Mixed primary mucinous cystadenocarcinoma and invasive ductal carcinoma of the breast: a case report and literature review.

Background: Mucinous cystadenocarcinoma (MCA) mainly occurs in the ovary, pancreas, and appendix, whereas the breast is a rare primary site of occurrence. Invasive ductal carcinoma (IDC) is the most common breast malignancy. Only 31 cases of the breast MCA have been reported in the English literature, and the coexistence of MCA and IDC in the breast are rare. Case Description: Here, we describe a 61-year-old postmenopausal woman with no family history of breast cancer or other breast-related diseases, who presented with a palpable mass in her left breast lasting for 2 months. On ultrasonography examination, the tumor was a cystic-solid lesion with clear boundary. Magnetic resonance imaging (MRI) showed a mass with low signal intensity on T1 weighted imaging and high signal intensity on T2 weighted imaging. Intraoperative frozen sections revealed metastatic tumor cells in one sentinel lymph node (1/4). She then underwent left modified radical mastectomy with axillary dissection. The post-operative pathological examination showed the tumor consisted mostly of MCA (60%), with a small proportion of intermediate-grade IDC. The MCA had a well-demarcated cystic structure with papillary projections and abundant mucoid material. The epithelium lining cystic spaces was tall columnar, with mucin-producing cells that had basally located nuclei. The degree of cytological atypia varied considerably. Axillary lymph nodes were normal (0/15). The MCA was triple-negative for estrogen receptor (ER), progesterone receptor (PR), and HER2, and positive for CK7 but negative for CK20. Through next-generation sequencing, no mutations in the BRCA1 and BRCA2 genes were identified in our case, which was not highlighted in prior cases. After surgery, the patient underwent eight cycles of chemotherapy, and she has been disease-free during the 10-month follow-up. In addition to detailing this instance of mixed MCA and IDC of the breast, we reviewed relevant literature and compare our findings with other patients who had breast MCAs. Conclusions: Our results improved the understanding of mixed MCA and IDC, especially MCA, and provided a basis for its diagnosis and differential diagnosis from other metastatic diseases.

Influence of bushenhuoxue on podocytes of focal segmental glomerulosclerosis mice.

OBJECTIVE: To observe the effects and mechanisms of Bushenhuoxue on desmin and nephrin expression in mice podocytes, and to investigate its effects on wt1 expression in Wilms' tumor. METHODS: Adriamycin (ADR) was used to induce focal segmental glomerulous sclerosis (FSGS) in mice. Bushenhuoxue was used to treat FSGS for 6 weeks. We measured body mass and right renal mass, and determined serum albumin (ALB) levels, protein content in urine, and urinary protein and albumin creatinine ratio (UACR). Changes in renal tissue morphology were evaluated by microscopy. wt1 and nephrin expression in podocytes were detected using immunofluorescence. Expression levels of desmin, wt1 and nephrin mRNAs in renal tissue were determined using reverse transcription polymerase chain reaction assays. RESULTS: Protein levels in urine and UACR were significantly increased in FSGS model mice compared with Bushenhuoxue-treated and control mice. Body mass and ALB levels were decreased in FSGS mice compared with control and Bushenhuoxue-treated mice. Expression of the wt1 protein was observed in control mice. Compared with controls, wt1 expression levels were reduced in Bushenhuoxue-treated mice, and to a greater extent in FSGS mice. Nephrin protein expression was widespread in FSGS mice, and significantly reduced in control and Bushenhuoxue mice. Expression levels of wt1 and nephrin mRNAs in FSGS mice were lower compared with those in control and Bushenhuoxue-treated mice. Desmin mRNA levels in FSGS mice were reduced compared with those in control and Bushenhuoxue-treated mice. CONCLUSION: Bushenhuoxue ameliorated albuminuria in FSGS mice; this was possibly related to the up-regulation of wt1 and nephrin, and down-regulation of desmin.

The effect of combination therapy of allicin and fenofibrate on high fat diet-induced vascular endothelium dysfunction and liver damage in rats.

BACKGROUND: It is designed to investigate the effects of combination therapy of allicin and fenofibrate on the endothelial and liver functions in rats with hyperlipidemia. METHODS: The healthy male Wistar rats fed high fat diet were treated with fenofibrate (80 mg/kg per day) alone, allicin (60 mg/kg per day) alone and a lower dosage of combined therapy (allicin 20 mg/kg per day and fenofibrate 30 mg/kg per day) respectively for 8 weeks. The serum levels of cholesterol, triglyceride, nitrogen oxidative, alanine transferase (ALT) and aspartate transferase (AST) were determined. Acetylcholine-induced endothelium-dependent vascular relaxation (EDVR) of aorta rings was tested, and the morphologic changes of liver tissue were observed. RESULTS: Compared with high fat diet control, fenofibrate alone or the combined therapy increased remarkably the levels of high density lipoprotein respectively (P<0.05). Both single and combined therapy of fenofibrate and allicin significantly enhanced the levels of NO (P<0.01 or P<0.05), but the combined therapy had greatest high EDVR responses (P<0.01). Furthermore, the reduced levels of ALT and AST were significantly obvious in the combined therapy groups (P<0.01 or P<0.05). In addition, the lower dosage of combined therapy significantly ameliorated severe fatty degeneration of liver cells occurred in the high fat diet fed rat although the single fenofibrate treatment showed spotty necrosis of liver cells and bile duct expansion. CONCLUSION: Combination therapy with allicin and fenofibrate can effectively enhance the protective effects on endothelial function and reduce the hepatic damage in rats with hyperlipidemia.

[Effect of JAK/STAT pathway activation on high glucose-induced transdifferentiation in renal proximal tubular epithelial cells].

OBJECTIVE: To evaluate the effect of JAK/STAT signaling pathway activation on the transdifferentiation and secretion of transforming growth factor-beta1 (TGF-beta1) induced by high glucose in renal proximal tubular epithelial cells. METHODS: Human kidney cells (HKC) were cultured and then divided into four groups: low glucose (LG) group, high glucose (HG) group, high mannitol (LG + M) group, and HG + AG490 group. Immunoprecipitation and Western blot analysis were used to determine the expression of tryosine phosphorylated Janus kinase 2 ( p-JAK2). The protein expressions of STAT1, STAT3, p-STAT1, and p-STAT3 and the expressions of alpha-SMA and E-Cadherin were observed by Western blot. The contents of TGF-B1, fibronectin and type I collagen in the supernatants of the cultured HKC were detected by enzyme-linked immunosorbent assay (ELISA). The expression of TGF-beta1 mRNA was measured by reverse transcription and polymerase chain reaction (RT-PCR). RESULTS: Compared with LG group, the expressions of JAK2, p-STAT1, p-STAT3, and TGF-beta1, mRNA were significantly increased in HG group from 6 to 72 hours. Meanwhile, the contents of TGF-beta1 and collagen I in the supernatants and the expression of alpha-SMA increased and the expression of E-Cadherin decreased. The expressions of JAK2, p-STAT1, p-STAT3, and TGF-beta mRNA as well as the levels of TGF-beta1 and collagen I in the supernatant s in HG + AG490 group were significantly lower than in the HG group. The expressions of alpha-SMA and E-Cadherin were also decreased in HG + AG490 group. CONCLUSION: Activation of JAK/STAT signaling pathway may be involved in the high glucose-induced transdifferentiation and overproduction of TGF-beta1, and ECM proteins in HKCs.