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Biomedical subjects

Y Endo

Publications and source records attributed to Y Endo.

At least 73 records · Page 4Linked to original sources
PubMed2001

Mesangial IgA2 deposits and lectin pathway-mediated complement activation in IgA glomerulonephritis.

Three pathways are recognized in complement activation. The aim of our study is to elucidate immunohistologically which complement pathway is associated with complement activation in immunoglobulin A (IgA) glomerulonephritis (GN) and which IgA subclass is related to complement activation. Immunohistological staining was performed on renal biopsy specimens obtained from 36 patients with IgA GN, 10 patients with systemic lupus erythematosus (SLE), and 16 patients with other GNs using polyclonal antibodies of IgG, IgA, IgM, C1q, C3c, and C4 and monoclonal antibodies of IgA1, IgA2, mannose-binding lectin (MBL), and MBL-associated serine protease-1 (MASP-1). Mesangial deposits of both IgA1 and IgA2 were found in 19 of 36 patients with IgA GN. Mesangial deposits of C3c, C4, MBL, and MASP-1 also were detected in these 19 patients, and IgA2, MBL, and MASP-1 deposits were colocalized in the mesangium in these patients. The remaining 17 patients showed mesangial deposits of IgA1 alone. Twelve of these 17 patients showed mesangial deposits of C3c without C4, MBL, or MASP-1. No deposition of C1q was evident in patients with IgA GN. Three of 10 patients with SLE showed glomerular deposition of MBL and MASP-1 without glomerular deposition of IgA2. None of the patients with other GNs showed glomerular deposition of IgA1, IgA2, MBL, or MASP-1. There was no correlation in clinical or pathological indicators between IgA2-positive and IgA2-negative patients with IgA GN. In conclusion, alternative pathway-involved complement activation is associated with mesangial deposits of IgA1 alone in patients with IgA GN. In those with mesangial deposits of both IgA1 and IgA2, both the alternative and lectin pathways are involved in complement activation. We first report that mesangial deposits of IgA2 may activate the lectin pathway in patients with IgA GN.

Adolescent↗
PubMed2001

Epidermal growth factor induces expression of decay-accelerating factor in human colonic cancer cells via the mitogen-activated protein kinase pathway.

The expression of decay-accelerating factor (DAF), a complement regulatory protein, is enhanced in colorectal cancer. In this study, to elucidate mechanisms for enhanced DAF expression, we studied the effects of growth factors on DAF expression in HT-29 human colonic cancer cells. Cells were treated with epidermal growth factor (EGF), insulin-like growth factor-I, platelet-derived growth factor, and transforming growth factor-beta. DAF protein expression and mRNA expression were determined with enzyme immunoassay and Northern blot analysis. The signaling pathways that target DAF expression in response to growth factor stimulation were characterized by using various inhibitors of the signal transduction pathway. EGF induced significant increases in DAF protein and mRNA expression in HT-29 cells; the other growth factors had a weak effect or no effect. The EGF-induced DAF expression was inhibited by mitogen-activated protein (MAP) kinase kinase inhibitor PD 98059 but not by phosphatidylinositol-3 kinase inhibitor, phospholipase Cgamma inhibitor, or protein kinase C inhibitor. When we analyzed the phosphorylation state of the MAP kinase by immunoblot analysis, phosphorylated p44/p42 MAP kinase was detected in EGF-stimulated HT-29 cells, and the addition of PD 98059 abrogated the phosphorylation. These results indicate that EGF regulates DAF expression in HT-29 cells via the signaling pathway that depends on the activation of MAP kinase.

Blotting, Northern↗
PubMed2001

Effective inhibition of HIV-1 replication in cultured cells by external guide sequences and ribonuclease.

We examined the suppression effect of HIV-1 expression by cleavage of the HIV-1 RNA gene, using the catalytic RNA subunit RNase P and the 3'-half tRNA [External Guide Sequence (EGS)] in vivo. The vectors were designed to express an anti-HIV EGS, U5, which targets the 5' leader sequence. We constructed an EGS expression vector, that used the tRNA(met) or U6 promoter as an expression cassette for EGS. RNase P cleaves the targeted HIV-1 mRNA when they are in a complex with the EGS. To test the antiviral efficacy of these EGS vectors, we have cotransfected into COS cells with the HIV-1 proviral DNA (pNL4-3 Luc) and the plasmid expressing the EGS from the tRNA(met) or U6 promoter. HIV-1 expression was inhibited by the tRNA-EGS-1 and U6-EGS-1 from the tRNA(met) and U6 promoters, respectively. No difference in the inhibitory effects on HIV-1 expression between the tRNA(met) and U6 promoters could be detected.

Animals↗
PubMed2001

Identification of essential amino acid residues of tRNA (Gm18)methyltransferase for methyl-transfer activity.

Recent computation analyses have pointed out an existence of conserved amino acid motifs among RNA ribose 2'-O-methyltransferases. However, the functions of these motifs are unclear yet. We carried out the site-directed mutagenesis studies systematically on Thermus thermophilus HB8 tRNA (Gm18) methyltransferase gene. Subsequent biochemical analyses with purified variant enzymes clearly revealed that five conserved amino acid residues (Asn35, Arg41, Glu124, Ser150, and Asn152) are involved in S-adenosyl-L-methionine binding. This is for the first time reporting the function of the conserved motifs among RNA ribose 2'-O-methyltransferases.

Amino Acid Motifs↗
PubMed2001

Substrate specificity of Ca(2+)/calmodulin-dependent protein kinase phosphatase: kinetic studies using synthetic phosphopeptides as model substrates.

Ca(2+)/calmodulin-dependent protein kinase phosphatase (CaMKPase) dephosphorylates and regulates multifunctional Ca(2+)/calmodulin-dependent protein kinases. In order to elucidate the mechanism of substrate recognition by CaMKPase, we chemically synthesized a variety of phosphopeptide analogs and carried out kinetic analysis using them as CaMKPase substrates. This is the first report using systematically synthesized phosphopeptides as substrates for kinetic studies on substrate specificities of protein Ser/Thr phosphatases. CaMKPase was shown to be a protein Ser/Thr phosphatase having a strong preference for a phospho-Thr residue. A Pro residue adjacent to the dephosphorylation site on the C-terminal side and acidic clusters around the dephosphorylation site had detrimental effects on dephosphorylation by CaMKPase. Deletion analysis of a model substrate peptide revealed that the minimal length of the substrate peptide was only 2 to 3 amino acid residues including the dephosphorylation site. The residues on the C-terminal side of the dephosphorylation site were not essential for dephosphorylation, whereas the residue adjacent to the dephosphorylation site on the N-terminal side was essential. Ala-scanning analysis suggested that CaMKPase did not recognize a specific motif around the dephosphorylation site. Myosin light chain phosphorylated by protein kinase C and Erk2 phosphorylated by MEK1 were poor substrates for CaMKPase, while a synthetic phosphopeptide corresponding to the sequence around the phosphorylation site of the former was not dephosphorylated by CaMKPase but that of the latter was fairly good substrate. These data suggest that substrate specificity of CaMKPase is determined by higher-order structure of the substrate protein rather than by the primary structure around its dephosphorylation site. Use of phosphopeptide substrates also revealed that poly-L-lysine, an activator for CaMKPase, activated the enzyme mainly through increase in the V(max) values.

Amino Acid Sequence↗
PubMed2001

Hypovolemic intolerance to lower body negative pressure in female runners.

PURPOSE: An attenuated baroreflex response and orthostatic intolerance have been reported in endurance-trained male athletes; however, it is still unknown whether this occurs also in females. The purpose of the present study was to examine whether endurance exercise-trained women had a predisposition to orthostatic compromise, and if so, what causative factor(s) may induce orthostatic intolerance. METHODS: We studied cardiovascular and hormonal responses to graded lower body negative pressure (LBNP) (0 to -60 mm Hg) in 26 middle-distance female runners (18.6 +/- 0.1 yr) as the exercise-trained (ET) subjects and 23 age-matched untrained (UT) control subjects. On the basis of the occurrence of syncope episodes during LBNP, ET and UT subjects were further allocated to two groups; ET with presyncope (ET+syncope) and without presyncope (ET-syncope) and UT with presyncope (UT+syncope) and without presyncope (UT-syncope). RESULTS: Occurrence of presyncope episodes during LBNP was higher in ET (65.4%, P < 0.05) than that for UT (34.8%). Leg compliance was higher (P < 0.05) in ET than in UT. LBNP reduced stroke volume (SV) more (P < 0.05), increased heart rate (HR) higher (P < 0.05), and increased forearm vascular resistance (FVR) more in ET+syncope as compared with the other groups. Response of vasoactive hormones to LBNP was higher in ET+syncope (P < 0.05) than that of the other groups except for norepinephrine (NE); high in both ET+syncope and UT+syncope. The relationship between SV and NE, an index of sympathetic neuronal response, had no training-related changes during LBNP. CONCLUSION: We conclude that exercise-trained females have a high incidence of orthostatic intolerance during LBNP, with a greater reduction of SV independent of changes in baroreflex and neurohumoral function. A lower incidence of LBNP intolerance in UT may be accounted for by a lower reduction of SV during LBNP. An increase in leg compliance in the exercise-trained females may play an important role in inducing pronounced reduction of SV and hence the intolerance to LBNP.

Adolescent↗
PubMed2001

The role of bacterial translocation on neutrophil activation during hemorrhagic shock in rats.

Some biological responses to hemorrhage have been reported to be associated with bacterial translocation (BT). While the relationship between peripheral blood neutrophils and BT in the late phase of hemorrhagic shock or burn injury has been reported, this relationship in the early phase has not been fully elucidated. We investigate the role of BT in neutrophil activation and priming during hemorrhagic shock. The experimental rats were divided into three groups: a group with normal intestinal flora (NF group), an antibiotic-decontaminated group (AD group), and a sham shock group with normal intestinal flora (sham group). Hemorrhagic shock was induced in the NF and AD groups (MAP 30 mm Hg for 30-90 min). The rats were sacrificed at 30, 60, or 90 min following the shock induction. Cultures were taken from the liver, spleen, mesenteric lymph nodes (MLNs), and systemic blood to assess the occurrence of BT. Hydrogen peroxide generation and CD11b/c expression were assayed by flow cytometry to evaluate peripheral blood neutrophil activation and priming, respectively. In the NF group, significant BT to the MLNs and spleen was noted from 30 min after the shock induction, and significant hydrogen peroxide generation was also noted from 30 min. The expression of CD11b/c on neutrophils was significantly up-regulated at 90 min after the shock induction. Furthermore, BT, as also the aforementioned parameters of neutrophil function, was significantly suppressed in the AD group. We, therefore, concluded that neutrophil activation and priming during hemorrhagic shock might be closely related to BT, and that infectious factors possibly influence the host responses starting from the early phase of damage, even in noninfectious stress-inducing conditions.

Animals↗
PubMed2001

Structure, expression and chromosome mapping of MLZE, a novel gene which is preferentially expressed in metastatic melanoma cells.

We isolated a novel gene, termed MLZE, from a B16-BL6 cDNA library after subtraction of B16-F10 mRNA. Expression levels of mouse MLZE (mMLZE) increased in accordance with metastatic ability of B16 melanoma sublines. Human homolog of mMlze (hMlze) contained one leucine zipper structure and two potential nuclear localizing signals. Northern blot analysis of multiple human tissues showed that hMLZE was expressed primarily in trachea and spleen. We mapped the hMLZE gene (by fluorescence in situ hybridization) to 8q24.1 - 2, which contains the c-myc gene and is often amplified in malignant melanoma. Immunohistochemistry revealed that the number of hMlze-positive cases was significantly larger in Clark levels III, IV and V melanomas (6 / 11 = 55%) than in Clark levels I and II melanomas (2 / 15 = 13%). In two cases of hMlze-positive melanomas, the strength of hMlze staining increased substantially in the deep component of the tumor. Considering that melanomas above Clark level II are more metastatic than those below Clark level III, these findings suggested that MLZE is one of the genes whose expression is upregulated during the course of acquisition of metastatic potential in melanoma cells.

Adult↗
PubMed2001

Deletion mutants of human deoxycytidine kinase mRNA in cells resistant to antitumor cytosine nucleosides.

We studied mutational events in deoxycytidine (dCyd) kinase mRNA expression, focusing on aberrant dCyd kinase mRNA, which has been frequently observed in established cell lines resistant to antitumor dCyd nucleoside analogues such as 1-beta-D-arabinofuranosyl cytosine (Ara-C), gemcitabine (dFdC) and 2'-C-cyano-2'-deoxy-1-beta-D-arabinofuranosylcytosine (CNDAC). We describe here the expression of aberrant dCyd kinase mRNAs identified as splicing mutants. These mutants included deletions of the fifth exon in CNDAC-resistant cells (originating from HT-1080 cells), of the third exon in Ara-C-resistant cells (originating from SK-MEL-28 cells) and of the fourth exon in 2'-deoxy-2'-methylidenecytidine (DMDC)-resistant cells (originating from SK-MEL-28 cells). Various nucleoside-resistant cells originating from the same parental HT-1080 cells were established. The resulting cells expressed the same mRNA with deletion of the fifth exon, and the location of splicing was independent of the type of nucleosides used for the establishment of resistant cells. The deletion of the fifth exon in dCyd kinase seems to be a target for acquisition of resistance to antitumor cytosine nucleosides. However, distinct mutations in the dCyd kinase gene seem to be associated with acquisition of resistance to different antitumor cytosine nucleosides.

Antimetabolites, Antineoplastic↗
PubMed2001

Alpha-glucosidase inhibitors with a 4,5,6,7-tetrachlorophthalimide skeleton pendanted with a cycloalkyl or dicarba-closo-dodecaborane group.

Previous studies of alpha-glucosidase inhibitors derived from thalidomide revealed that 4,5,6,7-tetrachloro-N-alkylphthalimide derivatives are superior lead compounds. Structure-activity relationship studies indicated that a hydrophobic group at the N(2) position is mandatory for potent activity. Accordingly, we have designed and synthesized some 4,5,6,7-tetrachloro-N-cycloalkylphthalimide and 4,5,6,7-tetrachloro-N-dicarba-closo-dodecaborane derivatives. The prepared compounds exhibited potent alpha-glucosidase-inhibitory activity. Among them, 4,5,6,7-tetrachloro-N-cycloheptylphthalimide (9) showed the most potent activity, being approximately 30 times more active than the classical inhibitor, 1-deoxynojirimycin (1).

Boranes↗
PubMed2001

[Induction of histidine decarboxylase in inflammation and immune responses].

Histamine is a classical, but still interesting inflammatory mediator. Many people have long believed that histamine is derived from mast cells or basophils alone. However, the histamine-forming enzyme, histidine decarboxylase (HDC), is induced in a variety of tissues in response (i) to gram-positive and gram-negative bacterial components (lipopolysaccharides, peptidoglycan, and enterotoxin A) and (ii) to various cytokines (IL-1, IL-3, IL-12, IL-18, TNF, G-CSF, and GM-CSF). HDC is induced even in mast-cell-deficient mice. The histamine newly formed via the induction of HDC is released immediately and may be involved in a variety of immune responses. Reviewing our work and that of Schayer and Kahlson, the pioneers in this field, lead us to the conclusion that nowadays we need to understand that histamine can be produced via the induction of HDC by a mechanism coupled with the cytokine network. We call this histamine "neohistamine", to distinguish it from the classical histamine derived from mast cells or basophils. Neohistamine is involved in physiological reactions, inflammation, immune responses and a variety of diseases such as periodontitis, muscle fatigue (or temporomandibular disorders), stress- or drug-induced gastric ulcers, rheumatoid arthritis, complications in diabetes, hepatitis, allograft rejection, allergic reactions, tumor growth, and inflammatory side effects of aminobisphosphonates.

Animals↗
PubMed2001

Involvement of cytochrome P450 metabolites in the vascular action of angiotensin II on the afferent arterioles.

Recent studies have demonstrated that cytochrome P450-dependent metabolites of arachidonic acid (CYP450-AA) play important roles in the control of renal vascular resistance (RVR). In the present study, we examined the possible involvement of CYP450-AA in the vasoconstrictor action of angiotensin II (Ang II) on the afferent arterioles (Af-Arts), a vascular segment crucial to the control of RVR. Rabbit Af-Arts were microperfused at 60 mmHg in vitro, and the vasoconstrictor action of Ang II (10(-11)-10(-8) M, added to both the bath and lumen) was examined with or without blocking the activity of CYP450 epoxygenase or hydroxylase. Ang II decreased the luminal diameter of Af-Arts in a dose-dependent manner (34+/-2% of control diameter at 10(-8) M, n=9, p<0.0001). Pretreatment with miconazole, an inhibitor of CYP450 epoxygenase, at 10(-6) M decreased the basal diameter by 14+/-1% (n=6, p<0.01) and augmented the vasoconstrictor action of Ang II (7+/-3% of control diameter at 10(-8) M, p<0.001 vs. without miconazole). This augmentation was abolished by blocking the Ang II type 2 (AT2) receptor with PD 123319 at 10(-7) M. In contrast, pretreatment with 17-octadecynoic acid (17-ODYA, 10(-6) M), which inhibits both epoxygenase and hydroxylase activity, had no effect on the basal diameter but attenuated the vasoconstrictor action of Ang 11(46+/-2% of control diameter at 10(-8) M, p<0.01 vs. without 17-ODYA). Our results demonstrate that in the Af-Art, endogenous CYP450-AA are involved not only in the control of basal tone but also in the action of Ang II. Further, it appears that the CYP450 epoxygenase pathway attenuates Ang II action via AT2 receptors.

Angiotensin II↗
PubMed2001

Sampling methods and residential factors affecting formaldehyde concentration in indoor air.

Formaldehyde (HCHO) is the most serious residential pollutant. In order to evaluate residential HCHO levels, two sampling methods have been recommended; one is a 30 minute sampling in a closed room, and the other is a 24 hour sampling with an ordinary lifestyle routine. The aim of this report was to clarify the difference between the HCHO levels obtained by the two sampling methods. Residential air in 58 rooms was sampled for 30 minutes by an active sampling method more than 5 hours after residents closed windows, and by a passive sampling method for 24 hours with an ordinary lifestyle routine. The HCHO concentration with the 30 minute sampling was 0.118+/-0.065 ppm (range: 0.034-0.295 ppm) and 36 rooms (62%) exceeded the Japanese guideline value of 0.08 ppm, while 5% were higher than 0.25 ppm. The HCHO concentration with the 24 hours sampling was 0.053+/-0.039 ppm (range: 0.02-0.167 ppm) and only 13 rooms (22%) exceeded 0.08 ppm. The relationship between the concentrations obtained by the two methods was linear. However, the level with the 24 hour sampling significantly reduced with prolonged window opening time, meaning that occupants made an effort to reduce the usual exposure to about 40% of the exposure in a closed room by opening windows in order to escape from irritation. Since major adverse effects of HCHO are irritation and sensitization, the occasional peak concentration must be focused. In order to evaluate residential HCHO levels, measurement in a closed room is recommended even if people are living there.

Air Conditioning↗
PubMed2001

Evidence of primary beta-cell destruction by T-cells and beta-cell differentiation from pancreatic ductal cells in diabetes associated with active autoimmune chronic pancreatitis.

OBJECTIVE: Diabetes associated with autoimmune chronic pancreatitis (ACP) is a subtype of diabetes that is responsive to corticosteroid treatment of progressive endocrine and exocrine dysfunction. However, little is known about pathological changes of islet and exocrine pancreas in ACP. RESEARCH DESIGN AND METHODS: We examined pancreatic specimens obtained on biopsy from four diabetic men with ACP (mean [range]: age 62 years [48-78], duration of ACP 3 months [1-5], duration of diabetes 1 month [0-3]) morphologically, immunohistochemically, and morphometrically. RESULTS: The pancreatic specimens in all cases exhibited inflammatory cell infiltration surrounding ductal cells and extensive fibrosis. Some islets were infiltrated with mononuclear cells with disrupted beta-cells. The subsets of T-cells infiltrated to the islets were mainly CD8(+). Islet beta-cell volume was decreased; the mean percentage area of beta-cells in the islets in four cases with ACP were 16% (range 13-20) (P = 0.0015 vs. type 2 diabetic patients, 48% [27-73], n = 8; P = 0.0002 vs. nondiabetic control subjects, 58% [39-77], n = 7). Preserved ductal cells were surrounded predominantly by CD8(+) or CD4(+) T-cells. Some cytokeratin 19-positive ductal cells contained insulin and glucagon, representing upregulated differentiation of islet cells from ductal cells. Insulin promoter factor-1 (IPF-1) was hyperexpressed in insulin-containing ductal cells. CONCLUSIONS: Diabetes associated with ACP is caused by T-cell-mediated mechanisms primarily involving islet beta-cells as well as pancreatic ductal cells. In ACP, ductal islet precursor cells were associated with IPF-1 hyperexpression, suggesting a critical role of IPF-1 on islet cell differentiation and eventual beta-cell restoration.

Acute Disease↗
PubMed2001

Three-dimensional computerized tomography angiography-guided surgery of acutely ruptured cerebral aneurysms.

OBJECT: The aim of this study was to assess whether aneurysm surgery can be performed in patients with ruptured cerebral aneurysms by using three-dimensional computerized tomography (3D-CT) angiography alone, without conventional catheter angiography. METHODS: In a previous study, 60 patients with subarachnoid hemorrhage (SAH) from ruptured aneurysms were prospectively evaluated using both 3D-CT and conventional angiography, which resulted in a 100% accuracy for 3D-CT angiography in the diagnosis of ruptured aneurysms, and a 96% accuracy in the identification of associated unruptured aneurysms. The results led the authors to consider replacing conventional angiography with 3D-CT angiography for use in diagnosing ruptured aneurysms, and to perform surgery aided by 3D-CT angiography alone without conventional angiography. Based on the results, 100 consecutive patients with SAH who had undergone surgery in the acute stage based on 3D-CT angiography findings have been studied since December 1996. One hundred ruptured aneurysms, including 41 associated unruptured lesions, were detected using 3D-CT angiography. In seven of 100 ruptured aneurysms, which included four dissecting vertebral artery aneurysms, two basilar artery (BA) tip aneurysms, and one BA-superior cerebellar artery aneurysm, 3D-CT angiography was followed by conventional angiography to acquire diagnostic confirmation or information about the vein of Labbé, which was needed to guide the surgical approach for BA tip aneurysms. All of the ruptured aneurysms were confirmed at surgery and treated successfully. Ninety-three patients who underwent operation with the aid of 3D-CT angiography only had no complications related to the lack of information gathered by conventional angiography. The 3D-CT angiography studies provided the authors with the aneurysm location as well as surgically important information on the configuration of its sac and neck, the presence of calcification in the aneurysm wall, and its relationship to the adjacent vessels and bone structures. CONCLUSIONS: The authors believe that 3D-CT angiography can replace conventional angiography in the diagnosis of ruptured aneurysms and that surgery can be performed in almost all acutely ruptured aneurysms by using only 3D-CT angiography without conventional angiography.

Adult↗
PubMed2001

Increased expression of S100A4 and its prognostic significance in esophageal squamous cell carcinoma.

S100A4 has been implicated in invasion and metastasis of cancer, but prognostic significance of its expression in esophageal squamous cell carcinoma remains unclear. In this study, we examined the expression of S100A4 by Western blot analysis and immunohistochemistry in surgically resected esophageal squamous cell carcinoma. The relationship between S100A4 tissue status and clinicopathological findings was analyzed to assess the prognostic significance of S100A4 in esophageal squamous cell carcinoma. The S100A4 protein level was significantly higher in tumor tissue than in corresponding normal esophageal mucosa (p<0.05) in 22 cases of esophageal carcinoma by Western blot analysis. S100A4 expression was detected in 25% of 52 cases of esophageal squamous cell carcinoma by immunohistochemistry and correlated with the depth of invasion (p<0.05). Patients with S100A4-positive carcinoma had significantly poorer prognosis than those with S100A4-negative carcinoma, which was also true in the cases with deep invasion of the primary cancer (T3, T4) (p<0.01 and p<0.05, respectively). Moreover, S100A4 tissue status remained the only independent prognostic parameter in the multivariate analysis. Our results suggest that S100A4 may play a key role in the progression of esophageal carcinoma and that immunohistochemical detection of S100A4 in the primary tumor may be useful for the prediction of a poor prognosis.

Adult↗
PubMed2001

Significance of integrin alpha2/beta1 in peritoneal dissemination of a human gastric cancer xenograft model.

In the present study, the role of integrin alpha2/beta1 in peritoneal dissemination of gastric cancer was investigated using an in vivo xenograft model for the highly metastatic MKN-45-P gastric cancer cells. Metastatic ability of MKN-45-P cells was significantly associated with the simultaneous expression of integrin alpha2 and alpha3 subunits. In an in vitro adhesion assay, neutralizing antibody for integrin alpha2 or beta1 subunit inhibited the adhesion of MKN-45-P cells to collagen type I and type IV. Moreover, the injection of anti-beta1 monoclonal antibody reduced the number of cancer cells on the peritoneum in nude mice that had been inoculated with MKN-45-P cells. These results suggest that integrin alpha2/beta1 represents a candidate target molecule available for the prevention of gastric cancer peritoneal dissemination.

Adenocarcinoma↗