Biomedical subjects

Y Yamanaka

Publications and source records attributed to Y Yamanaka.

At least 19 recordsLinked to original sources

PubMed2002

Primary tumour resection of tongue carcinoma based on response to preoperative therapy.

The purpose of this study was to investigate the selection of resection techniques for primary lesions of advanced tongue carcinoma based on the effectiveness of our current preoperative therapy. Forty-three patients with advanced but potentially resectable squamous cell carcinoma of the tongue were included in this study. All patients were treated with preoperative concurrent chemoradiotherapy followed by conventional surgical resection. Semiserial sections of whole surgical specimen of primary lesion were evaluated histopathologically. In patients who achieved 85% and above regression, the extent of residual tumours two-dimensionally and in the deep layers was lesser, and the rate of tumour cell survival was lower, than in other patients. Furthermore, residual tumours tended to be localized to the superficial layers in the centre. These findings suggest that even in advanced tongue carcinomas it is possible to avoid extended resection and perform a less invasive surgery in which the extent of resection is reduced to preserve morphology and function in patients who achieved 65% and above regression following preoperative chemoradiotherapy.

Adult↗

PubMed2001

Protective effect of histidine on para-nonylphenol-enhanced hydroxyl free radical generation induced by 1-methyl-4-phenylpyridinium ion (MPP+) in rat striatum.

The present study examined the antioxidant effect of histidine, a singlet oxygen ((1)O(2)) scavenger, on para-nonylphenol (an environmental estrogen-like chemical)-enhanced hydroxyl radical (.OH) generation induced by 1-methyl-4-phenylpyridinium ion (MPP+) in extracellular fluid of rat striatum. Rats were anesthetized, and sodium salicylate in Ringer's solution (0.5 nmol/microl/min) was infused through a microdialysis probe to detect the generation of.OH as reflected by the non-enzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) in the striatum. Introduction of para-nonylphenol (10 microM) significantly enhanced MPP+ -induced.OH generation. Histidine (25 mM) decreased the para-nonylphenol-enhanced.OH formation. Although the level of MPP+ -induced.OH formation trapped as DHBA after para-nonylphenol treatment increased, para-nonylphenol failed to increase either the level of dopamine and DHBA formation in the reserpinized animals. These results indicate that para-nonylphenol and MPP+ -enhanced.OH generation was based on 1O(2) production, and histidine may have a preventive effect on para-nonylphenol and MPP+ -induced.OH generation in rat striatum.

1-Methyl-4-phenylpyridinium↗

PubMed2001

Gene expression profiles of human small airway epithelial cells treated with low doses of 14- and 16-membered macrolides.

Although long-term treatment with low doses of 14-membered macrolides is widely applied in management of patients with chronic inflammatory diseases, e.g., diffuse panbronchiolitis, chronic bronchitis, or chronic lung damage in newborns, the physiological mechanisms underlying the action of macrolides in these conditions are unclear. To clarify the pathological basis of these diseases and also to aid in the design of novel drugs to treat them, we chose to investigate the molecular target(s) of macrolides. Our experiments involved long-term culture of human small airway epithelial cells (hSAEC) in media containing 14-membered macrolides erythromycin (EM) or clarithromycin (CAM), or a 16-membered macrolide, josamycin (JM), which lacks clinical anti-inflammatory effects. We then analyzed gene expression profiles in the treated cells using a cDNA microarray consisting of 18,432 genes. We identified nine genes whose expression was significantly altered during 22 days of culture with EM, and seven that were altered by CAM in that time. Four of those genes revealed similar behavior in cells treated with either of the 14-membered macrolides, but not JM. The products of these four genes may be candidates for mediating the ability of 14-membered macrolides to suppress chronic inflammation.

Anti-Bacterial Agents↗

PubMed2001

Release of dopamine by perfusion with 1-methyl-4-phenylpyridinium ion (MPP(+)) into the striatum is associated with hydroxyl free radical generation.

In Parkinson's disease (PD), the dopamine (DA) neuronal cell death in the nigrostriatal system has been proposed to be mediated by reactive oxygen radicals such as hydroxyl radicals (.OH). This.OH production may cause lipid peroxidation of cell membranes leading to neuronal cell death. This paper report that the DA-selective neurotoxin, 1-methyl-4-phenylpyridinium ion (MPP(+)), (1 nmol/microl per min for 1 h) infusion into the striatum of rats induces elevation of extracellular DA and.OH formation. These elevations seem to induce lipid peroxidation of striatum membranes, as detected by increases in non-enzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) levels. To test the involvement of DA release in the.OH generation and lipid peroxidation, the rats were pretreated with reserpine (5 mg/kg, i.v., 24 h before MPP(+) or without MPP(+)) to deplete presynaptic DA. Reserpine treatment alone did not change the levels of DA or 2,3-DHBA, while the combined treatment with both MPP(+) and reserpine clearly decreased 2,3-DHBA, as well as DA levels, compared to those in the group treated with MPP(+) alone. After injection into reserpinized rats, DA at various doses (2, 5 and 10 microM) small increased 2,3-DHBA levels dose-dependently, as compared to the MPP(+) alone-treated group. These results clearly indicate that MPP(+) perfusion into the striatum increases extracellular DA levels and this increase may concomitantly induce the formation of reactive free oxygen radicals, such as.OH free radicals. These events may contribute, at least in part, to the nigrostriatal neurons cell death after MPP(+).

1-Methyl-4-phenylpyridinium↗

PubMed2001

Allopurinol suppresses para-nonylphenol and 1-methyl-4-phenylpyridinium ion (MPP(+))-induced hydroxyl radical generation in rat striatum.

We recently demonstrated that para-nonylphenol, an environmental estrogen-like chemical, enhances hydroxyl radical (*OH) generation in the rat striatum. In the present study we have examined whether para-nonylphenol enhanced 1-methyl-4-phenylpyridinium ion (MPP(+))-induced *OH generation in the rat striatum using a microdialysis technique. Para-nonylphenol significantly enhanced MPP(+)-induced *OH generation. Further, we studied the effect of allopurinol, a xanthine oxidase inhibitor, on para-nonylphenol and MPP(+)-induced *OH generation. Allopurinol significantly suppressed para-nonylphenol and MPP(+)-induced *OH generation. The results indicate that para-nonylphenol enhanced *OH generation based on superoxide anion production, and allopurinol may have preventive effect on para-nonylphenol and MPP(+)-induced *OH generation.

1-Methyl-4-phenylpyridinium↗

PubMed2001

Nitric oxide enhances MPP(+)-induced hydroxyl radical generation via depolarization activated nitric oxide synthase in rat striatum.

We examined the effect of N(G)-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, on extracellular potassium ion concentration ([K(+)](o))-enhanced hydroxyl radical (.OH) generation due to 1-methyl-4-phenylpyridinium ion (MPP(+)) was examined in the rat striatum. Rats were anesthetized, and sodium salicylate in Ringer's solution (0.5 nmol/microl per min) was infused through a microdialysis probe to detect the generation of.OH as reflected by the non-enzymatic formation of 2,3-dihydroxybenzoic acid (DHBA) in the striatum. Induction of KCl (20, 70 and 140 mM) increased MPP(+)-induced.OH formation trapped as 2,3-dihydroxybenzoic acid (DHBA) in a concentration dependent manner. However, the application of L-NAME (5 mg/kg i.v.) abolished the [K(+)](o) depolarization-induced.OH formation with MPP(+). Dopamine (DA; 10 microM) also increased the levels of DHBA due to MPP(+). However, the effect of DA after application of L-NAME did not change the levels of DHBA. On the other hand, the application of allopurinol (20 mg/kg i.v., 30 min prior to study), a xanthine oxidase (XO) inhibitor was abolished the both [K(+)](o)- and DA-induced.OH generation. Moreover, when iron(II) was administered to MPP(+) then [K(+)](o) (70 mM)-pretreated animals, a marked increase in the level of DHBA. However, when corresponding experiments were performed with L-NAME-pretreated animals, the same results were obtained. Therefore, NOS activation may be no relation to Fenton-type reaction via [K(+)](o) depolarization-induced.OH generation. The present results suggest that [K(+)](o)-induced depolarization augmented MPP(+)-induced.OH formation by enhancing NO synthesis.

1-Methyl-4-phenylpyridinium↗

PubMed2001

Effect of fluvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, on nitric oxide-induced hydroxyl radical generation in the rat heart.

We examined the effect of fluvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, on the production of hydroxyl radical (*OH) generation via nitric oxide synthase (NOS) activation by an in vivo microdialysis technique. The microdialysis probe was implanted in the left ventricular myocardium of anesthetized rats and tissue was perfused with Ringer's solution through the microdialysis probe at a rate of 1 microl/min. Sodium salicylate in Ringer's solution (0.5 nmol/microl/min) was infused directly through a microdialysis probe to detect the generation of *OH. Induction of [K(+)](o) (70 mM) or tyramine (1 mM), significantly increased the formation of *OH trapped as 2,3-dihydroxybenzoic acid (DHBA). The application of N(G)-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, significantly decreased the K(+) depolarization-induced *OH formation, but the effect of tyramine significantly increased the level of 2,3-DHBA. When fluvastatin (100 microM), an inhibitor of low-density lipoprotein (LDL) oxidation, was administered to L-NAME-pretreated animals, both KCl and tyramine failed to increase the level of 2,3-DHBA formation. The effect of fluvastatin may be unrelated to K(+) depolarization-induced *OH generation. To examine the effect of fluvastatin on ischemic/reperfused rat myocardium, the heart was subjected to myocardial ischemia for 15 min by occlusion of the left anterior descending coronary artery (LAD). When the heart was reperfused, a marked elevation of the level of 2,3-DHBA was observed. However, in the presence of fluvastatin (100 microM), the elevation of 2,3-DHBA was not observed in ischemia/reperfused rat heart. Fluvastatin, orally at a dose of 3 mg/kg/day for 4 weeks, significantly blunted the rise of serum creatine phosphokinase and improved the electrocardiogram 2 h after coronary occlusion. These results suggest that fluvastatin is associated with a cardioprotective effect due to the suppression of noradrenaline-induced *OH generation by inhibiting LDL oxidation in the heart.

Animals↗

PubMed2001

Regulation of dharma/bozozok by the Wnt pathway.

The zebrafish homeobox gene dharma/bozozok (boz) is required for the formation and/or function of the Nieuwkoop center and the subsequent induction of the Spemann organizer. dharma is expressed soon after the midblastula transition in the dorsal blastomeres and the dorsal yolk syncytial layer (YSL). We found that the expression of dharma was upregulated or ectopically induced by misexpression of a Wnt protein and cytoplasmic components of the Wnt signaling pathway and downregulated by the expression of dominant-negative Tcf3. A 1.4-kbp fragment of the dharma promoter region contains consensus sequences for Tcf/Lef binding sites. This promoter region recapitulated the Wnt-dependent and dorsal dharma expression pattern when it was fused to luciferase or GFP. Deletion and point mutant analyses revealed that the Tcf/Lef binding sites were required to drive this expression pattern. These data established that dharma/boz functions between the dorsal determinants-mediated Wnt signals and the formation of the Nieuwkoop center.

Animals↗

PubMed2001

Singlet oxygen generation from phosphatidylcholine hydroperoxide in the presence of copper.

This study pursued whether singlet oxygen ((1)O2) is generated from phosphatidylcholine hydroperoxide (PCOOH), the oxidized modification product of a major constituent of biomembranes and serum lipoproteins. The (1)O2 formation was detected, by utilizing the oxidation of 2,2,6,6-tetramethyl-4-piperidone (TMPD) by (1)O2 to yield 2,2,6,6-tetramethyl-4-piperidone-1-oxyl (TEMPONE), which generates electron spin resonance (ESR) signals. The TEMPONE signal was detected in human plasma with addition of PCOOH by ESR determination after introducing copper(II). The TEMPONE formation was proportional to the amounts of PCOOH added according to moles of active oxygen. The TEMPONE signal intensity was weakened significantly in the presence of beta-carotene and histidine in a concentration-dependent manner, but was not at all decreased by mannitol, Mn-superoxide dismutase and catalase. In addition, HPLC-chemiluminescence analysis demonstrated that incubation with the PCOOH/Cu(II) combination oxidized cholesterol, a relatively oxidation-resistant component, to the cholesterol hydroperoxide. These results reveal that (1)O2 is generated from PCOOH in contact with copper(II). In conclusion, this in-vitro study provides directly the (1)O2 formation in living organisms following the advancement of peroxidation of constitutive lipids.

Catalase↗

PubMed2001

EGF family ligand-dependent phenotypic modulation of smooth muscle cells through EGF receptor.

The phenotypic modulation of smooth muscle cells (SMCs) is closely associated with the development and progression of various SMC diseases. We investigated the molecular mechanism of phenotypic modulation triggered by EGF family ligands using a primary culture system of differentiated SMCs. Among four EGF-receptor (EGFR) family members, the EGFR was solely activated by EGF, heparin-binding EGF (HB-EGF), transforming growth factor alpha (TGF alpha), epiregulin (ER), and betacellulin (BTC), resulting in induction of phenotypic modulation of SMCs. This effect was mediated through the coordinated activation of the extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (p38MAPK) pathways. These results suggest that EGF family ligand- and EGFR-triggered signaling pathways are critically involved in the phenotypic modulation of SMCs.

Animals↗

PubMed2001

Growth condition-dependent synchronized changes in transcript levels of type II hexokinase and type 1 glucose transporter in tumor cells.

Transcript levels of hexokinase (HK) isozymes and glucose transporter (GLUT) isoforms in RNA samples of AH130 cells obtained from dish cultures and ascites were evaluated in a quantitative manner. In AH130 cells cultured in dishes, HKI and HKII were expressed at a similar level, but HKIII and HKIV were not. GLUT1 and GLUT3 were also expressed, and messages of these two isoforms represented 27% and 71%, respectively, of the total GLUT messages. A faint signal of GLUT2 was also observed. On the contrary, in cells grown as ascites, the transcript of HKII was dominant, and its level was about 15-fold over that of dish-cultured AH130 cells. Transcript levels of GLUT1 and GLUT3 were 4.5- and 2-fold, respectively, higher than those in dish-cultured cells. Thus, GLUT1 was more susceptible to changes in culture conditions than GLUT3. Based on these results, we concluded that the change in growth conditions caused synchronized changes in the transcript levels of HKII and GLUT1 in AH130 cells. However, such marked changes in the transcript levels of HKII and GLUT1 were not observed when AH130 cells were cultured in dishes under a hypoxic condition, indicating that the observed changes were not solely attributable to the difference in oxygen concentration between the ascites and cell culture conditions. Accordingly, other factors such as growth factors may be responsible for this difference in levels of HKII and GLUT1 between the two growth conditions.

Animals↗

PubMed2001

Nitric oxide induces hydroxyl radical generation in rat hearts via depolarization-induced nitric oxide synthase activation.

We examined the effect of NG-nitro-L-arginine methyl ester (L-NAME), a NOS inhibitor, on extracellular potassium ion concentration ([K+]o) and induced hydroxyl free radical (.OH) generation by an in vivo microdialysis technique. A flexibly mounted microdialysis technique was used to detect the generation of .OH in in-vivo rat hearts. The microdialysis probe was implanted in the left ventricular myocardium of anesthetized rats and tissue was perfused with Ringer's solution through the microdialysis probe at a rate of 1.0 microl/min. To measure the level of .OH, sodium salicylate in Ringer's solution (0.5 nmol/microl per min) was infused directly through a microdialysis probe to detect the generation of .OH as reflected by the nonenzymatic formation of 2,3-dihydroxybenzoic acid (2,3-DHBA). Induction of high-concentration [K+]o (20, 70 and 140 mM) significantly increased formation of .OH trapped as 2,3-DHBA in a concentration-dependent manner. However, the application of L-NAME (50 mg/kg, i.v.) and allopurinol, a xanthine oxidase inhibitor, abolished the [K+]o depolarization-induced .OH generation. Tyramine (1.0 mM) increased the level of 2,3-DHBA. However, the application of L-NAME did not change the level of 2,3-DHBA. On the other hand, pretreatment with allopurinol (10 mg/kg, i.v.) abolished the KCl- or tyramine-induced .OH generation. Moreover, when iron (II) was administered to [K+]o (70 mM)-pretreated animals, there was a marked increased in the level of 2,3-DHBA. However, the application of L-NAME was not related to a Fenton-type reaction via [K+]o depolarization-induced .OH generation. To examine the effect of L-NAME on ischemic/reperfused rat myocardium, the heart was subjected to myocardial ischemia for 15 min by occlusion by left anterior descending coronary artery branch (LAD). When the heart was reperfused, a marked elevation of the level of 2,3-DHBA was observed. However, L-NAME attenuated .OH generation by ischemic/reperfused rat heart. These results suggest that NOS inhibition is associated with a cardioprotective effect due to the suppression of [K+]o depolarization-induced .OH generation.

Allopurinol↗

PubMed2001

A study of 13 patients with gastric tube in place after esophageal resection: use of omeprazole to decrease gastric acidity and volume.

STUDY OBJECTIVE: To investigate whether oral omeprazole 20 mg decreases the risk of aspiration pneumonia in patients with gastric tube reconstruction. DESIGN: Consecutive study. SETTING: Operation room of cancer center. PATIENTS: Thirteen patients with gastric tube reconstruction for esophageal cancer. INTERVENTIONS: Oral omeprazole 20 mg was given the night before surgery. A rapid-sequence induction with cricoid pressure was employed for induction of anesthesia. After tracheal intubation, a nasogastric catheter was inserted into the gastric tube and the contents were aspirated. MEASUREMENTS AND MAIN RESULTS: The pH and volume of the gastric contents were measured. The pH and volume of the gastric tube contents were 4.5 +/- 1.6 (range from 2.5 to 7.0) and 9.5 +/- 10.2 mL (range from 0 to 30 mL), respectively. Food residue was recognized in nine patients. There was no patient with a pH below 2.5 and a volume of 25 mL or greater. CONCLUSIONS: Omeprazole 20 mg decreased the acidity and volume of the gastric tube contents and reduced the risk of aspiration pneumonia in patients with a gastric tube in place.

Adult↗

PubMed2001

Prognostic value of response to preoperative chemoradiotherapy and residual tumor grades in tongue carcinoma.

OBJECTIVE: The purposes of the present study were to analyze our experience with preoperative chemoradiotherapy followed by surgery for advanced tongue carcinoma and to assess the prognostic value of response to preoperative therapy in these tumors. STUDY DESIGN: Between May 1988 and December 1999, a total of 43 patients with advanced but potentially resectable squamous cell carcinoma of the tongue were candidates for this study. A minimum tumor size of 3 cm was required. The mean age was 59.8 years (range, 26-85 years); 13 cases were advanced stage II, 23 cases were stage III, and 7 cases were stage IV. All patients were treated preoperatively with cisplatin- or carboplatin-based chemotherapy in combination with simultaneous irradiation to a target volume of 40 Gy; 2-6 weeks later, they underwent curative surgery. Tumor regression rate, residual tumor grade, and histologic regression grade to the preoperative therapy were analyzed to determine their influence on the prognosis. RESULTS: With a median follow-up of 60.5 months, overall survival rates were 86.0% for all cases, 92.3% for stage II cases, 77.3% for stage III cases, and 100% for stage IV cases. The progression-free survival rates according to tumor regression rate were 33.3% for group 1 (< 50% tumor regression), 66.7% for group 2 (> or = 50% and < 75% regression), 100% for group 3 (> or = 75% and < 100% regression), and 96.0% for group 4 (complete regression). The higher the tumor regression rates, the higher the survival rates. When patients who achieved a regression rate of 75% or higher were compared with those who did not, there was a significant difference in survival (P < .0001). The factors of residual tumor grade and histologic regression grade also had good correlations with the prognosis (residual tumor grade, P =.0324; histologic regression grade, P < .0001). CONCLUSIONS: The findings of the present study suggest that response to preoperative chemoradiotherapy, such as tumor regression rate, residual tumor grade, and histologic regression grade, could be of prognostic value in patients with tongue carcinoma.

Adult↗

PubMed2001

[Parkinsonism induced by MPTP and free radical generation].

Oxygen free radical formation has been implicated in dopaminergic toxicity caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and iron. Although MPTP produces a parkinsonian syndrome after its conversion to 1-methyl-4-phenylpyridine (MPP+) by type B monoamine oxidase (MAO-B) in the brain, the etiology of this disease remains obscure. MPP+ is one of the most potent dopamine (DA)-releasing agents. Iron-catalyzed DA autoxidation and oxidative stress may be involved in the pathogenesis of Parkinson's disease. If indeed the effect of MPP+ on hydroxyl radical (.OH) formation is due to DA release, reserpine-induced DA depletion may reduce MPP(+)-induced .OH formation. Imidapril, an angiotensin converting enzyme (ACE) inhibitor, can resist MPP(+)-induced .OH formation via suppression of release of DA by angiotensin. Histidine, a singlet oxygen (1O2) scavenger, protects MPP(+)-induced .OH formation. Fluvastatin, an inhibitor of low-density lipoprotein (LDL) oxidation, can resist MPP(+)-induced .OH formation. The inhibitory effect on the susceptibility of LDL oxidation can reduce .OH generation. These drugs may be applied as antiparkinsonian agents. Further clinical investigation is necessary in the future.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2001

Protective effect of Ninjin-yoei-to on damage to isolated hepatocytes following transient exposure to tert-butyl hydroperoxide.

To establish a simple screening system for estimating efficacy of an agent for an oxidative-related lesion, we investigated the damage in isolated rat hepatocytes exposed to 75 microM tert-butyl hydroperoxide (t-BuOOH) and then subsequently incubated the cells in fresh medium. By electron spin resonance spectroscopy analysis using 5,5-dimethyl-1-pyrroline-N-oxide (DMPO), DMPO adducts of tert-butoxyl radicals and carbon center radicals were detected during the t-BuOOH exposure, and DMPO-OH formation was detected after t-BuOOH removal. In t-BuOOH-exposed cells, the level of phosphatidylcholine hydroperoxide (PCOOH), a peroxidative product of biomembranes in the hepatocytes, and the leakage of enzymes into the culture medium were significantly increased. An increase in acid phosphatase (AP) activity representing lysosome destabilization preceded the aspartate oxoglutarate aminotransferase (AST), alanine oxoglutarate aminotransferase (ALT) and lactate dehydrogenase (LDH) leakage. Ninjin-yoei-to added to the culture medium following the t-BuOOH exposure significantly inhibited the PCOOH formation and the leakage of AP, AST, ALT and LDH, concentration-dependently. Ninjin-yoei-to at 1 mg/ml in culture medium completely diminished these increases in enzyme activities down to the background levels found in control experiments and this reduction was greater than the most effective alpha-tocopherol concentration of 20 micromol/ml. Considering all of these results, it is likely Ninjin-yoei-to may exert its protective effect by antioxidative action and membrane stabilization.

Acid Phosphatase↗

PubMed2001

Familial adult onset primary alveolar hypoventilation syndrome.

A 41-year-old man fell into type II respiratory failure after catching a cold, and became dependent on a respirator. Chest radiography showed no abnormalities and the hyperventilation test showed improved arterial blood gas findings. His sleep study showed marked nocturnal desaturation due to hypopnea and apnea with a decrease of thoracic and abdominal movement during sleep. Therefore, we diagnosed him as primary alveolar hypoventilation syndrome (PAH). Seven years previously, his 2-year elder sister had suffered from similar respiratory failure during her second pregnancy and had been diagnosed as PAH. While myopathy was suspected in both cases, attenuation of muscle strength was slight and it appeared not to be the main cause of alveolar hypoventilation. Since medication was not effective in each case, they underwent non-invasive positive pressure ventilation (NIPPV). While sustained mild hypercapnia remained during the daytime, it improved their respiratory failure. To our knowledge, this is the first study of familial adult onset PAH.

Adult↗

PubMed2001

[Immunohistochemical analysis with anti-cytokeratin antibody in the prostatic epithelium].

PURPOSE: We performed immunohistochemical studies of the prostatic epithelium using three different anti-cytokeratin monoclonal antibodies (35 beta-H11, RCK108, and 34 beta-E12), and also investigated the immunoreactivity of various prostatic lesions with basal cell specific anti-cytokeratin antibody (34 beta-E12). MATERIALS AND METHODS: One hundred and thirty one prostatic specimens were obtained at surgery or biopsy. H-E stained sections were available for review in all cases. They were classified according to histopathology; benign prostatic hyperplasia (BPH), prostatic cancer (PCA), atrophic acini, atypical adenomatous hyperplasia (AAH), and prostatic intraepithelial neoplasia (PIN). ABC or LSAB method was utilized for immunohistochemical staining with 3 anti-cytokeratin monoclonal antibodies. RESULTS: 35 beta-H11 was mainly stained in the luminal cells and RCK108 was stained both in the luminal and the basal cells in BPH. 35 beta-H11 showed highly positive staining in the prostatic cancer regardless of degree of differentiation. RCK108 tended to be less stained in the prostatic cancer cells with lower grades of tumor differentiation compared to those with higher grades. 34 beta-E12 was stained only in the basal cells, but neither in the normal luminal cells nor the cancer cells. Using 34 beta-E 12, basal cells were positively stained in most of the cases with BPH, while not in PCA. Atrophic acini and AAH was stained with 34 beta-E12 as positively as BPH. Basal cells were discontinuously or negatively stained in many cases with high-grade PIN. CONCLUSIONS: The luminal cells in BPH were highly positively stained using 35 beta-H11 or RCK108. RCK108 tended to be less stained in the prostatic cancer cells with lower grades of tumor differentiation. Positive staining of 34 beta-E12 strongly suggested a benign lesion, therefore immunohistochemistry using this antibody would be useful as an aid for pathological diagnosis.

Antibodies, Monoclonal↗