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Biomedical subjects

O Tokunaga

Publications and source records attributed to O Tokunaga.

At least 37 records · Page 2Linked to original sources
PubMed1999

Formation of multinucleated variant endothelial cells in vitro and investigation of MVECs' features.

Multinucleated variant endothelial cells (MVECs) have frequently been observed in the human aorta, and the ratio of MVECs to typical endothelial cells correlates well with the severity of atherosclerosis. MVECs showed no capacity of proliferation in vitro, making their study extremely difficult. We attempted to obtain reproducible MVECs in vitro in order to understand their functional characteristics and their roles in atherosclerosis. This study was designed to derive MVECs from human umbilical cord vein endothelial cells (HUVECs) with different reagents such as Meso-4,4'-(2,3-butanediyl) bis (2,6-piperazinedione) (ICRF-193), low density lipoprotein (LDL), interleukin-4 (IL-4), polyethylene glycol (PG), H2O2, and linoleic acid hydroperoxide (LAHO). We found that 10 microM ICRF-193 was most effective in inducing MVECs. We then investigated the features of aortic endothelial cells (AECs) and ICRF-193 treated HUVECs (I-HUVECs) in the following four aspects: morphology, by light microscopy; cell cycle phase, by uptake of BrdU; expression of endothelial cell (EC) related markers such as von Willebrand Factor (vWF), endothelin-1 (ET-1), prostacyclin (PGI2) and intercellular adhesion molecule CD34 by immunocytochemistry; and biological activity by analyzing their uptake of low density lipoprotein (LDL). Furthermore, we compared aortic MVECs (AMVECs) and other aortic endothelial cells (A-others), as well as A-MVECs and ICRF-193 induced MVECs (I-MVECs) in every parameter examined. We found: 1. Compared with A-others, A-MVECs expressed more vWF (p < 0.01), more ET-1 (p < 0.05) and less CD34 (p < 0.01). In the uptake of LDL, A-MVECs took up more nLDL than A-others; 2. Both A-MVECs and I-MVECs contained multiple nuclei, but the nuclei differed in shape. A-MVECs and I-MVECs were similar in the nuclear incorporation of BrdU, in the uptake of nLDL and oxLDL, and in the expression of vWF, ET-1 and PGI2, but different in the expression of CD34 (p < 0.01). Our findings suggested that A-MVECs may transfer more plasma LDL to the subendothelial space because they took up more LDLs. I-MVECs were similar to A-MVECs morphologically and functionally. Thus, I-MVECs could be considered as substitutes in the study of A-MVECs.

Arteriosclerosis↗
PubMed1999

Loss of retinoblastoma protein expression in laryngeal squamous cell carcinoma.

Laryngeal carcinomas are among the most curable malignancies, but some of them show poor clinical outcomes with local recurrence or regional neck metastasis. Multiple genetic alterations of oncogenes and tumor suppressor genes are thought to occur in the development some tumors. The frequency, however, and the prognostic significance of these genes or gene products still remain unknown in laryngeal carcinoma. Epidemiologic data suggest that cigarette smoking is closely related to the development of these neoplasms; and human papillomavirus (HPV) infections have also been postulated to play a role in development of laryngeal tumor. The objective of this study was to investigate the presence of retinoblastoma protein (pRb), p53 protein, and HPV infection in laryngeal squamous cell carcinoma, as well as the correlation of these factors with clinicopathologic and carcinogenic factors. Tumors from 79 patients with primary laryngeal squamous cell carcinoma were studied. The expression of pRb was immunohistochemically assessed in 79 such tumors, and the expression of p53 was assessed in 76 tumors. HPV Type 16 expression was estimated by nonisotopic in situ hybridization in 78 cases. Follow-up periods ranged from 15 to 90 months. pRb was detected in 82% of the tumors and p53 in 43%. Lack of staining for pRb was significantly associated with a high-histologic grade (P<.05), high T classification (P<.05), recurrence (P<.05), and a relatively short disease-free interval (P<.01). p53 overexpression was observed frequently in heavy smokers with an average Brinkman index of more than 800, but it was not associated with any of the clinicopathologic factors studied. These findings suggest that tumors exhibiting loss of pRb expression have a more aggressive biologic behavior than do those that express pRb and that loss of pRb expression might predict clinical outcome in patients with primary laryngeal squamous cell carcinoma.

Aged↗
PubMed1998

Activation mechanism of anticoagulant protein C in large blood vessels involving the endothelial cell protein C receptor.

Protein C is an important regulatory mechanism of blood coagulation. Protein C functions as an anticoagulant when converted to the active serine protease form on the endothelial cell surface. Thrombomodulin (TM), an endothelial cell surface receptor specific for thrombin, has been identified as an essential component for protein C activation. Although protein C can be activated directly by the thrombin-TM complex, the conversion is known as a relatively low-affinity reaction. Therefore, protein C activation has been believed to occur only in microcirculation. On the other hand, we have identified and cloned a novel endothelial cell surface receptor (EPCR) that is capable of high-affinity binding of protein C and activated protein C. In this study, we demonstrate the constitutive, endothelial cell-specific expression of EPCR in vivo. Abundant expression was particularly detected in the aorta and large arteries. In vitro cultured, arterial endothelial cells were also found to express abundant EPCR and were capable of promoting significant levels of protein C activation. EPCR was found to greatly accelerate protein C activation by examining functional activity in transfected cell lines expressing EPCR and/or TM. EPCR decreased the dissociation constant and increased the maximum velocity for protein C activation mediated by the thrombin-TM complex. By these mechanisms, EPCR appears to enable significant levels of protein C activation in large vessels. These results suggest that the protein C anticoagulation pathway is important for the regulation of blood coagulation not only in microvessels but also in large vessels.

Antibodies, Monoclonal↗
PubMed1998

Expression of c-Met in laryngeal carcinoma.

Expression of c-Met, a gene for the hepatocyte growth factor/scatter factor (HGF/SF) receptor, is known to be associated with tumour development in several human carcinomas. The expression of c-Met was examined using immunohistochemistry in 82 cases of primary laryngeal carcinoma to evaluate the tissue distribution of c-Met and the clinicopathological significance of c-Met expression. In normal larynx, c-Met expression was observed only in some minor salivary glands. Positive reaction for c-Met in neoplastic epithelium was noted in 45 out of 82 (54.9%) cases. In 44 cases, structures adjacent to the carcinoma (noncancerous squamous epithelium, some stromal fibroblastic cells, and endothelial cells) showed positive reaction for c-Met. c-Met expression in cancerous epithelium was significantly correlated with lymph node status (P<0.04) and proliferating activity expressed by the Ki-67 labelling index (P<0.02). There was no correlation between c-Met expression and age, sex, histological type, T category, distant metastasis or clinical stage. The data suggest that overexpression of c-Met in laryngeal carcinomas represents a growth advantage for cancer cells, which may be conferred by the mitogenic effect of HGF/SF. Simultaneous c-Met expression in noncancerous components of the larynx may represent a paracrine modification of c-Met.

Adult↗
PubMed1998

Autoreactive CD4- CD8- alpha beta T cells to vaccinate adjuvant arthritis.

Studies suggested that experimental autoimmune diseases can effectively be prevented and treated by application of normal autoreactive T cells or autoreactive T cells in an attenuated form. In this study, several autoreactive CD4- CD8- T-cell clones (A2, A6, and A13 cells) were isolated for the first time from the draining lymph nodes of Lewis rats with adjuvant arthritis (AA). Surprisingly, intraperitoneal inoculation with A13 cells, but not A2 or A6 cells protected rats from AA both clinically and histologically. It was demonstrated that A13 cells were CD4- CD8- alpha beta T cells, and showed proliferative responses to irradiated syngeneic spleen cells (antigen-presenting cells; APC). Interestingly, A13 cells proliferated against concanavalin A (Con A) and staphylococcal enterotoxin B (SEB), but did not show any proliferation to Mycobacterium tuberculosis (Mt), or its 65 000 MW heat-shock protein (HSP). Rats protected from AA by inoculation with A13 cells showed a specific anti-idiotypic delayed-type hypersensitivity reaction compared with other autoreactive T cells (A2 or A6 cells). These findings demonstrate that AA can be suppressed by autoreactive CD4- CD8- alpha beta T cells, and these cells may be used as therapeutic agents in experimental autoimmunity.

Adoptive Transfer↗
PubMed1998

Multinucleated variant endothelial cells (MVECs) in human aorta: chromosomal aneuploidy and elevated uptake of LDL.

The vascular endothelial cell is generally small and round and has a single small nucleus. It is called a typical endothelial cell (TEC). In human aortas, however, unusually large endothelial cells are often seen. They have multinuclei in a large cytoplasm and are called multinucleated variant endothelial cells (MVECs). MVECs exist individually or in a group, being surrounded by the majority of typical endothelial cells. The number of MVECs is increased with atherosclerosis grade and age. FISH analysis revealed that endothelial cells derived from young subjects had diploid chromosomes. However, aneuploidy was increased with aging in TECs as well as in MVECs, ranging from one to five or even more than five. Expression of LDL receptor on endothelial cells was generally low but greatly elevated in MVECs. Accordingly the uptake of LDL cholesterol was increased when observed in LDL-gold uptake by electron microscopy, whereas those of TECs remained low. These results indicate that human aortic endothelial cells change their characteristics, including shape and even gene, with aging, and that MVECs appear on the human aorta. MVECs actively participate in the development and advancement of atherosclerosis by transporting LDL to the subendothelial intima.

Adolescent↗
PubMed1998

Multinucleated variant endothelial cells (MVECs) of human aorta: expression of tumor suppressor gene p53 and relationship to atherosclerosis and aging.

Multinucleated variant endothelial cells (MVECs) generally exist in atherosclerotic human aorta and even in nonatherosclerotic aorta. Because the number of nuclei is increased in every MVEC, and because DNA instability was suspected, a series of oncogene expressions was conducted to clarify the nature of nuclear abnormality. The tumor suppressor gene p53 was found to be specifically expressed in the multinuclei of MVECs, while double nuclei were sometimes positive, and mononuclear typical endothelial cells were always negative for p53. Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) revealed extra bands in exons 5 and 7 of the p53 gene, but no additional band in exons 6 and 8. In a BCL family, BCL-2 was coexpressed in one or two nuclei in the perinuclear space of the multinuclei of MVECs, whereas MCL-1, BCL-XS/L, and BAX were all negative, indicating that the BCL-2 coding gene is expressed only in the corresponding one or two nuclei of the multinuclei. Another oncogene, c-MET (hepatocyte growth factor receptor), was universally expressed in either type of endothelial cells, but other oncogenes, k-RAS and c-ERBB2, were not expressed in either type. MVECs were derived from human aorta and therefore non-tumorous somatic cells. No morphologic evidence of apoptosis was found. Although it is unclear that the extra bands came from the MVECs or just from ECs associated with atherosclerosis, combined immunocytological studies and PCR analysis suggest that MVECs express mutant type p53.

Adolescent↗
PubMed1998

Expression of MMP-1, TIMP-1, and type I collagen in laryngeal carcinoma.

Matrix metalloproteinases (MMPs) are thought to play an important role in tumor invasion and metastasis. To our knowledge, however, no previous report examined the histologic localization of matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinase-1 (TIMP-1) and Type I collagen in laryngeal carcinoma from the same samples. In this study, immunohistochemical staining for MMP-1, TIMP-1, and Type I collagen was performed on paraffin-embedded sections from 83 laryngeal squamous cell carcinomas. Twenty of the 83 tumors were examined for MMP-1 and TIMP-1 mRNA using in situ hybridization (ISH). Immunohistochemical and ISH analyses indicated that squamous cancer cells as well as stromal cells such as fibroblasts, macrophages, and mononuclear and endothelial cells expressed MMP-1 and TIMP-1 in the area adjacent to the tumor. The localization of MMP-1 and TIMP-1 protein is similar to that of their respective transcripts. Dense or moderate patterns of Type I collagen were associated with a tendency toward positivity for TIMP-1 and negativity for MMP-1 (P < .002). A sparse pattern of Type I collagen was associated with a tendency toward positivity for MMP-1 and negativity for TIMP-1 (P < .004). The patterns of Type I collagen staining correlated significantly with imbalances in MMP-1 and TIMP-1 expression (P < .001). Matrix degradation and remodeling in squamous cell carcinoma of the larynx might be attributable to an imbalance in the expression of MMP-1 and TIMP-1.

Adult↗
PubMed1997

The relationship between primary splenic malignant lymphoma and chronic liver disease associated with hepatitis C virus infection.

BACKGROUND: An etiologically important role has been suggested for hepatitis C virus (HCV) infection in the development of B-cell non-Hodgkin's lymphoma (NHL). HCV has been recognized as the major cause of non-A, non-B chronic hepatitis throughout the world. Moreover, the occurrence of primary splenic malignant lymphoma (PSML) has been demonstrated in patients with chronic liver disease. METHODS: In this study, the authors describe three patients with PSML. The clinical, histologic, and immunohistochemical features of the lymphomas were studied. Clonal immunoglobulin heavy chain gene rearrangement was investigated by polymerase chain reaction. RESULTS: All three cases of PSML were detected by imaging studies performed in routine follow-up of cases of chronic liver disease associated with HCV infection. Macronodular lesions were found in the three spleens; two of them were of normal weight and another was moderately enlarged. The former two were the smallest PSMLs reported to date. The histology was B-cell NHL in all cases. All 3 patients were alive after splenectomy with an average follow-up of 51.7 months (range, 35-74 months). CONCLUSIONS: HCV infection may play an etiologic role in the development of splenic B-cell lymphoma. The long survival of the patients in this study may have been due to early splenectomy.

Aged↗
PubMed1997

The prognostic significance of p53 and bcl-2 expression in lung adenocarcinoma and its correlation with Ki-67 growth fraction.

BACKGROUND: The p53 and bcl-2 gene deregulations are frequently involved in several types of epithelial malignancy. The aims of this study were to determine the relationships between the Ki-67 labeling index (LI) and the expression of p53 and bcl-2 protein in lung adenocarcinoma and to investigate the clinicopathologic features of the tumors and the prognostic significance of p53 and bcl-2. METHODS: Immunohistochemical staining for p53, bcl-2, and Ki-67 was performed on paraffin embedded sections from 114 lung adenocarcinomas from patients who had been treated with complete and potentially curative surgery. To define a cutoff value for p53 immunopositivity, 37 of 114 tumors were examined for p53 gene mutations using cDNA sequencing. The results were compared with clinical outcomes. RESULTS: Expression of p53 protein was defined as nuclear staining in more than 20% of tumor cells, and the concordance rate between p53 expression and gene mutation was 73%. Expression of p53 (39%) was significantly associated with higher Ki-67 LI (P < 0.001) and with several poor prognostic factors, such as poor histologic grade of differentiation (P < 0.05), lymphatic permeation (P < 0.001), and vascular permeation (P < 0.001). Expression of bcl-2 (38%) was significantly associated with favorable T classification (P < 0.001) and smaller tumor size (<2 cm) (P < 0.05) and tended to be associated with lower Ki-67 LI (P = 0.054). In univariate analysis, p53 expression was significantly correlated with poor prognosis (53% vs. 90% at 5 years, P < 0.001) and bcl-2 expression with favorable prognosis (90% vs. 68% at 5 years, P < 0.05). Proliferative activity was highest when only p53 was expressed; by contrast, proliferative activity was lowest when only bcl-2 was expressed. Among four groups of patients, the group that was positive only for p53 had the shortest survival; this difference was statistically significant. Multivariate analysis showed that T classification (P = 0.002), vascular permeation (P = 0.011), and p53 expression (P = 0.03) were independent prognostic factors. CONCLUSIONS: The results of this study indicated an inverse relationship between the proliferative activity of p53 and bcl-2. Expression of p53 was an independent factor associated with poor prognosis, whereas bcl-2 expression was associated with favorable prognosis.

Adenocarcinoma↗
PubMed1997

Apoptotic index in ovarian carcinoma: correlation with clinicopathologic factors and prognosis.

The apoptotic index (apoptotic cells/1000 tumor cells, AI) was evaluated in 71 ovarian carcinomas, all surgically resected. Apoptosis was examined by modified terminal deoxynucleotidyltransferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) method in histologic sections. High AI (>/=2.8) significantly correlated with high mitotic index (P = 0.05), high histologic grade of the tumor (P = 0. 018), and short overall survival (P = 0.017). An inverse relationship between AI and bcl-2 protein expression was also observed (P = 0.007). In addition, AI was assessed in 5 ovarian epithelial tumors of borderline malignancy, and all were categorized as low AI (<2.8). No significant correlation was found between AI and other clinicopathologic factors, such as age, clinical stage, lymph node metastasis, tumor size, histology of the tumor, and expression of p53 protein. Multivariate survival analysis showed that only clinical stage (P = 0.0395) and mitotic index (P = 0.0387) had independent prognostic value, whereas AI did not. Our results suggest that counting apoptosis can be useful for predicting the patient survival in ovarian carcinoma, although AI is not an independent prognostic factor. It is also suggested that bcl-2 protein is an important regulator of apoptosis in ovarian carcinoma.

Apoptosis↗
PubMed1997

Polypoid adenomyoma of the gallbladder.

We describe a distinctive polypoid lesion of the gallbladder (16 mm in diameter) at the fundus, associated with a granulomatous mass in the liver adjacent to the gallbladder fossa, in a 64-year-old Japanese woman. Preoperatively, the lesion was diagnosed as advanced gallbladder cancer infiltrating the liver, and hepatopancreato-duodenectomy was performed. In the resected specimen, the polyp was round and pedunculate in shape, and, microscopically, it consisted of a mixture of small glandular and surrounding muscular elements, but atypia was not noted. The constituent elements were identical with those of adenomyoma, but the polypoid appearance was unusual. The hepatic lesion proved to be a foreign body granuloma containing multiple barium fragments and giant cells. A deep gastric ulcer, which penetrated into the gallbladder fossa, was also noted, near the granuloma. The histologic features indicate that the polypoid appearance of the tumor was due to a secondary modification of pre-existing adenomyoma by hepatic granuloma. To our knowledge, this is the second reported case of an adenomyomatous lesion of the gallbladder with a polypoid appearance.

Adenomyoma↗
PubMed1997

Endoscopic ultrasonography for demonstrating loss of multiple-layer pattern of the thickened gallbladder wall in the preoperative diagnosis of gallbladder cancer.

The purpose of this study was to elucidate the roles of endoscopic ultrasonography (EUS), conventional US, CT, and MRI in differential diagnosis of gallbladder wall thickening. We scrutinized images for the presence of the multiple-layer patterns of the thickened gallbladder walls during preoperative images (EUS, n = 22; US, n = 23; CT, n = 20; MRI, n = 15) and retrospectively correlated them with surgical results in 25 patients. The pathological diagnoses included 7 gallbladder cancers, 9 cases of chronic cholecystitis, 5 cases of xanthogranulomatous cholecystitis, and 4 cases of adenomyomatosis. Multiple-layer patterns of gallbladder wall were observed in patients with inflammatory and benign diseases by US, EUS, CT, and MRI. This pattern was demonstrated by EUS more efficiently compared with other means of imaging. All subjects with loss of multiple layers were finally diagnosed by use of EUS as having gallbladder cancer at surgery. Loss of multiple-layer patterns of the gallbladder wall demonstrated by EUS was the most specific finding in diagnosing gallbladder cancer.

Adenomyoma↗
PubMed1997

Immunohistochemical and ultrastructural examination of smooth muscle cells in aortocoronary saphenous vein grafts.

In this study, phenotypic modulation and remodulation of smooth muscle cells and associated intermediate filament expression were demonstrated by means of immunohistochemistry and ultrastructure to understand the development of intimal hyperplasia in aortocoronary saphenous vein grafts. In nongrafted saphenous veins, all smooth muscle cells expressed vimentin and desmin and were of a contractile form. In saphenous vein grafts showing stenotic intimal hyperplasia (luminal stenosis < 75%), expression of desmin was notably lower, whereas that of vimentin was higher. The cells were shown to be of a synthetic phenotype, suggesting modulation from the original contractile form. In saphenous vein grafts showing occlusive intimal hyperplasia (luminal stenosis > 76%), desmin expression in smooth muscle cells was increased again, and such cells were of a contractile form, suggesting remodulation from the synthetic phenotype. Some of the smooth muscle cells of the synthetic phenotype were positive for an antibody against proliferation cell nuclear antigen. Smooth muscle cells of the contractile form were negative for this antibody. The study suggests that smooth muscle cells of synthetic phenotype are highly responsible for "growing" intimal hyperplasia of aortocoronary saphenous vein grafts.

Actins↗
PubMed1997

Ultrastructural demonstration of mast cells in varicose veins of lower limbs: presence of mast cell-mediated mechanism.

OBJECTIVE: Mast cells are suggested to play an essential role during development of varices in the lower limbs. EXPERIMENTAL DESIGN: Investigation of the ultrastructure of mast cells in varicose lesions. SETTING: Saga Medical School, Yamamoto Surgical Hospital. PATIENTS: Eighteen varicose veins of 17 patients and 9 normal saphenous veins of 9 patients were examined. Patients who had undergone sclerotherapy for varices were excluded. INTERVENTIONS: Radical stripping surgery was performed on all varicose veins. MEASURES: Ultrastructural observations. RESULTS: In normal saphenous veins, mast cells usually singly embedded in dense collagen bundles as resident cells. They have characteristic crystalline granules of storage type. In varicose veins, mast cells show different features such as an increase of altered granules of discharging type, degranulation and intimate relationship with fibroblasts and lymphocytes. CONCLUSIONS: The observations suggest the presence of mast cell-mediated mechanism by releasing some mediators in the development of varices.

Adult↗
PubMed1996

Spontaneous apoptosis in gallbladder carcinoma. Relationships with clinicopathologic factors, expression of E-cadherin, bcl-2 protooncogene, and p53 oncosuppressor gene.

BACKGROUND: Although valuable information regarding spontaneous apoptosis in various human cancers has recently been obtained, spontaneous apoptosis in carcinoma of the gallbladder has not been studied. METHODS: Apoptotic cells were visualized using the nick end labeling method in 49 cases of gallbladder carcinoma. The relationships between frequency of apoptosis, which was expressed as the maximal apoptotic index (MAI), and clinicopathologic factors, immunoreactivity of E-cadherin (E-CD), bcl-2 protooncogene, and p53 oncosuppressor gene were investigated. RESULTS: MAI was significantly correlated with the maximum dimension of the tumor (P = 0.020) and high T category (P = 0.034). A closer correlation between high MAI and high T category was observed in E-CD positive cases (P = 0.0035), whereas no such correlation was evident in E-CD negative cases (P = 0.536). No relationship was observed between MAI and age, sex, histology, grading, stromal volume, venous or lymphatic permeation, and lymph node status. Overexpression of bcl-2 and p53 was observed in 18.4% (9 of 49) and 34.7% (17 of 49) of the cases, respectively, and there was a positive correlation between bcl-2 and p53 (P = 0.035). No notable relationship was observed between apoptosis and overexpression of bcl-2 or p53. CONCLUSIONS: These results indicate that the frequency of apoptosis may increase with the progression of gallbladder carcinoma, and in this process, cell-to-cell interaction may affect the cancer's capacity to undergo apoptosis. Oncogenic changes of bcl-2 and p53 may play a role in tumorigenesis of gallbladder carcinoma, but such changes were not correlated with spontaneous apoptosis.

Aged↗
PubMed1996

Gastric lesions in 76 patients with adult T-cell leukemia/lymphoma. Endoscopic evaluation.

BACKGROUND: Adult T-cell leukemia/lymphoma (ATLL) is caused by human T-lymphotropic virus type I. Gastric lesions in ATLL have not been described precisely, whereas the clinical features of ATLL have been well documented. The goal of the present study was to review gastric lesions, including gastric involvement, of patients with ATLL who were admitted to our hospital. METHODS: Endoscopic examination of the upper gastrointestinal tract was performed on 76 of 110 patients who were admitted to our hospital between 1981 and 1994. Gastric involvement was diagnosed by histologic examination of biopsy specimens of gastric lesions. Types of gastric lesions, histologic features, and survival periods in patients with ATLL were summarized. RESULTS: Of the 76 patients with ATLL who underwent an endoscopic examination, 23 had gastric involvement (30.3%). Twenty-seven patients had other gastric lesions: 10 with peptic ulcers (13.2%), 8 with gastric erosions (10.5%), 3 with submucosal tumors (3.9%), 2 with hyperplastic polyps (2.6%), 1 with gastric adenoma (1.3%), and 3 with gastric carcinomas (3.9%). The most frequent endoscopic configuration of gastric involvement with ATLL was the diffuse type with ulceration, and the most common histology was large cell type. Among those with the acute type ATLL, the survival period of those patients with gastric involvement was less than that of the patients without gastric involvement. In contrast, the survival period for lymphoma type ATLL did not differ among the groups regardless of gastric involvement. CONCLUSIONS: This study demonstrated that 30.3% of patients with ATLL had gastric involvement and 13.2% had peptic ulcers. Gastric involvement of ATLL was one of the prognostic factors in acute type ATLL, whereas it had no influence on the prognosis of lymphoma type ATLL.

Female↗