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Fong-Fu Chou

Publications and source records attributed to Fong-Fu Chou.

22 records · Page 2Linked to original sources

Overexpression of tumor susceptibility gene TSG101 in human papillary thyroid carcinomas.

Functional inactivation of tumor susceptibility gene tsg101 leads to cellular transformation and tumorigenesis in mice. While human TSG101 is located in a region where frequent loss of heterozygosity can be detected in a variety of cancers, no genomic deletion in TSG101 gene has been reported, casting a doubt on the role of TSG101 as a classical tumor suppressor. Some studies have revealed that TSG101 is a frequent target of splicing defects, which correlate with cellular stress and p53 status. Furthermore, recent reports have identified TSG101 as a part of the MDM2/p53 regulatory circuitry, a well-recognized circuitry that upon deregulation results in tumorigenesis. Interestingly, overexpression of tsg101 from an adventitious promoter also leads to neoplastic transformation. On the basis of this information, we have analysed TSG101 gene expression in 20 human papillary thyroid carcinomas (PTCs) by immunohistochemistry and demonstrated that the overexpression of TSG101 protein is closely associated with human PTCs. Further sequence analysis reveals no mutation in cDNA region encoding steadiness box in these PTC specimens, indicating that the upregulation of TSG101 protein is not caused by the alteration of this region. In situ hybridization analysis confirms that overexpression of TSG101 also occurs at the transcriptional level. In addition, semi-quantitative RT-PCR and subsequent Southern hybridization verify that the amounts of TSG101 transcripts are indeed lower in three normal thyroid tissues than in PTC specimens. Here we report the upregulation of TSG101 expression in PTC cells, providing the first evidence of the association of TSG101 overexpression with human tumors and suggesting that upregulation of TSG101 steady-state level might play a role in mediating tumorigenesis of human PTC.

Antibody Specificity↗

Intraoperative parathyroid hormone measurement in patients with secondary hyperparathyroidism.

HYPOTHESIS: Secondary hyperparathyroidism decreases renal clearance of parathyroid hormone (PTH). OBJECTIVE: To determine whether rapid PTH assays can be used to predict the success of a total parathyroidectomy to treat symptomatic secondary hyperparathyroidism. DESIGN: Case series from August 1 to December 31, 2000. SETTING: Tertiary referral center. PARTICIPANTS: Patients with symptomatic secondary hyperparathyroidism (n = 24) who underwent total parathyroidectomy and autotransplantation were included in the study. INTERVENTIONS: Blood samples for rapid PTH analyses were drawn from an indwelling catheter at the induction of anesthesia (baseline) and before (0 minutes), 10 minutes, and 30 minutes after the removal of the last parathyroid gland. Regular intact PTH (iPTH) assays were conducted later. MAIN OUTCOME MEASURE: If a patient's regular iPTH levels were below 65 pg/mL at 1 week or 3 months postoperatively, the operation was considered successful. RESULTS: All 24 patients had successful operations. Rapid PTH and regular iPTH correlated significantly at 0, 10, and 30 minutes. Rapid PTH levels decreased significantly at each time period and were 176 +/- 40.9 pg/mL (mean +/- SE) at 10 minutes. The percentage decrease in rapid PTH levels was 39.5% +/- 12.7% at 0 minutes, 75.1% +/- 6.2% at 10 minutes, and 91.0% +/- 0.1% at 30 minutes (mean +/- SE). A decrease of 60% or more from baseline PTH levels at 10 minutes and/or a decrease of 85% or more at 30 minutes predicted the successful removal of all parathyroid glands. CONCLUSIONS: A drop in PTH levels is delayed until 30 minutes after total parathyroidectomy; however, a rapid PTH assay 10 minutes after the removal of the last parathyroid gland is as accurate as an assay performed at 30 minutes postoperatively. Intraoperative PTH monitoring demonstrates relevant decreases in rapid PTH levels after parathyroidectomy that are similar to those previously documented in patients with primary hyperparathyroidism.

Alkaline Phosphatase↗

Persistent and recurrent hyperparathyroidism after total parathyroidectomy with autotransplantation.

OBJECTIVE: To conduct a retrospective study of 15 patients with persistent (n = 4) and recurrent (n = 11) hyperparathyroidism. SUMMARY BACKGROUND DATA: Secondary hyperparathyroidism may persist or recur because of hyperfunction of the parathyroid remnant or transplanted parathyroid tissue. It is a great challenge to localize the parathyroid tissue either in the neck or at the arm before surgery. METHODS: From June 1994 to June 2000, 15 patients with recurrent and persistent secondary hyperparathyroidism were selected for surgery for the removal of parathyroid tissue. The indications for surgery included bone pain, hypercalcemia, general weakness, and skin itching. Their ages ranged from 23 to 66 years. The average period of persistent hyperparathyroidism after total parathyroidectomy with autotransplantation was 3.8 months; that of recurrent hyperparathyroidism was 53 months. Serum levels of calcium, phosphorus, parathyroid hormone (iPTH), and alkaline phosphatase were measured before surgery and 1 week after surgery. Before surgery, the parathyroid gradient in the blood draining the graft-bearing arm versus the contralateral arm was measured. A 99mTc-sestamibi (MIBI) scan was performed including the neck and the arm area, and a computed tomography (CT) scan of the neck was performed to confirm the localization. The neck and mediastinal exploration was done directly at the side of localization under general anesthesia to remove the parathyroid tissue that had been located with the MIBI scan or CT scan. An arm exploration was done under local anesthesia to remove all parathyroid tissues detected in the MIBI scan or palpable masses during surgery. If all glands were removed, 0.5 x 0.5 x 0.5 cm of tissue (60-100 mg) was maintained in situ or the same amount of tissue was reimplanted. RESULTS: The average ratio of iPTH in the graft-bearing arm to the contralateral arm in the 5 patients with parathyroid tissue in the neck was 1.17 +/- 0.16, and that in the 10 patients with parathyroid at the arm was 14.15 +/- 16.62. A significant difference was found between the two groups. MIBI scans showed parathyroid tissues in the neck in four of five patients and in seven of eight patients at the arm. Computed tomography showed the parathyroid tissues in the neck and mediastinum in five of five patients (100%). Five glands were removed from these five patients, three in the neck, one in the mediastinum, and one in the carotid sheath. In total, 20 glands and 2 half-glands were removed from 10 patients; among these, 14 glands were shown in the MIBI scan. All patients had improvements of symptoms and signs after surgery. Serum levels of calcium, phosphorus, and iPTH decreased rapidly after surgery, but alkaline phosphatase did not. CONCLUSIONS: With the results obtained from the ratio of iPTH of the graft-bearing arm to the contralateral arm, clinical palpation of the arm, MIBI scan, CT scan, careful surgical exploration, and adequate resection, recurrent and persistent secondary hyperparathyroidism can be successfully treated with surgery in the neck or at the arm.

Adult↗

Massive hemobilia.

BACKGROUND/AIMS: Massive hemobilia is a relatively rare, but potentially life-threatening cause of upper gastrointestinal hemorrhage. We report our experiences in the treatment of 15 cases of massive hemobilia with different underlying pathologies. METHODOLOGY: Massive hemobilia is defined as a patient with blood discharge from the biliary tree and requiring whole blood transfusion for at least 4 u (1 u = 250 cc). Fifteen such patients were collected during an 8.5-year period (from January 1986 to July 1994), and the clinical courses of these patients were retrospectively reviewed. RESULTS: Among these 15 patients, 11 were males and 4 were females. Age distribution was from 33 to 78 years old. Mean age was 59.7 years. The cause of hemobilia included: percutaneous transhepatic biliary drainage in 7 patients, surgical trauma in 3, choledochoscopic extraction of biliary calculi in 1, pancreatic cancer in 1, radiotherapy for cholangiocarcinoma in 1, after operation for biliary lithiasis in 1, and rupture of the pseudoaneurysm in 1. In 11 patients, hemobilia was first noted by bleeding from percutaneous transhepatic biliary drainage tube (n = 10) or T-tube (n = 1). Three patients had hemobilia during choledocholithotomy. The other one was diagnosed by choledochoscopy. Treatment included pitressin infusion from angiographic catheter in one patient, transarterial embolization in 1, hepatic artery ligation in 1, hepatic artery ligation and transarterial embolization in 1, choledochotomy or choledocholithotomy in 2, and blood transfusion only in 9. Two of the four mortality cases had underlying malignancy. CONCLUSIONS: The most common cause of massive hemobilia was percutaneous transhepatic biliary drainage procedures. Eight cases were successfully treated with blood transfusion only. Transarterial embolization, hepatic artery ligation and open drainage were effective non-surgical and surgical procedures, but the former two procedures might not be successful if sudden and severe hemobilia developed, or when an aberrant hepatic artery existed. Main hepatic artery had better been isolated before removal of the percutaneous transhepatic biliary drainage tube during operation.

Adult↗