Junko Nagata

Clinical implications of interleukin (IL)-10 induced by non-small-cell lung cancer

BACKGROUND The type 2 cytokine interleukin (IL)-10 has been reported to inhibit the antitumour activity of the regional immunity against various neoplasms. Certain lung cancers produce IL-10, but the clinical significance of IL-10 expression is not well understood. PATIENTS AND METHODS We examined IL-10 and IL-10 receptor (IL-10R) mRNA expression in 82 non-small-cell lung cancers (NSCLC) by reverse transcription-polymerase chain reaction (RT-PCR) assay. Immunohistochemistry (IHC) and enzyme immunoassay (EIA) were applied to evaluate the cellular localisation and the serum levels of IL-10. RESULTS RT-PCR assay revealed IL-10 mRNA expression in 68 (83%) of 82 NSCLC surgical specimens (40 of 50 adenocarcinomas, 22 of 26 squamous cell carcinomas, 5 of 5 large-cell carcinomas, 1 of 1 adenosquamous-cell carcinoma). RT-PCR assay also revealed IL-10R mRNA expression in 79 cases of NSCLC (96.1%). IL-10 expression was confirmed within tumour cells by IHC. EIA showed no significant serum IL-10 elevation in the 12 NSCLC positive for IL-10 mRNA expression (0-2.99 pg/ml). The NSCLC patients with IL-10 production showed significantly poorer prognosis than those without IL-10 production (P < 0.05, Kaplan Meier, log-rank test). CONCLUSIONS These results suggested that the cytoplasmic IL-10 correlated to clinical prognosis, and that IL-10 expression is a prognostic factor for NSCLC.

Adenocarcinoma and multiple adenomas of the large intestine, associated with Cronkhite-Canada syndrome

The Cronkhite-Canada syndrome is a rare non-hereditary disorder with generalised gastrointestinal polyposis, associated with ectodermal changes. We report here a case of adenocarcinoma and multiple adenomas of the large intestine associated with Cronkhite-Canada syndrome in a 61-year-old Japanese man. Histologically, the rectal tumour was composed of well-differentiated tubular adenocarcinoma, admixed with foci of adenomatous components, and associated with hyperplastic mucosa of Cronkhite-Canada syndrome. Multiple polyps, >20 polyps < or = 2.0 cm in diameter, were found near the carcinoma of the resected rectum. Histologically, superficial parts of the polyps were composed of tubular adenomas, and basal parts of the polyps were hyperplastic dilated glands. It was speculated that, in the present case, the rectal adenocarcinoma arose from mucosal hyperplasia (Cronkhite-Canada polyp)-adenoma-carcinoma pathway. This suggested that Cronkhite-Canada syndrome has definite malignant potential, although the frequency of malignant transformation is thought to be low in Cronkhite-Canada syndrome.

Balloon-occluded arterial stump pressure before balloon-occluded transarterial chemoembolization

Abstract Objective To evaluate balloon-occluded arterial stump pressure (BOASP), which is responsible for effective balloon-occluded transarterial chemoembolization (B-TACE), at each hepatic arterial level before B-TACE using a 1.8-French tip microballoon catheter for unresectable hepatocellular carcinoma (HCC). Material and methods The BOASP at various embolization portions was retrospectively investigated. “Selective” and “non-targeted” BOASP was defined as the BOASP at the subsegmental or segmental artery and the lobar artery, respectively. Results The measurement of the BOASP was carried out in 87 arteries in 47 patients. BOASP > 64 mmHg was revealed in the caudate lobe artery (A1) and the left medial segmental (A4), right anterior superior segmental (A8), anterior segmental, right and left hepatic arteries. Significant difference was noted in the incidence of BOASP above 64 mmHg between “non-targeted” and “selective” BOASP (p = 0.01). “Non-targeted” BOASP was significantly greater than “selective” BOASP (p = 0.0147). In addition, the BOASP in A1, 4, 8 and the anterior segmental arteries were significantly greater than in the other subsegmental and segmental arteries (p = 0.0007). Conclusion “Non-targeted” B-TACE should be avoided to perform effective B-TACE and “selective” B-TACE at A1, 4, 8 and the anterior segmental arteries may become less effective than at the other segmental or subsegmental arteries.