced gestational age (r=0.24, p<0.001). Amniotic fluid leptin levels in the pregnant women carrying a female fetus (5.6±0.3 ng/ml) were significantly higher than those carrying a male fetus (4.7±0.2 ng/ml) (p = 0.004). Conclusion. Higher amniotic fluid leptin levels were observed in the preeclamptic pregnant women, and they decreased as gestational age advanced. Furthermore, the women with a female fetus were noted to have higher amniotic fluid leptin levels.

Decreased serum leptin levels in women with uterine leiomyomas.

Objective. To analyze the possible involvement of leptin in uterine leiomyomas.

Positive Association between STAT3 and Ki-67 in Cervical Intraepithelial Neoplasia

Signal transducer and activator of transcription 3 (STAT3) has been regarded as an oncogene in many types of cancers. However, its role in cervical carcinogenesis is not well determined. The purpose of this study was to evaluate the expression patterns of STAT3 in cervical intraepithelial neoplasia (CIN), normal cervix (NC), and squamous cell carcinoma (SCC) to explore its possible role in cervical carcinogenesis. Paraffin‐embedded sections from 83 patients including 20 CIN 1, 10 CIN 2, 26 CIN 3, and 27 comparative cases of 10 NC and 17 stage Ib SCC were collected in this study. Immunohistochemistry was performed to analyze the expression patterns of STAT3, and the results obtained were categorized by a semiquantitative method and were further correlated with the CIN histopathologic grade and the proliferation marker, Ki‐67, using the c2 test. Our results showed that nuclear STAT3 expression was predominantly in the squamous epithelial cells, and that high‐grade CIN and stage Ib SCC lesions had a higher nuclear STAT3 expression when compared with NC and CIN 1. Furthermore, the nuclear STAT3 expression in CIN was significantly correlated with Ki‐67 expression (p= 0.025), but not CIN lesion grade. In summary, our results indicate that an altered STAT3 expression in CIN is correlated with cell proliferation but may not have a direct contribution to cervical carcinogenesis.

Retroperitoneal leiomyomas: a rare tumor of the pelvis.

Retroperitoneal leiomyomas are extremely rare and have a good prognosis. Long-term follow-up reveals no metastasis but local recurrences do occur. These tumors, like uterine leiomyomas, are frequently accompanied by hyaline or myxoid changes as well as a trabecular pattern. Most are positive for estrogen and progesterone receptors. Herein, we report a 46-year-old woman with retroperitoneal leiomyomas who had undergone laparoscopically assisted vaginal hysterectomy 5 years previously due to uterine leiomyomas. Treatment by laparoscopic excision was successful and immunohistochemical staining of the tumor tissue was negative for estrogen and progesterone receptors.