Peptic ulcer-induced acute aortogastric fistula occurring 7 years after a pharyngogastrostomy following a resection for carcinoma of the esophagus: report of a case.

A 46-year-old woman underwent a pharyngogastrostomy, following a laryngoesophagectomy for esophageal carcinoma. Although she had been disease-free for 7 years, she subsequently was admitted to undergo a workup due to fever along with chest and back pain. A few days after admission, the patient suddenly vomited a large volume of blood and went into shock. Bleeding was stopped with a Sengstaken-Blakemore tube, and an emergency thoracotomy was performed. A fistula between the thoracic aorta and an ulcer of the gastric tube was identified. We decided to close the aortic lesion directly because the adhesions were extremely dense and her blood circulation was poor. One week later, we resected the thoracic part of the gastric tube, debrided the fistula, and wrapped the aortic lesion with a patch. However, on the 18th postoperative day, she developed massive hematemesis due to rupture of an infected pseudoaneurysm in the thoracic aorta and died.

NF-kappa B-dependent induction of cyclin D1 by retinoblastoma protein (pRB) family proteins and tumor-derived pRB mutants.

The retinoblastoma protein (pRB) and its homologues, p107 and p130, prevent cell cycle progression from G(0)/G(1) to S phase by forming complexes with E2F transcription factors. Upon phosphorylation by G(1) cyclin-cyclin-dependent kinase (Cdk) complexes such as cyclin D1-Cdk4/6 and cyclin E-Cdk2, they lose the ability to bind E2F, and cells are thereby allowed to progress into S phase. Functional loss of one or more of the pRB family members, as a result of genetic mutation or deregulated phosphorylation, is considered to be an essential prerequisite for cellular transformation. In this study, we found that pRB family proteins have the ability to stimulate cyclin D1 transcription by activation of the NF-kappaB transcription factor. The cyclin D1-inducing activity of pRB is abolished by adenovirus E1A oncoprotein but not by the deletion of the A-box, the B-box, or the C-terminal region of the pocket, indicating that multiple pocket sequences are independently involved in cyclin D1 activation. Intriguingly, tumor-derived pRB pocket mutants retain the cyclin D1-inducing activity. Our results reveal a novel role of pRB family proteins as potential activators of NF-kappaB and inducers of G(1) cyclin. Certain pRB pocket mutants may give rise to a cellular situation in which deregulated E2F and cyclin D1 cooperatively promote abnormal cell proliferation.

Staged hepatectomy following arterial embolization for ruptured hepatocellular carcinoma.

BACKGROUND/AIMS: While hemostasis by transcatheter arterial embolization is often the first choice in the initial treatment of ruptured hepatocellular carcinoma, post-transcatheter arterial embolization treatment has not fully been established. We studied the prognoses of ruptured hepatocellular carcinoma cases where hepatectomy was possible after transcatheter arterial embolization. METHODOLOGY: We retrospectively reviewed 10 cases of ruptured hepatocellular carcinoma which had been treated in our institution between 1989 and 1998. In all the 10 cases, emergency transcatheter arterial embolization was performed, which successfully achieved hemostasis. RESULTS: Following the achievement of hemostasis by transcatheter arterial embolization, hepatectomy was carried out in 5 cases after evaluation of general condition, functional liver reserve and extent of tumor spread. There was neither operative nor hospital death. One-year and 3-year survival rates were 100% and 40%, respectively, and 50% survival time was 36 months. In the other 5 patients, hepatectomy was decided to be impossible after evaluation of general condition, functional liver reserve and extent of tumor spread; all of them died within 0.5-10 months after transcatheter arterial embolization. CONCLUSIONS: Among the patients with ruptured hepatocellular carcinoma, those in which hepatectomy was decided to be possible after evaluation of general condition, functional liver reserve and extent of tumor spread, following successful hemostasis by transcatheter arterial embolization, had fairly good prognoses.

Role of pRB-family/E2F complex in the inhibition of IL-3-dependent lymphoid cell proliferation.

Interleukin 3 (IL-3)-dependent proliferation of haematopoietic cells is specifically inhibited by p130, a member of the pRB-family proteins. p130 interacts with the cell-cycle regulatory E2F transcription factors, notably E2F-4 and E2F-5, and affects promoters containing E2F-binding sites through two distinct mechanisms. First, upon complex formation with E2F, it blocks transcriptional activation by E2F. Second, the formed p130-E2F complex binds to E2F sites and actively represses transcription by inhibiting the activity of surrounding enhancer elements on the promoter. To pursue the relative contributions of each mechanism in the p130-mediated inhibition of IL-3-dependent cell proliferation, we employed a dominant-negative DP-1, which suppresses both E2F-dependent transactivation and the formation of active transcriptional repressors. Ectopic expression of the dominant negative DP-1 in the IL-3-dependent BaF3 lymphoid cells gave rise to an inhibition of cell proliferation, which was concomitantly associated with a decrease in levels of cyclin E, an indispensable molecule for G1 to S-phase cell-cycle progression. Our results indicate that blocking E2F-dependent transactivation, but not the formation of p130-E2F transcriptional repressor complexes, is responsible for the inhibition of IL-3-dependent cell growth by p130.