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Biomedical subjects

T Furukawa

Publications and source records attributed to T Furukawa.

At least 181 records · Page 10Linked to original sources
PubMed1999

Phlebosclerosis of the colon with positive anti-centromere antibody.

A 56-year-old woman with symptoms of chronic bowel disease presented a peculiar calcification of the mesenteric vein of the ascending to transverse colon on barium enema study. The resected colon was hard and black. Histo-pathologic examinations demonstrated fibrous change of the colon with a calcified and hyaline-deposited mesenteric vein. No cell infiltration was observed. These findings were compatible with phlebosclerosis and also with systemic sclerosis. Positive anti-centromere antibody and Raynaud's phenomenon, hallmarks of a variant systemic sclerosis, the CREST syndrome were observed. We therefore speculated that the pathogenesis of the phlebosclerosis of the colon is related to the CREST syndrome.

Autoantibodies↗
PubMed1999

Adenovirus-mediated delivery of the PTEN gene inhibits cell growth by induction of apoptosis in endometrial cancer.

PTEN, a gene encoding a dual specificity phosphatase, is frequently altered in endometrial carcinoma. Moreover, these alterations are observed even in atypical hyperplasia of the endometrium. This evidence suggests that mutation of PTEN is an early genetic alteration involved in endometrial carcinogenesis. Adenovirus-mediated gene transfer was carried out using Ishikawa 3 H 12 and RL95-2, the endometrial cancer cell lines with completely inactivated PTEN, together with endometrial cancer cell lines HEC1-A and KLE expressing wild-type PTEN as the control. The PTEN transgene significantly suppressed cell growth in vitro through induction of apoptosis in cells lacking wild-type PTEN. Furthermore, the ex vivo tumor formation by Ishikawa 3 H 12 cells was completely inhibited by the introduction of wild-type PTEN. However, neither regression nor progression was observed in inoculated tumors of either cell line by in vivo introduction of the PTEN gene. These results suggest that PTEN may be a good candidate for gene therapy in patients with endometrial carcinoma.

Adenoviridae↗
PubMed1999

[Effect of adrenaline on vagus nerve reflexes].

INTRODUCTION: Dizziness or syncope may occur during treatment of nasal disease. These symptoms are considered imputable to the vagovagal reflex, which is partly involved in neurogenic syncope. In response to trigeminal nerve stimulation, the vagus nerve causes a sudden fall in heart rate and blood pressure. Elevation in blood adrenaline level during pain or tension was noted, and its effects on vagovagal reflexes were studied. MATERIALS AND METHODS: Ten cats were used in the experiment. The vagus nerve was exposed on the right side of the neck by making an incision in the trachea, and a platinum electrode was attached to the vagus nerve on nerve's distal side. The head was tilted a 30 degree angle. The cats were divided into control and adrenaline-treated groups, and changes in cerebral blood flow, heart rate, and arterial pressure were compared between the two groups after electric stimulation of the vagus nerve. Cerebral blood flow was measured by the hydrogen clearance method. 1) Control group The vagus nerve was electrically stimulated for 1 minute. 2) Adrenaline-treated group The vagus nerve was electrically stimulated for 1 minute following 30 seconds of intravenous administration of adrenaline. RESULTS: Cerebral blood flow was significantly decreased in both the control and adrenaline-treated groups after electric stimulation, but the decrease was significantly greater in the latter group at all sites of measurement. Whereas heart rate and arterial pressure were significantly decreased in the control group, these variables in the adrenaline-treated group showed no significant change despite the greater decrease in cerebral blood flow. DISCUSSION: Heart rate, blood pressure, and cerebral blood flow were all significantly decreased after electric stimulation of the vagus nerve. These changes were considered owing to a fall in blood pressure due to vasodilation resulting from bradycardia and a relative decrease in sympathetic nervous tension resulting from electric stimulation. On the other hand, in the adrenaline-treated group, neither heart rate nor blood pressure showed any significant change, but cerebral blood flow was significantly decreased at all sites of measurement despite an adrenaline load. This contradictory results may be accounted for by the powerful beta 2-activity of adrenaline. The greater decrease in cerebral blood flow in the adrenaline-treated than in the control group can be attributed to decreased peripheral vascular resistance by its beta 2-activity. In the field of otorhinolaryngology the trigeminal region is often involved in the treatment of nasal disorders so that vagovagal reflexes are often encountered. The results of this study counsels caution in the treatment involving the trigeminal region.

Adrenergic beta-2 Receptor Agonists↗
PubMed1999

ATP-Dependent efflux of CPT-11 and SN-38 by the multidrug resistance protein (MRP) and its inhibition by PAK-104P.

Non-P-glycoprotein-mediated multidrug-resistant C-A120 cells that overexpressed multidrug resistance protein (MRP) were 10.8- and 29. 6-fold more resistant to 7-ethyl-10-[4-(1-piperidino)-1-piperidino]carbonyloxycamptothecin (CPT-11) and SN-38, respectively, than parental KB-3-1 cells. To see whether MRP is involved in CPT-11 and SN-38 resistance, MRP cDNA was transfected into KB-3-1 cells. The transfectant, KB/MRP, which overexpressed MRP, was resistant to both CPT-11 and SN-38. 2-[4-Diphenylmethyl)-1-piperazinyl]ethyl-5-(trans-4,6-dimethyl-1,3 , 2-dioxaphosphorinan-2-yl)-2, 6-dimethyl-4-(3-nitrophenyl)-3-pyridinecarboxylate P-oxide (PAK-104P) and MK571, which reversed drug resistance in MRP overexpressing multidrug-resistant cells, significantly increased the sensitivity of C-A120 and KB/MRP cells, but not of KB-3-1 cells, to CPT-11 and SN-38. The accumulation of both CPT-11 and SN-38 in C-A120 and KB/MRP cells was lower than that in KB-3-1 cells. The treatment with 10 microM PAK-104P increased the accumulation of CPT-11 and SN-38 in C-A120 and KB/MRP cells to a level similar to that found in KB-3-1 cells. The ATP-dependent efflux of CPT-11 and SN-38 from C-A120 and KB/MRP cells was inhibited by PAK-104P. DNA topoisomerase I expression, activity, and sensitivity to SN-38 were similar in the three cell lines. Furthermore, the conversion of CPT-11 to SN-38 in KB-3-1 and C-A120 cell lines was similar. These findings suggest that MRP transports CPT-11 and SN-38 and is involved in resistance to CPT-11 and SN-38 and that PAK-104P reverses the resistance to CPT-11 and SN-38 in tumors that overexpress MRP.

ATP-Binding Cassette Transporters↗
PubMed1999

Identification of three commonly deleted regions on chromosome arm 6q in human pancreatic cancer.

Pancreatic cancer has one of the poorest prognoses among malignant diseases. To understand its molecular mechanisms, we studied allelic losses on the long arm of chromosome 6. Using 55 paired DNAs of tumors and their corresponding normal tissues and 30 microsatellite markers that spanned the entire 6q chromosome arm, we found three distinct regions of common allelic loss: region A, a less than 500-kb region bordered by D6S449 and D6S283 on 6q21 with a loss of heterozygosity (LOH) frequency of 69% (38/55); region B, a 7-cM region bordered by D6S292 and D6S308 on 6q23-q24 with a LOH frequency of 60% (33/55); and region C, a 13-cM region bordered by D6S305 and D6S264 with a LOH frequency of 51% (28/55). We further focused on region A and constructed a physical map using yeast artificial chromosome (YAC) clones, their derived cosmid clones, and bacterial artificial chromosome (BAC) clones. Region A was completely covered by three overlapping BAC clones. Our results in the present study should shed light on the cloning and characterization of tumor suppressor genes in pancreatic carcinogenesis.

Adult↗
PubMed1999

Resistance to cisplatin.

Resistance to cis-diamminedichloroplatinum(II) (cisplatin), a DNA damaging agent, is a major obstacle for its clinical effectiveness. Multiple mechanisms may be involved in cisplatin resistance. Frequently cited mechanisms include reduced accumulation, elevated levels of glutathione (GSH) and metallothionein, and enhanced DNA repair. Alterations in oncogene expression and in signal transduction pathways involved in apoptosis have been associated with cisplatin resistance. Of these mechanisms, decreased accumulation of cisplatin is the most common finding. Efflux of cisplatin by an organic anion transporter has been proposed, and one of the organic anion transporters, canalicular multispecific organic anion transporter, is associated with cisplatin resistance. Sensitivity to cisplatin has been increased by inhibitors of DNA repair, agents that increase accumulation of cisplatin and depletion of GSH. None of the agents tested that modulate cisplatin sensitivity completely reverses cisplatin resistance. These observations indicate that multiple mechanisms of resistance arise in the same cell line when cells are selected in vitro.

Animals↗
PubMed1999

[Fusion of medicine and technology in endoscopic surgery].

Although endoscopic surgery has become widespread and is currently used in a wide range of general, thoracic, urologic, gynecologic, and orthopedic procedures, many major difficulties remain because sensorial information is restricted to a two-dimensional image, and effector instruments have limited maneuverability due to the rigid shaft axis fixed to the abdominal wall by the entry trocar. To overcome these problems, advanced engineering technology has been introduced in laparoscopic surgery which includes three-dimensional video imaging, robotic laparoscopic cameraholders, telemanipulated flexible effector instruments, and tactile feedback. A voice-controlled robotic laparoscopic holder (AESOP200, Computer Motion Inc. USA) provides stable support for the laparoscope during laparoscopic surgery performed by a single surgeon. A new computer-assisted telemanipulation robot (Intuitive Surgical Inc. USA) permits the performance of completely endoscopic coronary artery bypass and Nissen fundoplication. Furthermore, price reductions and technological advances in telecommunications have made telementoring in endoscopic surgery available for routine clinical use, and intercontinental surgical video teleconferences fruitful opportunities for discussing technical details. The fusion of medicine and technology in endoscopic surgery would overcome difficulties in the conventional endoscopic approach.

Humans↗
PubMed1999

Contribution of nitric oxide to the presynaptic inhibition by endothelin ETB receptor of the canine stellate ganglionic transmission.

We previously reported that endothelin (ET) 3 inhibited presynaptically the dog stellate ganglionic transmission. Here, we report the investigation of the possible involvement of nitric oxide pathway in the endothelin-induced inhibition of the ganglionic transmission. The amount of acetylcholine released by preganglionic stimulation for 10 min was concentration-dependently inhibited after exposure to ET-3 (10(-9)-10(-6) M) or IRL-1620, endothelin ET(B) receptor agonist (10(-8)-10(-5) M). The inhibition was antagonized by pretreatment with a nonselective endothelin receptors antagonist (bosentan) and an ET(B) receptor antagonist (BQ-788) or a neuronal nitric oxide synthase inhibitor, 3-bromo-7-nitroindazole, but was not inhibited by a selective ET(A) receptor antagonist, BQ-123. The reduction induced by ET-3 was also antagonized by treatment with a selective inhibitor of soluble guanylyl cyclase, 1H-[1,2, 4]oxadiazolo[4,3-a]quinoxalin-1-one. In addition, similar reductions were also mimicked by exposure to cGMP analog, 8-bromoguanosine-3, 5-cyclic monophosphate and nitric oxide donor, S-nitroso-N-acetylpenicillamine. Exposure to ET-3 or IRL-1620 for a 30-min period increased the levels of total nitric oxide (NO), nitrite plus nitrate NO(x) concentration in the incubation medium, with the increase in NO(x) also being antagonized by BQ-788 at the same concentration. The ET-3-induced increase in NO(x) was antagonized by treatment with the same concentration of 3-bromo-7-nitroindazole or a selective inhibitor of receptor-mediated Ca(2+) entry, 1-[b-[3-(4-methoxyphenyl) propoxy]-4-methoxyphenethyl]-1H-imidazole (10(-5) M), and with a calmodulin antagonist, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide. These results indicate that ET(B) receptor activation inhibits the sympathetic ganglionic transmission via reducing acetylcholine release from presynaptic nerve terminals, although this inhibition also seems to involve the ET(B) receptor-operated Ca(2+)-calmodulin-dependent activation of endogenous nitric oxide production.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1999

[Mode of onset and two years outcome of a broad spectrum of affective disorders].

In recent years emphasis has tended to be placed on assessing and diagnosing low-grade affective disorders. If mild affective symptoms are also considered a broad spectrum of affective disorders, this spectrum can be seen, not only in the manifestation of major symptoms of such illnesses as manic-depressive illness, but also in symptoms of various mental disorders. The present study was undertaken to analyze the clinical features of a broad spectrum of affective disorders in a prospective follow-up study. Ninety mentally ill patients who visited our outpatient clinic were followed for 2 years, to investigate the mode of onset, the course and outcome of their disorders. Using a semistructured interview method specially developed for this survey, these patients were divided into a broad spectrum of affective disorder group and the other groups. Forty-nine patients were allocated to a spectrum of affective disorder group characterized by four-day (or longer) persistence of at least one of the following symptoms, depressed mood, loss of interest or elevated, expansive, or irritable mood. Of the forty-nine patients there were only two patients with manic symptoms. And the forty-seven patients with depressive symptoms were compared with the other groups as a main subject. The other groups were composed of eighteen patients with psychotic symptoms (the psychotic group) and 23 patients with neurotic symptoms (the neurotic group). The psychotic and neurotic groups did not satisfy the criteria shown above. There was no significant differences in male-to-female ratio or age between these three groups. When the mode of onset of symptoms were compared, the percentage of cases in whom symptoms could be identified early (within 10 days after onset) was 64.4% in the depressive group, 41.2% in the psychotic group and 30.4% in the neurotic group. The percentage of cases who remitted 2 years later was 70.2%, 38.9%, 45.5% in the depressive group, psychotic and neurotic groups, respectively. The GAS score (mean +/- SD), assessed 2 years later, was 76.2 +/- 12.5, 62.8 +/- 11.7, 78.2 +/- 9.9 points for these three groups, respectively. These results suggest that a broad spectrum of depressive disorders develops more acutely and patients with this spectrum are more likely to recover from symptoms and in function. Thus, the course of disorders was more favorable in the depressive group than in the psychotic group or the neurotic group.

Adult↗
PubMed1999

Selectivities of dihydropyridine derivatives in blocking Ca(2+) channel subtypes expressed in Xenopus oocytes.

Some dihydropyridines (DHPs), such as amlodipine and cilnidipine, have been shown to block not only L-type but also N-type Ca(2+) channels; therefore, DHPs are no longer considered as L-type-specific Ca(2+) channel blockers. However, selectivity of DHPs for Ca(2+) channel subtypes including N-, P/Q-, and R-types are poorly understood. To address this issue at the molecular level, blocking effects of 10 DHPs (nifedipine, nilvadipine, barnidipine, nimodipine, nitrendipine, amlodipine, nicardipine, benidipine, felodipine, and cilnidipine) on four subtypes of Ca(2+) channels (L-, N-, P/Q-, and R-types) were investigated in the Xenopus oocyte expression system with the use of the two-microelectrode voltage-clamp technique. L-type Ca(2+) channels expressed as alpha(1C)alpha(2)beta(1a) combination were profoundly blocked by all DHPs examined, whereas blocking actions of these DHPs on R-type (alpha(1E)alpha(2)beta(1a)) channels were equally weak. In contrast, 5 of the 10 DHPs (amlodipine, benidipine, cilnidipine, nicardipine, and barnidipine) significantly blocked N-type (alpha(1B)alpha(2)beta(1a)) and P/Q-type (alpha(1A)alpha(2)beta(1a)) Ca(2+) channels. These selectivities of DHPs in blocking Ca(2+) channel subtypes would provide useful pharmacological and clinical information on the mode of action of the drugs including side effects and adverse effects.

Animals↗
PubMed1999

[Judgment at medico-legal dispute].

As the number of medical malpractice court cases has been increasing recently, it is critical for the sound development of surgery to give appropriate expert medical opinions to enable fair judicial decisions. Surgeons are asked to give such opinions in response to requests from the courts and from the parties involved in trials. To make expert opinions easily understandable to judges and lawyers, it is important to clarify general aspects of disease and the characteristics of the case at issue, give detailed descriptions of cause-and-effect relationships, indicate the evidence for every assertion, detail medical reasons prior to evaluation, and recognize the differences between clinical practice and retrospective analysis. One of the major causes of prolongation of medical malpractice trials is the difficulty in finding people qualified to give expert medical opinions. Surgeons should therefore take a positive attitude toward participation in legal procedures.

Expert Testimony↗
PubMed1999

[A case of synchronous bilateral double primary lung cancer successfully treated by Nd-YAG laser therapy and chemotherapy].

A 61-year-old man was admitted to our hospital with the chief complaint of hemosputum. He was a heavy smoker. A chest radiograph revealed a tumor shadow in right S3 which invaded the pulmonary artery. There was also an associated patchy shadow in the periphery as well as ipsilateral pleural effusion. Bronchoscopy revealed a near occlusion with superficial infiltration at the right B3 bronchus and a nodular tumor at the bifurcation between the left upper and lingual division bronchi, which was consistent with endoscopic early lung cancer. Although both tumors were histologically diagnosed as squamous cell carcinoma, this was considered to be a case of synchronous double primary lung cancer due to their mutual isolation. The left tumor was subsequently diagnosed as carcinoma in situ. Following Nd-YAG laser therapy for carcinoma in situ and 4 courses of systemic chemotherapy using TXT and CDDP, bronchoscopy revealed no residual cancerous tissue and no tumor apart from the nodular shadow in right S3 was seen on a radiograph. Subsequent right upper and middle lobectomy and lymph node (R2a) dissection revealed no residual tumors.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1999

[Mechanisms for resistance to anticancer agents and the reversal of the resistance].

MDR results from overexpression of P-glycoprotein (Pgp) and multidrug resistance protein (MRP or MRP1) that function as ATP-dependent efflux pumps. Lung resistance related protein (LRP) is also supposed to be involved in MDR. The human canalicular multispecific organic anion transporter (cMOAT) gene that is responsible for the defects in Dubin-Johnson syndrome was isolated. cMOAT is homologous to MRP1 and supposed to be involved in drug resistance. Human cMOAT cDNA transfected LLC-PK1 cells, LLC/cMOAT-1, have increased resistance to vincristine (VCR), 7-ethyl-10-hydroxycamptothecin (SN-38), and cisplatin. The multidrug resistance (MDR)-reversing agents, cyclosporin A (CsA) and PAK-104P, almost completely reversed the resistance to VCR, SN-38 and cisplatin of LLC/cMOAT-1 cells by interacting with the substrate binding site of cMOAT. Treatment of human colorectal carcinoma SW-620 cells with sodium butyrate(NaB) induced LRP in the cells and conferred resistance to Adrianycin(ADM), VCR, VP-16, gramicidin D and taxol. Two LRP-specific ribozymes inhibited the NaB-induced expression of LRP in SW-620 cells and almost completely abolished their acquisition of the MDR phenotype. The accumulation of ADM, VCR and taxol was not decreased in NaB-treated cells, suggesting that ATP-binding cassette transporters are not involved in the MDR of NaB-treated cells. ADM was mainly located in the nuclei of untreated and the cytoplasm of NaB-treated cells. The accumulation level of ADM in the nuclei isolated from untreated cells or those from treated cells in the presence of anti-LRP polyclonal antibody was higher than that from treated cells in the absence of the antibody. Efflux of ADM from nuclei isolated from NaB-treated cells was enhanced compared with those from untreated cells and NaB-treated cells transfected with a LRP-specific ribozyme. The polyclonal antibody against LRP inhibited the enhanced efflux of ADM from nuclei isolated from NaB-treated cells. These findings indicate that LRP is involved in resistance to ADM, VCR, VP-16, taxol and gramicidin D, and has an important role in the transport of ADM from the nucleus to the cytoplasm.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Dendritic cells stimulate the expansion of PML-RAR alpha specific cytotoxic T-lymphocytes: its applicability for antileukemia immunotherapy.

Dendritic cells (DC), the most potent "professional" antigen-presenting cells, hold promise for improving the immunotherapy of cancer. In this study, we investigated the ability of normal donor DC pulsed ex vivo with 12 mer PML-RAR alpha (A) peptide (SGAGEAAIETQS) to generate peptide specific autologous cytotoxic T-lymphocytes. The peptide pulsed DC-primed peripheral blood lymphocytes (PBL) displayed significantly higher cytotoxic activity compared with that of peptide non-pulsed DC-primed PBL against peptide-pulsed autologous macrophages (P<0.001). Both CD8+ and CD4+ T lymphocytes were involved in the effector cell populations. The PML-RAR alpha peptide-pulsed DC-primed T-cells were significantly superior in their production of GM-CSF and TNF-alpha, compared with peptide non-pulsed DC-primed T-cells. These intriguing preclinical studies, suggest that PML-RAR alpha pulsed-DC could be a promising immunotherapeutic modality for patients with acute promyelocytic leukemia.

CD4-Positive T-Lymphocytes↗
PubMed1998

Prevention of hypoxia-induced apoptosis by the angiogenic factor thymidine phosphorylase.

The angiogenic factor platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP) is expressed at higher levels in a wide variety of solid tumors compared to adjacent normal tissues. Patients with PD-ECGF/TP-positive colon and esophageal tumors have a poorer prognosis than those with negative tumors. The expression of PD-ECGF/TP is a prognostic factor independent of microvessel density suggesting that TP has effects on tumor progression independent of its angiogenic activity. Evidence that hypoxia and apoptosis affect tumor growth prompted us to determine whether increased expression of PD-ECGF/TP prevents apoptosis induced by hypoxia. KB/TP cells transfected with a PD-ECGF/TP cDNA were resistant to hypoxia-induced apoptosis. Among the degradation products of thymidine produced by PD-ECGF/TP, 2-deoxy-D-ribose and thymine partially prevented hypoxia-induced apoptosis. The ability of 1 microM 2-deoxy-D-ribose in combination with the same concentration of thymine to prevent hypoxia-induced apoptosis was similar to that of the overexpressed TP in KB cells. A concentration of 1 microM 2-deoxy-L-ribose abrogated the effects of these degradation products of thymidine. These findings suggested that TP can confer resistance to apoptosis induced by hypoxia and the degradation products of thymidine are involved in this resistance. Expression of PD-ECGF/TP may play an important role in the progression of solid tumors, and inhibitors of TP and analogs of the degradation products of thymidine may suppress the growth of tumors by promoting apoptosis.

Angiogenesis Inducing Agents↗
PubMed1998

Childhood parental loss and schizophrenia: evidence against pathogenic but for some pathoplastic effects.

Childhood parental loss has been associated with a number of psychiatric disorders in adulthood. The present article aims to examine, firstly, the etiologic relationship between early parental loss and later development of schizophrenia and, secondly, the pathoplastic effect of the former on the symptomatology of the latter. We have administered semi-structured interviews inquiring into psychopathology and early separation experiences to a representative sample of first-visit patients to the 31 hospitals and clinics all over Japan (n=1963) and also to a community sample in a small city in Japan (n=218). When 225 patients diagnosed with schizophrenia according to DSM-III-R criteria were compared with 122 healthy control subjects without any lifetime psychiatric disorder, controlled for sex and age, there was no statistically significant difference in the rates of childhood parental loss (death or separation). As regards the pathoplastic effects, it was found that schizophrenic men were less likely to present with negative symptoms if they had experienced separation from the father, and were more likely to show panic attacks if they had experienced separation from the mother. Schizophrenic women were more likely to present with hallucinations if they had suffered any loss of the father. Childhood parental loss is not pathogenic of schizophrenia but appears to exert some pathoplastic influences on its presenting symptoms.

Adult↗
PubMed1998

Loss of chromosome 18q is an early event in pancreatic ductal tumorigenesis.

Cytogenetic and molecular studies demonstrated that pancreatic cancer frequently shows specific chromosomal abnormalities, such as losses of 9p, 17p, and 18q, and gains of 8q and 20q. We have analyzed alterations in the copy number of specific chromosomal regions in cells from the pancreatic juices of 32 patients with various pancreatic disorders by fluorescence in situ hybridization (FISH) technique to pursue the possible clinical use of early diagnosis of pancreatic cancer. None of the chromosomal abnormalities were found in 13 specimens from individuals who had no neoplastic lesions. On the other hand, 12 specimens (63%) derived from the remaining 19 patients who had neoplastic lesions showed at least one chromosomal abnormality. Ten of these specimens were from pancreatic cancer patients; 7 cases (70%) showed chromosomal abnormalities. All but one of the 12 tumors with chromosomal abnormalities had loss of 18q. Furthermore, we detected a tumor in one patient in whom the routine cytological method and endoscopic retrograde chorangiopancreatography found nothing. Based on the results by FISH, we performed endoscopic ultrasonography and found a small serous cystadenoma in this patient. These results indicate that: (a) FISH analysis of cells from pancreatic juices obtained during endoscopic retrograde chorangiopancreatography is quite useful for detecting pancreatic ductal tumors; and (b) loss of chromosome 18q is one of the early genetic changes that provide very useful information in diagnosing pancreatic neoplasias.

Adolescent↗