Rare common bile duct metastasis of breast cancer: A case report and literature review.

BACKGROUND: Breast cancer is the most common tumor in women, and about one-third of cases develop metastatic disease. However, metastatic breast cancer rarely invades the common bile duct (CBD) directly without involving the liver, and involvement of the gastrointestinal tract is rare. Cases of such metastases pose a particular diagnostic challenge. CASE SUMMARY: A 55-year-old female presented to the Department of Gastroenterology with complaint of a 2 mo history of right upper abdominal pain accompanied by pain in the right back, aggravated after eating greasy diet. The patient had received a diagnosis of breast cancer 3 years prior. Physical examination showed obvious superficial protuberant erythema on the left neck and chest skin, with slight tenderness and burning sensation. Endoscopic retrograde cholangiopancre-atography showed an obstruction at the end of the CBD. Histopathology of the CBD and symptomatic skin biopsies showed positivity for cytokeratin 7 and trans-acting T-cell-specific transcription factor breast cancer biomarkers. A cancer embolus was also found in the skin vasculature. Accordingly, the diagnosis of breast cancer metastases to the skin and biliary ducts was made. A plastic biliary sent was placed, which relieved the right upper abdominal pain and protected against unnecessary hepatectomy surgery. CONCLUSION: Although rare, biliary metastasis should be considered in patients with bile duct stenosis and a history of breast cancer.

CAPS1 promotes colorectal cancer metastasis via Snail mediated epithelial mesenchymal transformation.

Colorectal cancer (CRC) is a common gastrointestinal cancer with high mortality rate mostly due to metastasis. Ca2+-dependent activator protein for secretion 1 (CAPS1) was originally identified as a soluble factor that reconstitutes Ca2+-dependent secretion. In this study, we discovered a novel role of CAPS1 in CRC metastasis. CAPS1 is frequently up-regulated in CRC tissues. Increased CAPS1 expression is associated with frequent metastasis and poor prognosis of CRC patients. Overexpression of CAPS1 promotes CRC cell migration and invasion in vitro, as well as liver metastasis in vivo, without affecting cell proliferation. CAPS1 induces epithelial-mesenchymal transition (EMT), including decreased E-cadherin and ZO-1, epithelial marker expression, and increased N-cadherin and Snail, mesenchymal marker expression. Snail knockdown reversed CAPS1-induced EMT, cell migration and invasion. This result indicates that Snail is required for CAPS1-mediated EMT process and metastasis in CRC. Furthermore, CAPS1 can bind with Septin2 and p85 (subunit of PI3K). LY294002 and wortmanin, PI3K/Akt inhibitors, can abolish CAPS1-induced increase of Akt/GSK3ß activity, as well as increase of Snail protein level. Taken together, CAPS1 promotes colorectal cancer metastasis through PI3K/Akt/GSK3ß/Snail signal pathway-mediated EMT process.

Auphen and dibutyryl cAMP suppress growth of hepatocellular carcinoma by regulating expression of aquaporins 3 and 9 in vivo.

AIM: To investigate whether the regulation of aquaporin 3 (AQP3) and AQP9 induced by Auphen and dibutyryl cAMP (dbcAMP) inhibits hepatic tumorigenesis. METHODS: Expression of AQP3 and AQP9 was detected by Western blot, immunohistochemistry (IHC), and RT-PCR in HCC samples and paired non-cancerous liver tissue samples from 30 hepatocellular carcinoma (HCC) patients. A xenograft tumor model was used in vivo. Nine nude mice were divided into control, Auphen-treated, and dbcAMP-treated groups (n = 3 for each group). AQP3 and AQP9 protein expression after induction of xenograft tumors was detected by IHC and mRNA by RT-PCR analysis. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay and histological evaluation were used to detect apoptosis of tumor cells, and the concentration of serum α-fetoprotein (AFP) was measured using RT-PCR and an ELISA kit. RESULTS: The volumes and weights of tumors decreased significantly in the Auphen- and dbcAMP-treated mice compared with the control mice (P < 0.01). The levels of AQP3 were significantly lower in the Auphen treatment group, and levels of AQP9 were significantly higher in thedbcAMP treatment mice than in the control mice (P < 0.01). The reduction of AQP3 by Auphen and increase of AQP9 by dbcAMP in nude mice suppressed tumor growth of HCC, which resulted in reduced AFP levels in serum and tissues, and apoptosis of tumor cells in the Auphen- and dbcAMP-treated mice, when compared with control mice (P < 0.01). Compared with para-carcinoma tissues, AQP3 expression increased in tumor tissues whereas the expression of AQP9 decreased. By correlating clinicopathological and expression levels, we demonstrated that the expression of AQP3 and AQP9 was correlated with clinical progression of HCC and disease outcomes. CONCLUSION: AQP3 increases in HCC while AQP9 decreases. Regulation of AQP3 and AQP9 expression by Auphen and dbcAMP inhibits the development and growth of HCC.

[The reason and management of the sunken upper eyelid after hydroxyapatite platform implantation].

OBJECTIVE: To study the reason and the management of the sunken upper eyelid after implanting a hydroxyapatite platform. METHODS: From 1998, we developed a method of subperiosteal implantation at the orbital floor to repair the introcession of the upper eyelid after hydroxyapatite platform implantation. 11 cases of the sunken upper eyelid were treated with this method. The implants included Medpor in 2 cases, hydroxyapatite plates in 7 cases and acellular dermal matrix in 2 cases. RESULTS: Postoperatively, all the patients obtained satisfactory results. Follow-up for 1 to 4 years showed no complications of extrusion or infection of the implants. Re-operation was needless in all of them. CONCLUSION: Subperiosteal implantation to correct the sunken upper eyelid is a safe and effective method.