Yunfeng Shan

Decreased Expression of LKB1 Correlates with Poor Prognosis in Hepatocellular Carcinoma Patients Undergoing Hepatectomy

AIM To study any correlation of LKB1 expression with prognosis in hepatocellular carcinoma (HCC) cases. METHODS A total of 70 HCC patients and 20 primary intrahepatic stone patients in the first affiliated hospital of Wenzhou Medical College were enrolled in this study. LKB1 expression was detected by immunohistochemistry. Patients were followed-up and prognostic factors were evaluated. RESULT LKB1 expression was decreased in the HCC samples. Loss of LKB1 expression in HCC was significantly related to histologic grade (P=0.010), vascular invasion (P=0.025) and TMN stage (P=0.011). Patients showing negative LKB1 expression had a significantly shorter disease-free and overall survival than those with positive expression (P = 0.001, P=0.000, respectively). Multivariate Cox regression analysis indicated that LKB1 expression level was an independent factor of survival (P = 0.033). CONCLUSION HCC patients with decreased expression LKB1 have a poor prognosis. The loss of LKB1 expression is correlated with a lower survival rate.

Correlation between tuberous sclerosis complex 2 and glycogen synthase kinase 3 beta levels, and outcomes of patients with hepatocellular carcinoma treated by hepatectomy.

Tuberous sclerosis complex 2 (TSC2), a tumor suppressor, may play an essential role in the regulation of cell growth and cell survival under energy stress conditions. In addition, TSC2 may act in concert with Wnt and energy signals by additional phosphorylation of glycogen synthase kinase 3β (GSK3β) to regulate cell growth. The expression levels and function of TSC2 and GSK3β in hepatocellular carcinoma (HCC) remain unclear.

Effect of NK4 Transduction in Bone Marrow-Derived Mesenchymal Stem Cells on Biological Characteristics of Pancreatic Cancer Cells

Pancreatic cancer usually has a poor prognosis, and no gene therapy has yet been developed that is effective to treat it. Since a unique characteristic of bone marrow-derived mesenchymal stem cells (MSCs) is that they migrate to tumor tissues, we wanted to determine whether MSCs could serve as a vehicle of gene therapy for targeting pancreatic cancer. First, we successfully extracted MSCs from SD rats. Next, MSCs were efficiently transduced with NK4, an antagonist of hepatocyte growth factor (HGF) which comprising the N-terminal and the subsequent four kringle domains of HGF, by an adenoviral vector. Then, we confirmed that rat MSCs preferentially migrate to pancreatic cancer cells. Last, MSCs expressing NK4 (NK4-MSCs) strongly inhibited proliferation and migration of the pancreatic cancer cell line SW1990 after co-culture. These results indicate that MSCs can serve as a vehicle of gene therapy for targeting pancreatic cancer.

Autophagy regulates proliferation and biliary differentiation of hepatic oval cells via the MAPK/ERK signaling pathway

Hepatic oval cells (HOCs) are thought to possess self‑renewal ability and a bipotential capacity for differentiation, which allows them to differentiate into hepatocytes and cholangiocytes. Autophagy serves an important role in self‑renewal and differentiation of stem cells; however, how autophagy contributes to proliferation and differentiation of hepatic progenitor cells has yet to be elucidated. In the present study, autophagy was regulated by rapamycin (Rapa) and chloroquine (Chlo) administration. The results demonstrated that Chlo‑treated HOCs exhibited decreased autophagic activity alongside a decreased tendency to proliferate, as determined by Cell Counting Kit‑8. In addition, activation of autophagy by Rapa enhanced the biliary differentiation of HOCs. Furthermore, increased phosphorylated (p)‑extracellular signal‑regulated kinase (ERK)/p‑p38 expression was observed following the induction of autophagy, thus indicating that the mitogen‑activated protein kinase (MAPK)/ERK signaling pathway was activated by autophagy to exert effects on the stimulation of HOC proliferation and differentiation. In conclusion, the present study demonstrated that autophagy regulates proliferation and biliary differentiation of HOCs via the MAPK/ERK signaling pathway. These results suggest a role for autophagy in stimulating the proliferation and differentiation of HOCs.

Discovery of a novel human lactate dehydrogenase A (LDHA) inhibitor as an anti-proliferation agent against MIA PaCa-2 pancreatic cancer cells

LDHA has recently emerged as an attractive target for cancer therapy. Herein, we present the discovery of a potent LDHA inhibitor 12, which has good inhibitory activity to LDHA (IC50 = 1.50 μM). Moreover, the inhibitor 12 strongly inhibits the proliferation of MIA PaCa-2 pancreatic cancer cells (EC50 = 3.16 μM), suggesting it could serve as a promising candidate for further investigation.

A rare case of primary chondrosarcoma arising from the sternum: A case report

The current study reports a case of an extremely rare tumor that presented in an uncommon location, which was successfully treated via radical resection and reconstruction. A 37-year-old female, with no notable medical history, with the exception of a cesarean delivery, was admitted to The First Affiliated Hospital of Wenzhou Medical University (Wenzhou, China) due to pain and a lump of the anterior chest wall. The mass was identified on the manubrium sterni and was not tender on palpation. A chest computed tomography (CT) scan reconstruction identified the abnormal mass on the manubrium sterni (size, 5×4 cm in diameter) and positron emission tomography-CT interpretation strongly indicated a type of well-differentiated malignant tumor, such as a giant cell tumor. An aspiration needle biopsy was not conducted, however, the patient underwent tumor radical resection and sternal reconstruction using steel wire and titanium mesh. Histopathological examination of the surgical specimen determined the diagnosis of chondrosarcoma. A postoperative chest X-ray revealed that the sternal defect had repaired well, therefore, this procedure may be highly beneficial in future for repairing defects in the sternum.

Undifferentiated embryonal liver sarcoma in childhood: A case report

In order to improve the diagnosis and therapy of undifferentiated embryonal liver sarcoma (UELS), the present study presents the case of a 9-year-old female with UELS and discusses UELS in childhood. The patient presented with abdominal pain and fever. The laboratory tests, radiographic examination and pathological features presented by the female were similar to those of typical cases of UELS reported in childhood. The patient initially received surgical treatment and the immunohistochemical findings suggested that the patient had UELS. The patient’s parents refused adjuvant chemotherapy and demonstrated a right prerenal mass 6 months post-surgery. Microscopic examination revealed that the tumor was evidence of undifferentiated embryonal sarcoma recurrence. However, the patient was comfortable and physical examination revealed no abnormal conditions. In addition, the laboratory results were normal. Abdominal computed tomography scan and ultrasound were performed every 3 months to monitor the tumor recurrence. At the time of writing, it has been 6 months after the second surgical procedure and there has been no appearence of abnormalities. Previous studies have shown that patients who receive combined therapy with complete tumor resection and adjuvant chemotherapy have a longer survival time than those who undergo surgical therapy alone. Complete tumor resection combined with adjuvant chemotherapy may reduce the risk of recurrence and enhance the survival time in patients with UELS.