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We present a patient with systemic lupus erythematosus receiving long-term steroid therapy, who had myometrial thinning, markedly thickened placenta, and fetal growth restriction (FGR). Blood flow profiles of the myometrium, decidua and placental villous vessels (VV) were described using superb microvascular imaging (SMI) at 35 weeks' gestation. Images showed no decidual blood flow underneath the placenta sitting on a thin myometrium and sparse VV distribution and non-visualization of peripheral VV flow. Emergency cesarean hysterectomy was performed at 36 weeks. Histological findings showed missing decidua on the thin myometrium, which indicated placenta accreta spectrum, and massive perivillous fibrin deposition and increased numbers of syncytial knots in the placenta. We speculated that the thick placenta and peculiar VV flow profiles resulted from congestion of the intervillous space and intervillous underperfusion/low intraplacental oxygenation, respectively, resulting in FGR. Superb microvascular imaging is useful for diagnosing placenta accreta spectrum and understanding the pathophysiology of thick placenta and FGR.

We present a case of a 34-year-old pregnant woman with a prior cesarean delivery presenting with placenta previa. Placenta previa accreta was diagnosed from missing decidual flow signals using superb microvascular imaging (SMI). At 31 weeks' gestation, B-mode ultrasonography showed that the placenta was attached to the anterior uterine segment, extending over the internal cervical os. In normally appearing myometrium, SMI demonstrated double layers of flow signals underneath the placental basal plate, corresponding to myometrial and decidual flows. The thin myometrium located on the bladder where sonolucent zones were not visible revealed three different flow patterns in the Doppler signals underneath the basal plate as follows: double layers (both myometrium and decidual tissues present); a single layer (myometrium alone) or no layers (decidual tissues missing). A cesarean hysterectomy was performed at 37 weeks, and histology confirmed the presence of placenta accreta.

The myc target gene Mina53 was reported to be overexpressed in esophageal cancer with a poor prognosis. The purpose of the present study was to examined Mina53 expression and its relationship to clinicopathological parameters in human renal cell carcinoma (RCC). Mina53 and Ki-67 expression was examined on immunohistochemistry for 64 surgically resected RCC and non-cancerous tissue. In addition, the relationship between Mina53 expression and clinicopathological prognostic factors of RCC such as age, stage, microvenous invasion (MVI), histological subtype, Ki-67 labeling index (LI), and prognosis, was examined. Mina53 was expressed in the nuclei of tumor cells and tubular nuclei of normal renal tissue. The expression level of Mina53 was significantly higher in patients with poor prognostic factors (stage IV, MVI-positive, and sarcomatoid RCC, and high Ki-67 LI). The prognosis of high Mina53-expressing tumors was significantly poorer than that of non-Mina53-high tumors (P < 0.0001). In conclusion, Mina53 is overexpressed in RCC tissue from patients with poor prognostic factors, suggesting that Mina53 overexpression is one of the factors for poor prognosis in RCC.

PURPOSE We investigated the effects of pegylated IFN-alpha2b (PEG-IFN-alpha2b) on the growth of human liver cancer cells. METHODS The effect of PEG-IFN-alpha2b on the proliferation of 13 liver cancer cell lines was investigated in vitro. Chronological changes in growth and IFN-alpha receptor-2 (IFNAR-2) expression were monitored in hepatocellular carcinoma (HCC) cells (HAK-1B) cultured with PEG-IFN-alpha2b. After HAK-1B cells were transplanted into nude mice, various doses of PEG-IFN-alpha2b or IFN-alpha2b were administered, and tumor volume, weight, histology, and IFNAR-2 expression were examined. RESULTS PEG-IFN-alpha2b inhibited the growth of nine cell lines with apoptosis in a dose- and time-dependent manner. Continuous contact with PEG-IFN-alpha2b induced time-dependent growth inhibition and down-regulation of IFNAR-2 expression. PEG-IFN-alpha2b induced a dose-dependent decrease in tumor volume and weight, a significant increase of apoptotic cells, and a decrease in IFNAR-2 expression in the tumor. The clinical dose for chronic hepatitis C was also effective. The antitumor effect of PEG-IFN-alpha2b was significantly stronger than that of non-PEG-IFN-alpha2b in vivo. CONCLUSIONS Continuous contact with PEG-IFN-alpha2b induces strong antitumor effects and the down-regulation of IFNAR-2 in HCC cells. The data suggest potential clinical application of PEG-IFN-alpha2b for the prevention and treatment of HCC.