The differential diagnosis of canine adrenal tumors was feasible based on triple-phase CT findings, including morphological features, CT values, and intratumoral contrast attenuation. Preoperative diagnosis using triple-phase helical CT may be useful for surgical planning in dogs with adrenal tumors.

Near-infrared fluorescence imaging may be feasible for intraoperative mapping of hepatocellular carcinomas in hepatic lobes and may help increase the chance of complete resection of hepatocellular carcinoma in dogs.

This prospective case study aimed to clarify the clinical significance of contrast-enhanced ultrasound (CEUS) for the differential diagnosis of canine adrenal tumors. Forty-three client-owned dogs with adrenal tumors were included. All dogs underwent CEUS, which was evaluated qualitatively and quantitatively. The peak signal intensity (PI), time to peak signal intensity (TPI), mean transit time (MTT), upslope, and downslope were calculated for each time-intensity curve. The histopathological diagnosis of each resected mass was compared with the CEUS findings and parameters. Enhancement distribution, vascularity, tortuous nourishing vessels, enhancement pattern, and late-phase enhancement did not differ significantly between adrenal cortical adenoma (CA), adenocarcinoma (CAC), and pheochromocytoma (PHEO) in qualitative assessment. In PHEO, the TPI was significantly more rapid compared with that in CA ( P =0.0287) and CAC ( P =0.0404). The MTT in PHEO was significantly shorter than that in CA ( P =0.0016) and CAC ( P =0.0003). Upslope in PHEO was larger than that in CAC ( P =0.0406). Downslope in PHEO was significantly larger than that in CA ( P =0.0048) and CAC ( P =0.0018). A receiver operating characteristic curve analysis demonstrated that the area under the MTT curve yielded 0.91 for distinguishing PHEO from adrenocortical tumors in dogs; an MTT cut-off value less than 6,225 msec yielded a sensitivity of 69%, specificity of 94%, and likelihood ratio of 12.46. CEUS appears to be clinically applicable for the differential diagnosis between cortical and medullary origins of primary adrenal tumors in dogs.

SUMMARY We report a case of primary aldosteronism in a 30-year-old woman without hypertension or any other characteristic symptoms. The condition was first suspected by hypokalemia (2.6 mEq/liter), which was incidentally found by routine checkup. There was evidence of suppressed plasma renin activity (PRA) and elevated plasma aldosterone levels. However, the blood pressure never reached a hypertensive level, and the circulating blood volume was within a normal range. A functioning right adrenal tumor was diagnosed by adrenal scintigraphy, computerized x-ray tomography, and adrenal venography. Adrenal venous catheterization suggested an aldosteronoma, which was confirmed by lateralized hypersecretion of aldosterone. After removal of the benign adenoma, the biochemical abnormalities were corrected, yet the blood pressure remained much the same. Hypertension is not necessarily a sign of primary aldosteronism. 1 There have also been cases with normokalemia.2 Although the hypertension is usually mild and may fluctuate, it is only recently that consistently normotensive cases of primary aldosteronism, due to adrenal adenoma 3 " 5 and idiopathic adrenal hyperplasia, 6 have been reported. All of the normotensive cases of aldosteronoma reported had been detected due to some symptoms related to hypokalemia. Herein, we report a case of aldosteronoma without hypertension which was first suspected because of persistent hypokalemia but revealed no symptoms characteristic of hypokalemia.

The purpose of this study was to evaluate the gene expression of growth factors and growth factor receptors of primary hepatic masses, including hepatocellular carcinoma (HCC) and nodular hyperplasia (NH), in dogs. Quantitative real-time reverse transcriptase-polymerase chain reaction was performed to measure the expression of 18 genes in 18 HCCs, 10 NHs, 11 surrounding non-cancerous liver tissues and 4 healthy control liver tissues. Platelet-derived growth factor-B (PDGF-B), transforming growth factor-α, epidermal growth factor receptor, epidermal growth factor and hepatocyte growth factor were found to be differentially expressed in HCC compared with NH and the surrounding non-cancerous and healthy control liver tissues. PDGF-B is suggested to have the potential to become a valuable ancillary target for the treatment of canine HCC.

Background: Neutrophilic leucocytosis as a paraneoplastic syndrome may occur in dogs with lymphoma, renal carcinoma, rectal polyps and metastatic fibrosarcoma.However, the information on canine lung adenocarcinoma with neutrophilic leucocytosis is lacking.Objective: This study aimed to describe the clinical features and cytokine profiles of canine patients with primary lung adenocarcinoma and neutrophilic leucocytosis.Methods: Two dogs (cases #1 and #2), each with a solitary lung adenocarcinoma, were included. Both cases had leucocytosis and underwent lung lobectomy. The resected tumours were analysed for the expression of granulocyte colony-stimulating factor (G-CSF), granulocyte macrophage colony-stimulating factor (GM-CSF) and interleukin-6 (IL6) by quantitative real-time PCR compared with normal lung tissues.Results: At the initial examination, neither patient had any clinical signs or fever. White blood cell count (WBC) was 58,300/μl and 32,900/μl in cases #1 and #2, respectively.The gene expression of G-CSF increased 6.7-and 19.7-fold in cases #1 and #2, respectively. The gene expression of IL6 markedly increased (30-fold) in case #1, whereas it increased slightly (1.9-fold) in case #2. On the other hand, that of GM-CSF was slightly changed in both cases. The WBC count postoperatively decreased to within the normal range in both cases. The postoperative survival times were 347 and 118 days in cases #1 and #2, respectively. Conclusions:This study describes G-CSF and IL6 producing lung adenocarcinoma associated with neutrophilic leucocytosis in dogs. Canine patients with pulmonary adenocarcinomas that have elevated G-CSF and IL6 levels may have a guarded prognosis. Further investigations are needed to clarify the prognosis of canine cytokineproducing lung adenocarcinoma.

Objective To characterize the multidrug resistance (MDR) phenotype in human urothelial cancers, the expression levels of four MDR‐related genes (multidrug resistance, mdrl; multidrug resistance‐associated protein, MRP; glutathione S‐transferase‐π, GST‐π; and DNA topoisomerase II, topo II) were analysed in urothelial cancers. Materials and methods Fifty‐two tumour tissue and three normal urothelial mucosa samples were obtained from 44 patients with urothelial cancers. The expression of each gene was analysed with a reverse‐transcription polymerase chain reaction (RT‐PCR) method using β2‐microglobulin (b2m) mRNA as an endogenous control. Levels of expression were expressed as the ratio of the specific products of the target gene to those specific to b2m. Results In primary urothelial cancer tissues, the mean (sd) expression of mdrl, MRP, GST‐πand topo II relative to b2m expression were 0.067 (0.061), 0.27 (0.23), 0.35 (0.31) and 0.12 (0.05), respectively. The mean expressions of MRP and GST‐πwere higher than those of mdrl and topo II. The mean ratios of mdrl/b2m, MRP/b2m, GST‐π/b2m and topo II/b2m in normal urothelial mucosa were 0.06 (0.03), 0.12 (0.09), 0.30 (0.32) and 0.14 (0.01), respectively. There was no significant association of the expression of each gene with either the grade or extent of the primary tumour. The level of MRP expression in each sample was correlated significantly with the expression of mdrl and GST‐πin the urothelial cancers (r=0.637 and 0.537, respectively). Chemotherapy did not markedly influence the induction of expression of the MDR‐related genes, except for one case in which mdrl expression was 15 times greater than before chemotherapy. The expression of GST‐πin the patients not receiving chemotherapy was significantly higher than in those that did. Conclusions These results suggest that the activation of MRP and GST‐πexpression occurs during the tumorigenesis of urothelial cancers and that it may confer de novo and acquired drug resistance on urothelial cancers. These results should provide further insight into the complex role postulated for MDR‐related genes in chemotherapy, carcinogenesis and tumour progression.

Hyperprolactinaemia induced by pituitary isografts in male host mice was confirmed by radioimmunoassay, but plasma testosterone levels determined by radioimmunoassay in these mice showed no changes. Immunoenzyme electron microscopic observations revealed large spherical-shaped immunoreactive prolactin granules in pituitary grafts in male hosts, regardless of the sex of the donor mice, indicating the disappearance of sexual dimorphism in prolactin-producing cells in hyperprolactinaemic mice. In hyperprolactinaemic host mice the male accessory sex glands, particularly the seminal vesicle and the ventral prostate, exhibited considerable proliferation and significant increase in weight. These phenomena do not seem to be mediated by the increased action of testosterone. Such biological effects in host mice were much greater when the donor was female rather than male, and were more noticeable in C57BL mice than in C3H mice.