Biomedical subjects

Yuichi Sugisaki

Publications and source records attributed to Yuichi Sugisaki.

At least 37 records · Page 2Linked to original sources

PubMed2003

Identification of an electron densification of the glomerular basement membrane in renal biopsy specimens.

Ultrastructural examination of renal biopsy specimens is often necessary to establish a diagnosis. We have noted, in some renal biopsies, that normal-appearing glomerular basement membrane (GBM) shows an electron densification. The aim of this study was to describe this phenomenon and assess the degree of its occurrence. We reviewed ultrastructural pathology records of 153 renal biopsy patients with special reference to the careful examination of the electron micrographs. Of these, 28 cases (18%) showed a definite and homogeneous electron densification of normal-appearing GBM in the glomeruli. The pathological diagnosis in these cases was IgA nephropathy in 15, minimal change nephrotic syndrome in 6, interstitial nephritis in 3, membranoproliferative glomerulonephritis in 2, and nephritis of Henoch-Schonlein purpura and membranous nephropathy in 1 case each. In addition, frequent deposition of IgG without C3 in the GBM (86%) and glomerular endothelial cell edema (96%) were observed. No apparent correlation could be ascertained between the presence of the electron densification and pathological diagnosis. It is suggested that electron densification of the GBM may be caused by the penetration of some electron-dense materials into the GBM as a result of an abnormality in the glomerular filtration barrier and that this could be considered as a sign of altered properties of the lamina densa.

Adolescent↗

PubMed2003

Central neurocytoma expressing characteristics of ependymal differentiation: electron microscopic findings of two cases.

We describe two cases of central neurocytoma in the lateral ventricle. Ultrastructural examination showed occasional cilia mixed in with sparse dense core vesicles and thin tumor cell processes containing parallel microtubules. These central neurocytomas revealed evidence of ependymal differentiation. We propose that central neurocytoma originates from multiple differentiation from the germinal matrix cell layer.

Adult↗

PubMed2003

Different influences of hyperglycemic duration on phosphorylated extracellular signal-regulated kinase 1/2 in rat heart.

Extracellular signal-regulated kinase (ERK) 1/2 is an important intracellular proteinase associated with myocardial protection against heart injury. Hyperglycemia was also reported to be highly involved in heart injury by the formation of advanced glycation end products (AGEs) in myocardial protein, resulting in its altered structure and function. However, the effect of this glycation on mitogen-activated protein kinases, particularly ERK1/2, in the myocardium is largely unclarified. In this study, we investigated whether the glycation of an intracellular protein, ERK1/2, would result in ERK1/2-AGEs formation that adversely affects ERK1/2 activation in the rat heart under hyperglycemia. Hyperglycemia was induced by injection of streptozotocin (STZ) and hearts were examined 4 and 20 weeks after STZ treatment. By immunohistochemical staining and Western blotting, it was determined that the level of phosphorylated ERK1/2 in the rat heart under hyperglycemia 20 weeks after STZ treatment decreased markedly by about 50% of that of the time-matched control group, whereas in the case of 4 weeks after STZ treatment, it increased by about 2.7-fold that of the time-matched group. The level of deposition of AGEs in proteins of the myocardium increased significantly depending on the duration of hyperglycemia. Twenty weeks after STZ treatment, two clear bands corresponding to 44- and 42-kDa AGEs were detected by Western blotting: these corresponded to protein sizes of ERK1/2. The immunoprecipitation method further confirmed the formation and the increased intensity of ERK1/2-AGEs in the rat heart under hyperglycemia for 20 weeks. These results demonstrate that long-term hyperglycemia may inhibit ERK1/2 phosphorylation in the myocardium, whereas a short-term (4 weeks) hyperglycemia enhances its phosphorylation. The ERK1/2 phosphorylation under long-term hyperglycemia is very different from that under short-term hyperglycemia. In addition, this inhibition of ERK1/2 activation appears to be dependent on the formation of ERK1/2-AGEs under long-term hyperglycemia, which may be related in part to the etiology of diabetic cardiomyopathy. It also suggests that the formation of AGEs in intracellular enzymes and proteins under hyperglycemia could play important roles in the development of diabetes complications.

Animals↗

PubMed2003

Transient and ectopic expression of lumican by acinar cells in L-arginine-induced acute pancreatitis.

Lumican is a member of a small leucine-rich proteoglycan family. We previously found that lumican mRNA and its protein were ectopically and highly expressed in acinar cells in chronic pancreatitis (CP)-like lesions close to pancreatic cancer cells. CP-like lesions are characterized by acinar and ductal-ductular cell proliferation with expanding fibrosis. This finding suggests that lumican is ectopically synthesized by acinar cells under chronic inflammatory conditions and plays a role in fibrosis of the pancreas. However, the expression and role of lumican in acute inflammatory changes of the pancreas are not completely elucidated. In the present study, we aim to clarify whether lumican mRNA and its protein are expressed in exocrine or endocrine components in acute pancreatitis (AP). For experimental AP, Wistar rats received an intraperitoneal injection of L-arginine. Western blot analysis showed an intense 50-kDa band corresponding to the lumican protein in normal and L-arginine-treated rat pancreas. After L-arginine injection, three intense bands at 42, 57, and 92 kDa were detected on day 1. Immunohistochemically, the lumican protein was localized in ductal and a few centroacinar cells in the normal pancreas. After L-arginine injection, an immature fibrosis with fragmented and loose collagen fibers was observed in AP on day 4 and lumican immunoreactivity was detected in the collagen fibers. Lumican mRNA was faintly detected in islet cells in the normal pancreas, but it was strongly expressed in acinar and islet cells on day 1. Furthermore, lumican mRNA was expressed in many proliferating fibroblasts on day 4 by in situ hybridization. These findings indicate that lumican is transiently synthesized by acinar cells and fibroblasts in AP. Lumican proteins synthesized by acinar cells, islet cells, and fibroblasts may contribute to immature and transient fibrosis of AP.

Acute Disease↗

PubMed2003

Tumorous deformity of mitral valve leaflet after chordal rupture in a child.

A case with tumorous deformity of the posterior mitral valve leaflet after spontaneous chordal rupture in a child is described. A partial rupture in the chordae tendineae of the posterior mitral leaflet was found by echocardiography in a 9-year-old Japanese boy. Tumorous bulging was gradually developed in the leaflet and was surgically excised 5 years later. Multiple nodular tumors were found on the atrial surface of the posterior mitral leaflet. Histological examination revealed that the tumorous bulging consisted of myxomatous materials in which collagen fibrils and very fine elastic fibers were distributed loosely and irregularly. Normal-looking endothelial cells covered the luminal surface of the bulging lesion. Vimentin-positive spindle-shaped mesenchymal cells were scattered in the bulge area. The labeling index of proliferating cell nuclear antigen (PCNA) in these cells was 29.3%. These spindle cells were positive for matrix metalloproteinase (MMP)-1 in the entire bulge area. The cells and matrix were positive for MMP-2 and tissue inhibitor of MMP (TIMP)-1 in the basal area of bulging, but were weakly positive or negative at the surface area. Reactivity for TIMP-2 in the cells in the bulge area was obviously weaker than that in the cells at the spongiosa of the anterior mitral leaflet, which was obtained from the patient at the valve replacement operation 9 months after the initial operation. These findings indicated that the tumorous deformity of the mitral valve was formed by the overgrowth of valve tissue under the stimulation of mitral regurgitation in this child, and the imbalance of MMP and TIMP might play an important role in the bulge formation.

Biomarkers, Tumor↗

PubMed2003

Expression of keratinocyte growth factor receptor (KGFR/FGFR2 IIIb) in vascular smooth muscle cells.

Keratinocyte growth factor receptor (KGFR), also known as fibroblast growth factor receptor (FGFR)2 IIIb, is located in many types of epithelial cells and is activated by four known ligands (FGF-1, FGF-3, FGF-7 (also known as KGF) and FGF-10) that are predominantly synthesized by mesenchymal cells. In the early stage of atherosclerosis, vascular smooth muscle cells (VSMC) transform from a contractile to a synthetic phenotype, proliferate and migrate into the intima. Previously, FGF-7 mRNA expression was reported in VSMC, but KGFR mRNA was not detected. In the present study, we attempted to determine whether KGFR is localized in VSMC cultured from rat aorta and VSMC in human normal and atherosclerotic coronary arteries. Expression of KGFR mRNA and its protein was detected in cultured rat VSMC by reverse transcription-polymerase chain reaction and western blot analysis, respectively. Immunohistochemically, KGFR was localized in the VSMC of the outer layer of the media in normal human coronary arteries. Furthermore, it was localized in the VSMC of the media and thickened intima of atherosclerotic arteries. Recombinant FGF-7 and/or FGF-10 proteins stimulated the growth of cultured rat VSMC. These findings indicate that KGFR localized in VSMC may contribute to the proliferation of VSMC in normal and atherosclerotic arteries.

Aged↗

PubMed2003

Basic FGF and Ki-67 proteins useful for immunohistological diagnostic evaluations in malignant solitary fibrous tumor.

Solitary fibrous tumor (SFT) is an uncommon soft tissue tumor initially reported in the pleura but recently described in other sites in the body. Morphological distinction between benign and malignant SFT is often difficult. An immunohistochemical study was performed in pleural and extrapleural sites. The aim of this study was to determine if an immunohistochemical method is helpful in distinguishing benign SFT from malignant SFT, and providing valid information to predict the prognosis associated with malignant SFT. Twenty-four cases of benign (14 patients) and malignant (10 patients) SFT in the pleura, pelvic space, prostate and other sites of soft tissue were analyzed. Tumors from 10 patients were diagnosed as malignant on the basis of markedly increased cellularity, mitotic activity (>4/10 high-power fields), nuclear pleomorphism and areas of necrosis. Immunohistochemically, we found a mean basic fibroblast growth factor (bFGF) labeling index of 48.67% (48.67 +/- 8.52%) for benign SFT and 74.5% (74.5 +/- 6.92%) for malignant SFT (P < 0.05). We also found a mean Ki-67 labeling index of 1.9% (1.9 +/- 0.43%) for benign SFT and 6.11% (6.11 +/- 1.05%) for malignant SFT (P < 0.05). Our results suggest that bFGF and Ki-67 are diagnostically relevant to the evaluation of malignant SFT and these proteins are thought to be potentially useful markers for prognosis of SFT.

Adult↗

PubMed2003

Anti-invasive effect of an anti-matrix metalloproteinase agent in a murine brain slice model using the serial monitoring of green fluorescent protein-labeled glioma cells.

OBJECTIVE: We aimed to analyze the anti-invasive effect of the anti-matrix metalloproteinase (anti-MMP) agent SI-27 by quantitative tracking of enhanced green fluorescent protein (EGFP)-labeled human malignant glioma cell lines in a brain slice model. METHODS: Persistent expression of EGFP in human malignant glioma cell clones (U87MG, U251MG, and U373MG) was established with the use of the pEGFP-C1 vector. Tumor spheroid in 1 microl Matrigel was implanted into the caudate nucleus-putamen of a severe combined immunodeficient mouse brain slice. To allow the quantitative assessment of tumor cell invasion, the invasion area index was measured on Days 1, 3, 5, and 7 with a fluorescence stereomicroscope and an image analyzer in the presence of various concentrations of SI-27 (0, 1, 10, 50, or 100 microg/ml). RESULTS: In the control group (0 microg/ml), all glioma cell lines invaded in a fingerlike fashion and reached the contralateral hemisphere through the corpus callosum. SI-27 at concentrations of 10, 50, and 100 microg/ml significantly suppressed the invasion area index on Days 5 and 7 in a dose-dependent manner, whereas 1 microg/ml had no effect. Transmission electron microscopy and laser confocal microscopy indicated that the tumor cells had penetrated the brain slice and that the normal structural integrity of the brain was maintained until Day 7. CONCLUSION: This model enabled unequivocal periodic tracking of individual invading tumor cells in normal brain. The significant suppression of glioma cell invasion by noncytotoxic concentrations of SI-27 indicates that anti-MMP treatment may represent an important future therapeutic strategy for malignant cerebral neoplasms.

Animals↗

PubMed2003

Expression of p73 and c-Abl proteins in human ovarian carcinomas.

The p73, a homologue of the p53 tumor suppressor protein, has a pro-apoptotic activity which is induced by the c-Abl, a protein tyrosine kinase appearing in the nucleus and cytoplasm of proliferating cells. However, the role of p73 and c-Abl in ovarian cancer is not well-defined. We investigated immunohistochemical expressions of p73 and c-Abl in 64 ovarian carcinomas, 13 borderline and 14 benign ovarian tumors to elucidate their clinicopathological relevances. Of the malignant, borderline, and benign ovarian tumors, respectively, 33 (51%), 10 (77%) and 13 (93%) had negative or low p73 expression, 31 (48%), 3 (23%) and 1 (7%) had high p73 expression, 23 (36%), 5 (38%) and 10 (71%) had negative or low c-Abl expression, and 41 (64%), 8 (61%) and 4 (29%) had high c-Abl expression. A high p73 or c-Abl expression was significantly associated with ovarian carcinomas as compared to benign tumors (p=0.003 and p=0.03 respectively). In addition, a significant correlation was found between the high p73 expression and disease stage (p=0.04) and patient's survival (p=0.02). No correlation was found with c-Abl expression. These results reveal an association of p73 overexpression with advanced ovarian carcinomas which may suggest the p73 overexpression as an indicator of poor prognosis.

Biomarkers, Tumor↗

PubMed2003

Prognostic suggestion in the evaluation of solid component in poorly differentiated adenocarcinoma of the lung.

UNLABELLED: Pulmonary adenocarcinoma composed of pure or predominant solid components is reported to be a highly malignant tumor. However, the existence of solid components and its connection with biological behavior have not been well documented. To answer this question, we histologically subclassified poorly differentiated adenocarcinoma (P/D Ad Ca) into solid type and non-solid type, and compared the biological behavioral characteristics. MATERIAL AND METHODS: All histological specimens of surgically resected primary lung carcinoma diagnosed as P/D Ca or large cell carcinoma in Nippon Medical School Hospital were re-evaluated according to the 1999 WHO manual. The cases re-evaluated as P/D Ad Ca were further divided into solid type and non-solid type according to our original definition: the solid type contains solid components where a glandular structure is not recognized in more than one high-power field, while in the non-solid type, a small glandular structure is observed in every high-power field. The differences in the occurrence of lymph node metastasis were assessed by Fisher's exact test. RESULTS: Among 109 cases satisfying both histological and clinical investigation, 45 cases were re-evaluated as P/D Ad Ca; solid type (n=22), and non-solid type (n=23). Lymph node metastases occurred at a higher rate in the solid type than in the non-solid type (p<0.01). CONCLUSION: Patients with solid type Ad Ca have reached a more advanced stage than patients having non-solid type due to high metastatic rate to lymph nodes. These results suggest that we should not overlook solid components even if the solid components are the focal lesion. This sub-typing alerts clinicians to survey metastases, and may contribute to therapeutic strategies in the future.

Adenocarcinoma↗

PubMed2003

[Comparative study on the sclerotic changes of cardiac valve and blood vessel].

BACKGROUND: Recently, there is an increase in number of surgical treatments for the aortic stenosis caused by valvular sclerosis with aging. Whether valvular sclerosis are related to aortic atherosclerosis, the prevention therapy of arteriosclerosis may benefit the clinical treatment of the valvular dysfunction due to aging. MATERIALS AND METHODS: Gross, histological and immunohistochemical studies were made on 159 autopsy cases (97 men, 62 women, mean age 65.1 years old). The degree of sclerotic change in aortic valve (AV), mitral valve (MV), aorta (Ao) and coronary artery (CA) was classified by gross examination to none, mild, moderate, and severe, scored as 0 to 3, respectively. The data were statistically analyzed by the correlation test. To observe the expression of bone related proteins in valve calcification, indirect immunostaining procedures were applied with antibodies to osteocalcin, osteopontin and osteonectin. RESULTS: Grossly, there was a significant correlation in sclerotic change between Ao and AV, Ao and MV, AV and MV, CA and AV, and CA and MV, respectively (p<0.01). Also, the degree of sclerotic change in each tissue was correlated with patients'age. However, the grade of sclerotic change of each tissue was variant in each case. On gross observation, all valvular sclerosis showed yellowish thickening and/or calcification. Microscopically, hyalinous change of the fibrosa was observed in the yellowish lesion of the valves. Accumulations of foamy macrophages were found focally at the surface area of the fibrosa, but no atheromatous change was observed in the valves. Calcified deposits, if present, were found in the fibrous valvular ring or fibrosa with hyalinous degeneration. In MV, calcification was usually localized in the fibrous ring. However, in AV, valvular calcification extended diffusely in the fibrosa and caused stenosis in some cases. These lesions were similar to calcified area in the intima with fibrous thickening of Ao and/or CA, but were different from atheromatous lesion of these tissues. Immunohistochemically, calcified areas of valves showed stronger reaction for osteocalcin than that of vessels. CONCLUSION: Among sclerotic change of cardiac valves and arteriosclerosis, statistical correlations were found, but pathological features were different. Main causes of these differences are thought to be 1) not only the shear stress, but also intramural pressure and mechanical stress with opening and closing may interfere the sclerotic change of cardiac valves, and 2) mechanism of valvular sclerosis may be different from arteriosclerosis because medial smooth muscle cells are absent in the valves.

Adolescent↗

PubMed2003

[Long-term remnants of coagulation necrosis of cardiomyocytes following myocardial infarction].

Remnants of cardiomyocytes showing coagulation necrosis in the scars caused by myocardial infarction were histopathologically studied. Among 305 autopsy cases of acute and/or healed myocardial infarction, 8 cases (7 men, 1 woman, ages 62 - 87 years, mean age 72.1) had masses of cardiomyocytes with coagulation necrosis at the center of the infarction scars more than 3 weeks (21 to 79 days) after the attack of myocardial infarction. All these cases had transmural infarction and more than 80% of the wall thickness of the left ventricle was involved in the infarction. No polymorphonuclear leukocytic infiltration or granulation tissue was found in the necrotic area, but macrophages were observed in the peripheral area adjacent to the scar tissue. Immunohistochemical staining for myoglobin showed no reaction in remnant necrotic cells or pericellular interstitium, which was similar to findings in the necrotic area more than 4 days after the infarction. These findings are important in the pathological diagnosis to distinguish remnant necrosis from acute necrosis, because 4 out of 8 present cases (50%) were misdiagnosed as acute myocardial infarction that superimposed on the previous old infarction.

Aged↗

PubMed2003

Identification of MG-160, a FGF binding medial Golgi sialoglycoprotein, in brain tumors: an index of malignancy in astrocytomas.

Malignant astrocytomas are highly invasive, vascular neoplasms that comprise the majority of nervous system tumors in humans. A strong association has previously been made between malignancy in human astrocytic tumors and increased expression of certain fibroblast growth factor (FGF) family members. MG-160 is an intrinsic type I cysteine-rich membrane sialoglycoprotein that resides in the medial cisternae of the Golgi apparatus, highly homologous to CFR, chicken fibroblast growth factor receptor, and ESL-1, E-selectin ligand. MG-160 binds fibroblast growth factors (FGFs) and may be involved in the intracellular trafficking of FGFs and the regulation of cellular response to FGFs. In the present study MG-160 expression was evaluated in human brain tumors exhibiting varying degrees of malignancy. At the mRNA level MG-160 expression was inversely correlated with the histological grade of astrocytomas such that high levels of MG-160 were observed in low-grade astrocytomas and low levels in malignant astrocytomas. This differential expression of MG-160 mRNA was verified at the protein level using immunohistochemistry. Grade II astrocytomas displayed consistent and intense staining for MG-160 as seen in normal brain. In contrast to the lower grade tumors, grade IV astrocytomas exhibited variable and weaker expression of MG-160. Our results suggest that, MG-160 may participate in malignant progression in astrocytomas. In addition, other brain tumors and human astrocytoma cell lines were characterized for MG-160 expression.

Astrocytoma↗

PubMed2002

Expression of lumican in thickened intima and smooth muscle cells in human coronary atherosclerosis.

Lumican is a member of a small leucine-rich proteoglycan family. Members of this family play an important role in cell migration and proliferation during embryonic development, tissue repair, and tumor growth. Lumican is reported to be overexpressed during the wound-healing process in the cornea and ischemic and reperfused heart. Recently, we found that lumican mRNA and its protein are expressed in cultured vascular smooth muscle cells (VSMCs) from the rat aorta. However, the expression and role of lumican in human atherosclerotic tissues are not clearly elucidated. In the present study, we aimed to clarify whether lumican is expressed in VSMCs and its localization in human coronary atherosclerotic tissues. The lumican protein and its mRNA were expressed in a small number of VSMCs in the media of normal coronary artery, but the lumican protein was not localized in the medial stroma. In contrast, the lumican protein and its mRNA were expressed in most of VSMCs that migrated into the thickened intima, but not in infiltrating foamy macrophages. The lumican protein was prominently localized in the thickened intimal stroma. The lumican protein and its mRNA were also expressed in VSMCs in the inner layer of the media and its protein was localized in medial stromal tissues. These findings indicate that the lumican protein is mainly synthesized by intimal and medial VSMCs in coronary atherosclerosis and that lumican contributes to collagen fibrillogenesis of coronary atherosclerosis.

Adult↗

PubMed2002

Differential distribution of fibroblast growth factor (FGF)-7 and FGF-10 in L-arginine-induced acute pancreatitis.

The regenerative process of the pancreas after acute pancreatitis (AP) is characterized by acinar and ductal cell proliferation with synthesis and transient deposition of extracellular matrices. Various growth factors were reported to be highly expressed in AP, but their regulation has not yet been clarified. Fibroblast growth factor (FGF)-7, also known as keratinocyte growth factor (KGF), and FGF-10 are members of the FGF family and show high structural homology and similar biological characteristics. Both are mainly synthesized by mesenchymal cells and stimulate epithelial cells via KGF receptor (KGFR) which is a splice variant of FGFR-2. In the present study, we attempted to immunohistochemically determine the localization of FGF-7 and FGF-10 in pancreatic tissues of an L-arginine-induced rat pancreatitis model. Furthermore, highly specific KGFR antibodies were prepared and used for Western blot analysis and immunohistochemistry. In the normal pancreas, FGF-7 was localized in alpha cells of islets, but FGF-10 was not detected. KGFR was also localized in islet cells, ductal cells, and centroacinar cells in the normal pancreas. In the pancreatic tissues of rats with L-arginine-induced pancreatitis, FGF-7 was localized in alpha cells, whereas FGF-10 was expressed in vascular smooth muscle cells (VSMCs). KGFR was not expressed in centroacinar cells and its level decreased after L-arginine treatment. However, KGFR was detected instead in some acinar cells and VSMCs in addition to islet cells. These findings suggest that FGF-7 and FGF-10 contribute to the regeneration and differentiation of acinar cells and angiogenesis in AP through KGFR.

Acute Disease↗

PubMed2002

Tracking cell invasion of human glioma cells and suppression by anti-matrix metalloproteinase agent in rodent brain-slice model.

Persistent expression of green fluorescent protein (GFP) in human malignant glioma cell clones (U87MG, U251MG, and U373MG) was established using the pEGFP-Cl vector. Tumor spheroid was implanted into the caudate nucleus-putamen of a severely compromised immunodeficient (SCID) mouse brain slice. To allow quantitative assessment of tumor cell invasion, the invasion area index was measured on days 1, 3, 5, and 7 by a fluorescence stereomicroscope and an image analyzer in the presence of varying concentrations of SI-27. In the control group (0 microg/ml), all glioma cell lines invaded in a fingerlike fashion, reaching the contralateral hemisphere via the corpus callosum. SI-27 at concentrations of 10, 50, or 100 microg/ml significantly suppressed the index on days 5 and 7 in a dose-dependent manner, whereas 1 microg/ml had no effect. Laser confocal microscopy indicated that the tumor cells penetrated through the brain slice. This model enabled unequivocal periodic tracking of individual invading tumor cells in the normal brain. The significant suppression of glioma cell invasion by SI-27 indicates that anti-matrix metalloproteinase (MMP) treatment may represent an important future therapeutic strategy for malignant cerebral neoplasms.

Animals↗

PubMed2002

Expression of lumican in human colorectal cancer cells.

Lumican is a member of a small leucine-rich proteoglycan family and its overexpression in human breast cancer tissues is reported to influence the growth of cancer cells. In the present study, we aimed to clarify the expression of lumican mRNA and its protein in human colorectal cancer cell lines and their localization in normal and cancerous colorectal tissues. Reverse transcription-polymerase chain reaction and western blot analysis revealed lumican mRNA and its protein expression in COLO 205, DLD-1, HCT-15, SW 480 and WiDr colorectal cancer cell lines. The lumican in colorectal cancer cells had non-sulfated or poorly sulfated polylactosamine side chains. Based on its immunoreactivity, the lumican protein was found to be localized in fibroblasts and stromal tissues of normal colorectal tissues, but not in colorectal epithelial cells. In colorectal cancer tissues, the lumican was strongly localized in cancer cells in eight of 12 cancer cases. The lumican protein was also localized in epithelial cells with mild reactive dysplasia and fibroblasts adjacent to cancer cells. Lumican mRNA was expressed in cancer cells and adjacent fibroblasts, and epithelial cells. These findings may indicate that the lumican protein synthesized by cancer cells, fibroblasts and epithelial cells with mild reactive dysplasia found adjacent to cancer cells may affect the growth of human colorectal cancer cells.

Blotting, Western↗

PubMed2002

Immunohistochemical localization of endothelial cell markers in solitary fibrous tumor.

Solitary fibrous tumor (SFT) is an uncommon tumor first reported in the pleura, but recently described in other tissues. CD34, which is expressed in hematopoietic stem cells, endothelial progenitor cells and vascular endothelial cells, is observed in most SFT and some investigators believe that its expression is a definitive marker of this tumor. In the present study, the expression of vascular endothelial cell markers, such as vascular endothelial growth factor receptor (VEGFR)-1 (flt-1), VEGFR-2 (flk-1/KDR), Tie-2 and c-Met, was examined in SFT to clarify the relationship between SFT and endothelial cells. By immunohistochemical staining of tumor cells from 26 patients, VEGFR-1 was detected in 24 (92%), VEGFR-2 in five (19%), Tie-2 in 14 (54%), and c-Met, a specific receptor of hepatocyte growth factor (HGF) in 23 patients (88%). Furthermore, VEGFR-3 (flt-4) immunoreactivity was detected in eight of 26 patients (31%). In contrast, VEGF, VEGF-C and HGF, which are ligands for the receptors, were not localized in the SFT cells. These findings indicate that most SFT may closely relate to vascular or lymphatic endothelial cells and the endothelial growth factors may contribute to the growth of SFT in a paracrine manner.

Adult↗