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K Goto

Publications and source records attributed to K Goto.

At least 343 records · Page 19Linked to original sources

Cloning and expression localization of cDNA for rat homolog of TRP protein, a possible store-operated calcium (Ca2+) channel.

A 3.2 kbp cDNA clone encoding a possible candidate for the store-operated Ca2+ channel was isolated from a rat brain cDNA library. The deduced amino acid sequence was 51.8% identical to TRP encoded by a Drosophila trp (transient receptor potential) gene and contained ankyrin motifs, a coiled-coil structure and six transmembrane segments similar to the previously identified TRP family and named as TRP-R (rat TRP). By in situ hybridization histochemistry of rat body on embryonic day 15, no significant expression signal for TRP-R was detected. On embryonic day 20 and postnatal day 1, the expression signals were most evident in the septum, cerebral cortical plate and hippocampal neuronal layers. On postnatal day 7 and thereafter the expression in the cerebral cortex and the septum decreased progressively, and weak expression remained only in the CA1 and CA2 neuronal layers of the hippocampus in the brain on postnatal day 21 and 49. This limited spatiotemporal expression of this novel molecule. TRP-R, suggests that it is involved in some specific functions related to the neuronal differentiation.

Amino Acid Sequence↗

Cloning and characterization of a 92 kDa soluble phosphatidylinositol 4-kinase.

A phosphatidylinositol (PtdIns) 4-kinase cDNA cloned from a rat brain cDNA library encoded a protein of 816 amino acids with a calculated molecular mass of 91654 Da. This molecule contained a lipid-kinase-unique domain and a presumed lipid/ protein kinase homology domain that are found in other PtdIns 4-kinases and PtdIns 3-kinases. Furthermore, this kinase molecule had 43.3% shared identity with the presumed catalytic domain of yeast PtdIns 4-kinase, PtdInsK1, and the two molecules had a region of similarity that is not conserved in other lipid kinases. By examining PtdIns kinase activity in transfected COS-7 cells using epitope tag immunoprecipitation as well as conventional methods, the product PtdIns phosphate was identified as phosphatidylinositol 4-phosphate (PtdIns4P), but not phosphatidylinositol 3-phosphate (PtdIns3P). The PtdIns 4-kinase activity was recovered predominantly from the soluble fraction and the activity was markedly enhanced in the presence of Triton X-100 and was relatively insensitive to inhibition by adenosine. In addition, the PtdIns 4-kinase activity was completely inhibited in the presence of 10 microM wortmannin. When examined by epitope tag immunocytochemistry, the immunoreactivity for the PtdIns 4-kinase molecule was dominantly aggregated in a cytoplasmic region juxtaposed to the nuclei and was faintly but widely dispersed in the cytoplasm. By in situ hybridization analysis, the mRNA for PtdIns 4-kinase was expressed ubiquitously and was detected in most neurons throughout the grey matter of the brain, with higher expression intensity found in fetal than in adult brain.

1-Phosphatidylinositol 4-Kinase↗

Inhibition of myocardial endothelin pathway improves long-term survival in heart failure.

Occlusion of the diseased coronary artery in humans causes acute myocardial infarction, survivors of which have a high risk for the development of chronic heart failure. Cardiac myocytes and vascular endothelial cells produce endothelin-1 (refs 2-4), which increases the contractility of cardiac muscle and of vascular smooth muscle cells. Endothelin-1 also exerts long-term effects such as myocardial hypertrophy, and causes cellular injury in cardiac myocytes. Production of endothelin-1 is markedly increased in the myocardium of rats with heart failure, and acute application of an endothelin-receptor antagonist decreases myocardial contractility in such rats, indicating that myocardial endothelin-1 may help to support contractility of the failing heart. But we report here that the upregulated myocardial endothelin system may contribute to the progression of chronic heart failure, because long-term treatment with an endothelin-receptor antagonist greatly improved the survival of rats with chronic heart failure. This beneficial effect was accompanied by significant amelioration of left ventricular dysfunction and prevention of ventricular remodelling, in which there is usually an increase in the ventricular mass and cavity enlargement of the ventricle.

Animals↗

Pulmonary hypertension caused by congestive heart failure is ameliorated by long-term application of an endothelin receptor antagonist. Increased expression of endothelin-1 messenger ribonucleic acid and endothelin-1-like immunoreactivity in the lung in congestive heart failure in rats.

OBJECTIVES: The purpose of this study was to investigate whether 1) endothelin-1, a potent vasoconstrictor peptide, is involved in progression of pulmonary hypertension caused by congestive heart failure (CHF); and 2) whether long-term treatment with BQ-123, an endothelin receptor antagonist, ameliorates pulmonary hypertension caused by CHF. BACKGROUND: Congestive heart failure accompanies pulmonary hypertension, and the severity of pulmonary hypertension is an important determinant of prognosis. Although we reported that production of endothelin-1 is increased in the failing heart in rats with CHF, it is not known whether production of endothelin-1 in the lung is altered by CHF. METHODS: Congestive heart failure was induced by coronary artery ligation in rats. Expression of preproendothelin-1 messenger ribonucleic acid (mRNA) in the lung and kidney was determined. Endothelin-1 staining (immunoreactivity) in the lung was studied by immunohistochemical analysis. Effects of long-term BQ-123 treatment on the rats were studied. RESULTS: Two weeks postoperatively, CHF accompanied by pulmonary hypertension developed in the rats (CHF rats). Expression of preproendothelin-1 mRNA in the lung was markedly higher in the CHF rats than in the sham-operated rats, whereas that in the kidney did not differ between the two groups. Endothelin-1 staining on the pulmonary vascular endothelial cells was more intense in the CHF rats. BQ-123 treatment over a 2-week period in the CHF rats greatly reduced right ventricular systolic pressure and central venous pressure, but it did not affect blood pressure or left ventricular contractility (peak positive first derivative of left ventricular pressure) in these rats. CONCLUSIONS: Long-term BQ-123 treatment greatly ameliorated pulmonary hypertension in the CHF rats. The present study suggests that endothelin-1 plays an important role in the progression of pulmonary hypertension caused by CHF and that an endothelin receptor antagonist may be a new therapeutic agent for CHF-induced pulmonary hypertension.

Animals↗

Monoamine neurotransmitter function and spontaneous recurrence of methamphetamine psychosis.

The process that triggered spontaneous recurrence of methamphetamine (MAP)-induced paranoid-hallucinatory psychosis, a phenomenon known as flashbacks, was studied in 41 subjects with flashbacks, along with 84 subjects with a history of previous MAP psychosis but no flashbacks. Plasma levels of norepinephrine (NE), dopamine, and 5-hydroxytryptamine, and their respective metabolites were assayed in 28 of the 41 flashbackers, 16 of the 84 non-flashbackers, 9 subjects with persistent MAP psychosis, and 28 healthy controls comprised of 20 MAP users and 8 non-users. None of the 28 controls had become psychotic. The 41 flashbackers had experienced significantly greater frequencies of threatening events and frightening paranoid-hallucinatory states during previous MAP use than the 84 non-flashbackers. The dominant factor that triggered flashbacks was a mild fear of other persons. The 41 flashbackers may have encoded threatening experiences as frightening images. Repeated MAP use with threatening experiences may induce sensitization to frightening images. Plasma NE levels during flashbacks were significantly higher than the levels during periods of normalcy, and the NE levels in the 20 user and 8 non-user controls. The 9 subjects with persistent MAP psychosis had significant higher levels of NE than the user and non-user controls. The 16 non-flashbackers had significantly higher MHPG levels than the user controls. The findings suggest that MAP use may induce changes at pharmacological levels in the process underlying sensitization to frightening images. We suggested that when the flashbackers experienced a mild fear of other persons, MAP-induced sensitization to frightening images may have been actualized. Thus, the flashbacks may have been caused through increased noradrenergic hyperactivity.

Adult↗

A 104-kDa diacylglycerol kinase containing ankyrin-like repeats localizes in the cell nucleus.

The cDNA corresponding to a fourth species of diacylglycerol (DG) kinase (EC 2.7.1.107) was isolated from cDNA libraries of rat retina and brain. This cDNA encoded a 929-aa, 104-kDa polypeptide termed DGK-IV. DGK-IV was different from previously identified mammalian DG kinase species, DGK-I, DGK-II, and DGK-III, in that it contained no EF-hand motifs but did contain four ankyrin-like repeats at the carboxyl terminus. These structural features of DGK-IV closely resemble the recently cloned, eye-specific DG kinase of Drosophila that is encoded by the retinal degeneration A (rdgA) gene. However, DGK-IV was expressed primarily in the thymus and brain with relatively low expression in the eye and intestine. Furthermore, the primary structure of the DGK-IV included a nuclear targeting motif, and immunocytochemical analysis revealed DGK-IV to localize in the nucleus of COS-7 cells transfected with the epitope-tagged cDNA, suggesting an involvement of DGK-IV in intranuclear processes.

Amino Acid Sequence↗

Identification of an osteoblastic silencer element in the first intron of the rat osteocalcin gene.

The osteocalcin gene has been used as a model for studying the regulation of gene expression by 1,25-dihydroxyvitamin D3, as well as for examining factors which contribute to osteoblast-specific regulation of gene expression. Most of these studies have focused on transactivation. We report the identification of a sequence in the first intron of the rat osteocalcin gene which suppresses the expression of osteocalcin-CAT fusion genes approximately 10-fold in ROS 17/2.8 and UMR 106 osteosarcoma cells. Mutation of a TTTCTTT motif in the first intron abolishes this suppression. The silencing effect of this motif is also observed after bone morphogenic protein-2 (BMP-2)-induced expression of the osteoblastic phenotype in the MLB13MYC clone 17 cell line. Mutation of the splice donor site does not affect suppression by these sequences in ROS 17/2.8 cells. When multimerized and placed upstream of the native osteocalcin promoter, these sequences retain their ability to mediate transcriptional repression. Electrophoresis mobility shift analysis demonstrates a specific protein-DNA interaction with the TTTCTTT motif in nuclear extracts from ROS 17/2.8, UMR 106, and MLB13MYC clone 17 cells but not those from COS-7 kidney cells. The mutation of this motif, which abolishes suppressing activity in the native context, also abolishes binding. The presence and activity of this suppressor in cells of the osteoblast lineage suggest that it is expressed with other cell-specific transcriptional regulators of the osteocalcin gene, coordinately regulating expression of this gene in bone cells.

Animals↗

Anticoagulant factor protein S inhibits the proliferation of rat astrocytes after injury.

The actions of protein S (PS) on the scratch injury-induced proliferation of rat astrocytes (AC) were studied. PS (10-300 nM) markedly inhibited [3H]thymidine incorporation into injured AC. The effect of 100 nM PS was comparable with that of transforming growth factor-beta 1 (TGF-beta 1; 20 ng/ml). The incorporation of bromodeoxyuridine, which is usually detectable in AC along the border of the wound, was undetectable in the presence of 300 nM PS. The level of PS mRNA in the injured AC was slightly increased 15 h after the injury, although the level of its receptor, Tyro 3 mRNA was not changed significantly. The results of the present study suggest that PS plays an important role in tissue repair processes in the central nervous system (CNS) by suppressing the proliferation of AC as in the case of TGF-beta 1.

Animals↗

Plasma monoamine metabolites and spontaneous recurrence of methamphetamine-induced paranoid-hallucinatory psychosis: relation of noradrenergic activity to the occurrence of flashbacks.

The relationship between monoamine neurotransmitter function and spontaneous recurrence of methamphetamine (MAP) psychosis, a phenomenon known as flashbacks, was studied in a group of incarcerated women. Plasma levels of norepinephrine (NE), dopamine, 5-hydroxytryptamine, and their respective metabolites were assayed in 28 flashbackers, 19 non-flashbackers with a history of previous MAP psychosis, and 9 subjects with persistent MAP psychosis. Control data were available from 61 physically healthy prisoners (41 MAP users and 20 non-users, none of whom became psychotic). The plasma NE levels of the 28 flashbackers during flashbacks were significantly higher than levels during periods of normality, and were significantly higher than those in the MAP user and non-user controls. Plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) levels during flashbacks were significantly higher than those in the user controls. The nine subjects with persistent MAP psychosis had significantly higher NE levels than the user and non-user controls. The 19 non-flashbackers had significantly higher MHPG levels than the user controls. Plasma levels of 3-methoxytyramine and dihydroxyphenylacetic acid contributed to the NE levels in the flashbackers, in contrast to the findings in the control group. Noradrenergic systems may be compromised in the flashbackers, suggesting increased vulnerability to psychotic decompensation. These findings suggest that aggravation in peripheral noradrenergic hyperactivity may be an important factor in the occurrence of flashbacks.

Adult↗

Endogenous endothelin-1 initiates astrocytic growth after spinal cord injury.

We developed a rat spinal cord injury model and investigated whether endogenous endothelin (ET)-1 plays a role in astrocytic growth after injury. Immunohistochemical study showed that the number of immature astrocytes (ACs) exhibiting strong reactivity to the monoclonal antibody, RC1, markedly increased 24 h after the injury. Injection of a potent nonselective ET receptor antagonist, SB209670, into the lesion sites significantly inhibited the appearance of RC1-positive cells 24 h after the injury. In conjunction with this result, the increase in immunostaining density of 5-bromo-2'-deoxyuridine in the spinal cord 24 h after the injury was inhibited by the injection of SB209670. The tissue content of ET-1-LI was significantly increased 12 and 24 h after the injury. These results suggest that endogenous ET-1 is involved in astrocytic growth after spinal cord injury.

Animals↗

Molecular genetic basis of red cell markers and its forensic application.

(1) The polymerase chain reaction (PCR) was used to amplify Rh-related cDNAs from erythroid cells cultured by the selective two-phase liquid culture system for human erythroid progenitors in peripheral blood. Two Rh polypeptide cDNAs have been isolated from the PCR products and tentatively designated RhPI cDNA and RhPII cDNA. Both cDNA clones have an open reading frame composed of 1251 nucleotides. The RhPI cDNA clone shows a single nucleotide substitution with no amino acid substitution compared with the published sequence. The RhPII cDNA clone differs from the above by 41 nucleotide substitutions in the open reading frame, resulting in 31 amino acid substitutions. Besides these cDNA clones, eleven and five truncated isoforms of the RhPI and RhPII cDNAs, have been isolated, respectively. (2) The promoter region of the Duffy gene was cloned by IPCR of 1.1 kb SacI fragment and the 3' flanking sequence was cloned by IPCR of 1.9 kb EcoRI fragment. The IPCR products contained the known Duffy cDNA sequence without introns. By comparing the coding area of the Duffy gene in 28 Duffy positive individuals, we elucidated that one base change that results in an amino acid substitution (GAT(Asp44)-->GGT(Gly)) is in accordance with the Fya/Fyb polymorphism. This fact proves that the Duffy cDNA and its gene encode the Duffy blood group system. (3) Two common alleles in Esterase D (EsD) polymorphism, EsD1 and EsD2 were characterized by the substitution of one amino acid (Gly-Glu) caused by the point mutation of one nucleotide (G-A). The point mutation between cDNAs of EsD1 and EsD2 alleles was detectable as restriction fragment length polymorphism (RFLP) using Ssp1. The RFLP makes it possible to determine the EsD phenotypes using DNA samples from forensic materials without EsD enzymatic activity. (4) The authors report studies on 19 pairs of donors and recipients in bone marrow transplantation. A broad range of genetic markers at 42 gene loci, including one DNA marker 11 red blood cell markers, five human lymphocyte antigen types, 12 serum protein markers, five red cell enzyme markers, and eight salivary markers was evaluated before and after BMT over about 2 months. As a result, 11 out of 42 gene loci of genetic markers in recipients were transformed into the donor type.

Base Sequence↗

An immuno-histochemical study of ferritin in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced hemiparkinsonian monkeys.

Iron is increased in the substantia nigra of patients with Parkinson's disease, but the mechanism of its accumulation is unknown. We report the distribution of ferritin in the basal ganglia of hemiparkinsonian monkeys made by MPTP. We stereotactically injected MPTP unilaterally into the caudate nucleus of four monkeys, and the substantia nigra and the basal ganglia regions were stained for L-ferritin by an immunohistochemical method. The ferritin immuno-staining was most intense in the pallidum and the pars reticulata of the substantia nigra on both injected and non-injected sides. No significant difference was noted in the immunostaining for ferritin in the pars compacta of the substantia nigra between the injected and the non-injected side. Iron was increased in the pars compacta of the substantia nigra of this hemiparkinsonian monkeys in our previous study. Normal ferritin immunostaining on the injected side would indicate that iron accumulation is not related to altered metabolism of L-ferritin in this model.

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

Cloning, expression, and localization of 230-kDa phosphatidylinositol 4-kinase.

A phosphatidylinositol (PI) 4-kinase cDNA was cloned from a rat brain cDNA library. This cDNA encoded a protein of 2041 amino acids with a calculated molecular weight of 231,317. The deduced amino acid sequence shared the identity of 52.3 and 34.4% in the presumed catalytic domain with two yeast PI 4-kinases, STT4 and PIK1, respectively, and showed 31.7% identity to p110alpha subunit of rat PI 3-kinase in the same domain. In addition, a 3' half coding region of the present cDNA was 89.6% identical to and its deduced amino acid sequence was 98.2% identical to the sequence for P14Kalpha, a recently reported human PI 4-kinase of type II, suggesting that P14Kalpha is an alternative form of the present PI 4-kinase molecule. The present cDNA contained sequences encoding the ankyrin repeat domain, lipid kinase unique domain, pleckstrin homology domain, presumed lipid kinase/protein kinase homology domain, proline-rich region, and SH3 domain. By examining PI kinase activity in transfected COS-7 cells using the epitope tag immunoprecipitation as well as the conventional way, the product phosphatidylinositol phosphate was identified as phosphatidylinositol 4-phosphate but not phosphatidylinositol 3-phosphate. This PI 4-kinase activity was markedly enhanced in the presence of Triton X-100 but relatively insensitive to inhibition by adenosine. By epitope tag immunohistochemistry, the immunoreactivity for this PI 4-kinase molecule was largely localized in close association with the membranes of the Golgi vesicles and vacuoles. By in situ hybridization analysis, the expression of mRNA for this PI 4-kinase was evident throughout the gray matter of entire brain with higher expression intensity in fetal brain. These data imply that this novel PI 4-kinase is involved in some processes essential to neuronal differentiation and maturation including the synaptogenesis and synaptic plasticity.

Amino Acid Sequence↗

Isolation of cDNA and genomic clones of a human Ras-related GTP-binding protein gene and its chromosomal localization to the long arm of chromosome 7, 7q36.

A Ras-related GTP-binding protein cDNA has been isolated from a human skin fibroblast cDNA library using a genomic subclone derived from a YAC clone as a probe. The polypeptide, consisting of 184 amino acids deduced from nucleotide sequences, contains five repeats of the Ras-related GTP-binding region and is highly homologous to the rat RHEB (Ras homologue enriched in brain) gene, which encodes a Ras-related growth factor- and synaptic activity-regulated protein, with 98.9% amino acid identity. Therefore, it is suggested to be a human homologue of the rat RHEB protein, and we have designated it human RHEB. Using fluorescence in situ hybridization, we concluded that this human RHEB gene was localized to band q36 on chromosome 7. Considering the chromosomal localization as well as the potential function of this protein, it will be very important to investigate whether it may play a role in the etiopathogenesis of holoprosencephaly type 3 or hereditary sacral agenesis, in which the disease susceptible locus is linked to the microsatellite marker, D7S22, in this chromosomal region, 7q36.

Amino Acid Sequence↗

Vasoconstriction by endothelin-1 in resistance and conduit portions of isolated human mesenteric arteries.

Although physiological processes related to vascular function differ greatly between resistance arteries and conduit arteries, it is not known whether the effects of endothelin-1 on these arteries differ in humans. In the present study, the conduit portion and the resistance portion of isolated human mesenteric arteries were suspended in a Krebs-Ringer solution. Norepinephrine and endothelin-1 produced concentration-dependent contractions in both portions. The EC50 value of norepinephrine in the resistance portion (3.7 x 10(-7) M, n = 8) did not differ from that in the conduit portion (3.4 x 10(-7) M, n = 7). However, the EC50 value of endothelin-1 in the resistance portion (3.0 x 10(-9) M, n = 8) was significantly lower than that in the conduit portion (1.1 x 10(-8) M, n = 7, P < 0.05). Although the maximum response to norepinephrine in the resistance portion (calculated as the percentage of 50 mM KCl-induced contraction) did not differ from that in the conduit portion, the maximum response to endothelin-1 in the resistance portion was significantly greater than that in the conduit portion. These results indicate that endothelin-1 induces more potent constriction in resistance portion than in conduit portion in isolated human mesenteric arteries.

Adult↗

Human apolipoprotein E receptor 2. A novel lipoprotein receptor of the low density lipoprotein receptor family predominantly expressed in brain.

Isolation and characterization of a human cDNA demonstrated a novel lipoprotein receptor designated apolipoprotein E receptor 2 (apoER2). The new receptor consists of five functional domains resembling the low density lipoprotein (LDL) and very low density lipoprotein (VLDL) receptors. LDL receptor deficient Chinese hamster ovary cells expressing human apoER2 bound apoE rich beta-migrating VLDL with high affinity and internalized. LDL was bound with much lower affinity to these cells. The 4.5- and 8.5-kb mRNAs for the receptor were most highly expressed in human brain and placenta. In rabbit tissues, multiple species of the mRNA with 4, 4.5, 5.5, 8.5, and 11 kb were detected most intensely in brain and testis and, to a much lesser extent, in ovary, but were undetectable in other tissues. In rat adrenal pheochromocytoma PC12 cells, the receptor mRNA was induced by treatment of the cells with nerve growth factor. The receptor transcripts were detectable most intensely in the cerebellar cortex, choroid plexus, ependyma, hippocampus, olfactory bulb and, to a much lesser extent, in the cerebral cortex as revealed by in situ hybridization histochemistry. In the cerebellar cortex, the receptor transcripts were densely deposited in Purkinje cell somata.

Amino Acid Sequence↗

Endogenous endothelin-1 participates in the maintenance of cardiac function in rats with congestive heart failure. Marked increase in endothelin-1 production in the failing heart.

BACKGROUND: Although it was demonstrated that circulating endothelin-1 (ET-1) levels are elevated in congestive heart failure (CHF), the production and roles of ET-1 in the failing heart are not known. We investigated the production of ET-1 in the heart and the density of myocardial ET receptors in rats with CHF. We also investigated the effects of intravenously infused BQ-123, an endothelin(A) (ETA) receptor antagonist, on both heart and myocardial contractility in rats with CHF. METHODS AND RESULTS: We used the left coronary artery-ligated rat model of CHF (CHF rats). Three weeks after surgery, the rats developed CHF. Plasma ET-1 concentration was significantly higher in the CHF rats than in the sham-operated rats (P<.01). In the left ventricle, the expression prepro-ET-1 mRNA was markedly higher in the CHF rats than in the sham-operated rats. The peptide level of ET-1 in the left ventricle was also significantly higher in the CHF rats than in the sham-operated rats (500+/-41 versus 102+/-10 pg/g tissue, P<.01). Myocardial ET receptors were significantly higher in the CHF rats than in the sham-operated rats (243+/-20 versus 155+/-17 fmol/mg protein, P<.05). In the CHF rats, intravenous BQ-123 infusion (0.1 mg x kg(-1) x min(-1) for 120 minutes) significantly decreased both heart rate (P<.01) and LV+dP x dt(max) (P<.05) but not mean blood pressure. BQ-123 infusion did not affect these hemodynamic parameters in the sham-operated rats. CONCLUSIONS: In the present study, we demonstrated that the production of ET-1 in the heart is markedly increased and that the density of myocardial ET receptors is significantly elevated in the CHF rats. Intravenous BQ-123 infusion significantly reduced both heart rate and LV+dP/dt(max) in the CHF rats but not in the sham-operated rats. Therefore, the ET receptor-mediated signal transduction system in the heart appears to be markedly stimulated in the CHF rats, and endogenous ET-1 may be involved in the maintenance of the cardiac function in these rats.

Animals↗

Cooperative clinical trial of photodynamic therapy with photofrin II and excimer dye laser for early gastric cancer.

BACKGROUND AND OBJECTIVE: Photodynamic therapy (PDT) is a recently developed endoscopic method for treating malignant tumors. For obtaining more photodynamic action with less thermal effect, we employed as the excitation light source for PDT an excimer dye laser, which is a pulsed laser with extremely high peak power, instead of an argon dye laser, which is a continuous wave laser and has been used conventionally. STUDY DESIGN/MATERIALS AND METHODS: The effect of PDT using Photofrin II and the excimer dye laser was evaluated in 27 patients with early gastric cancer. RESULTS: Complete responses (CR) were obtained in 88% of 24 assessable patients and the response rate was 100%. CR was observed in all cases of lesions of superficial depressed type without ulceration and/or with tumor diameter less than 2 cm. Regarding toxicity, mild cutaneous reaction and photosensitivity were seen and lasted several weeks. There were no serious abnormalities in laboratory tests. CONCLUSION: We conclude that PDT is a promising modality for early gastric cancer.

Aged↗