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National Cancer Institute®
Ultima Vez Modificado: 1 de octubre del 2002
UI - 11962262
AU - Nakaji S; Fukuda S; Sakamoto J; Sugawara K; Shimoyama T; Umeda T; Baxter
TI - D Relationship between mineral and trace element concentrations in drinking water and gastric cancer mortality in Japan.
SO - Nutr Cancer 2001;40(2):99-102
AD - Department of Hygiene, Hirosaki University School of Medicine, Hirosaki 036-8562, Japan. firstname.lastname@example.org
It is well known that the incidence and mortality from gastric cancer in Japan are the highest in the world. This is thought to be due, in part, to dietary habit, including a high salt intake. There are, however, no epidemiological reports to describe the relationship between ingestion of mineral and trace elements and gastric carcinogenesis. In this study, we determined the concentrations of 14 elements in drinking water from 34 water treatment plants in Aomori Prefecture, Japan, and studied how element concentrations were geographically associated with gastric cancer mortality rate. Gastric cancer mortality was calculated from the data of the Annual Aomori Health Report. Multiple regression analysis (stepwise method of decreasing the number of variables) was performed by using age-adjusted mortality of gastric cancer by gender as objective variables and each element concentration as an explanatory variable. The standardized partial regression coefficient was significant in men for zinc (-0.59, P = 0.004), lead (1.01, P = 0.013), strontium (1.23, P = 0.007), and selenium (-1.62, P = 0.004), whereas it was significant in women for lead (-0.65, P = 0.022), strontium (0.51, P = 0.035), and gold (0.70, P = 0.019). It is suggested that selenium and zinc may aid in the prevention of gastric carcinogenesis. However, the significant relationship of sodium (a component of salt) to gastric carcinogenesis was not observed, although many previous epidemiological studies in Japan have shown this relationship.
UI - 12003993
AU - Nardini E; Rizzi S; Menard S; Balsari A
TI - Molecular phenotype distinguishes two subsets of gastric low-grade mucosa-associated lymphoid tissue lymphomas.
SO - Lab Invest 2002 May;82(5):535-41
AD - Molecular Targeting Unit, Department of Experimental Oncology, National Cancer Institute, University of Milan, Italy.
Isotype switch recombination together with somatic mutation of immunoglobulin variable genes is indicative of B-cell maturation stage. Because aberrant isotype switch events occur in a proportion of gastric mucosa-associated lymphoid tissue (MALT) lymphomas, we tested whether gastric MALT lymphomas with or without aberrant rearrangements in the switch regions differ in B-cell maturation stage. Southern blot analysis of DNA from six gastric MALT lymphoma cases revealed the presence of aberrant isotype switch events in three cases. Somatic common mutations were present in all immunoglobulin variable heavy chain genes of the six cases, and homology with the closest germline ranged from 89.5% to 98.8%. Replacement versus silent mutation ratio analysis of complementarity-determining regions and frameworks indicated the positive selective pressure of an antigen in four cases. In the remaining two cases, protein translated from the third complementarity-determining region suggested the selective pressure of an autoantigen. The three cases with aberrant isotype switch events showed no uncommon mutations, whereas two of three cases without evidence of aberrant isotype switch showed high levels of such mutations. Moreover the three cases with aberrant isotype switch, compared with the three cases without, showed an increased number of common mutations and of N segment additions. These data raise the possibility of two distinct subsets of gastric low-grade MALT lymphomas, one with aberrant isotype switch and no intraclonal diversification, and one with no aberrant isotype switch but with intraclonal diversification. The first subset may originate from a post-germinal center environment and the second from a germinal center. Alternatively, the first subset may derive from the second after maturation or after a transformation event that blocks the mutational process.
UI - 12136247
AU - Kataoka H; Tanaka M; Kanamori M; Yoshii S; Ihara M; Wang YJ; Song JP; Li
TI - ZY; Arai H; Otsuki Y; Kobayashi T; Konno H; Hanai H; Sugimura H Expression profile of EFNB1, EFNB2, two ligands of EPHB2 in human gastric cancer.
SO - J Cancer Res Clin Oncol 2002 Jul;128(7):343-8
AD - First Department of Pathology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
PURPOSE: We have previously reported that EPHB2 is overexpressed in gastric cancer; however, the expression profiles of its ligands, EFNB1 and EFNB2, are unknown. This study was designed to investigate the expression of EPHB2 and its ligands, EFNB1 and EFNB2, in human gastric cancer. METHODS: Semi-quantitative RT-PCR using (32)P was performed on human gastric cancer tissues and corresponding normal tissues (29 gastric cancer patients). RESULTS: EPHB2 was more highly expressed in tumor tissues than in normal tissues in 21 out of 29 (72.4%), in gastric cancer patients ( P = 0.01); EFNB1 and EFNB2 were highly expressed in 21 out of 29 (72.4%) ( P = 0.037) and 14 out of 29 (48.3%) patients, respectively. The overexpression of EPHB2 was frequently detected in both well-differentiated adenocarcinoma and poorly differentiated adenocarcinoma [10/13 (76.9%) and 9/14 (64.3%), respectively]. On the other hand, the overexpression of EFNB1 was more frequently detected in poorly differentiated adenocarcinoma than in well-differentiated adenocarcinoma [12/14 (85.7%) and 7/13 (53.8%), respectively. P =0.027]. Elevated levels of EPHB2 and EFNB1 were detected in substantial subsets of early gastric cancers. Genomic alterations to these three genes in gastric cancer specimens were either not found or rarely found except for several rare variations of EPHB2. CONCLUSIONS: These findings suggest that not only the expression of EPHB2, but the expression of its ligand EFNB1 may have some relation with the oncogenesis of gastric cancer.
UI - 12174360
AU - Liu LX; Liu ZH; Jiang HC; Qu X; Zhang WH; Wu LF; Zhu AL; Wang XQ; Wu M
TI - Profiling of differentially expressed genes in human gastric carcinoma by cDNA expression array.
SO - World J Gastroenterol 2002 Aug;8(4):580-5
AD - Department of Surgery, the First Clinical College, Harbin Medical University, No.23 Youzheng Street, Nangang District, Harbin 150001, Heilongjiang Province, China. email@example.com
AIM: To investigate the expression of cancer related genes in gastric carcinoma (GC) through the use of Atlas Human Cancer Array membranes with 588 well-characterized human genes related to cancer and tumor biology.METHODS: Hybridization of cDNA blotting membrane was performed with (32)P-labeled cDNA probes synthesized from RNA isolated from gastric carcinoma and adjacent noncancerous gastric epithelial tissue. AtlasImage, which is a software specific to array, was used to analyze the result.RESULTS: The differentially expression cell cycle/growth regulator in GC showed a stronger tendency toward cell proliferation with 2.7-fold up-regulation of CK1. The promoter genes of apoptosis were down-regulated, including caspase-8 precursor, caspase-9 and caspase-10. Among the oncogene/tumor suppressor genes, ABL2 was down-regulated. In addition, some genes were up-regulated, including matrix metalloproteinse 2(MMP-2), MMP-16(MT3-MMP), SKY, CD9 and semaphorin V. A number of genes were down-regulated, including neuroendocrine-dlg (NE-dlg), retinoic acid receptor gamma and tumor suppressor DCC colorectal. In general, The expression of the cancer progression genes were up-regulated, while the expression of anti-cancer progression genes were down-regulated.CONCLUSION: Investigation of these genes should help to disclose the molecular mechanism of the onset, progression and prognosis of GC. Several genes are reported herein to be altered in GC for the first time. The quick and high-throughout method of profiling gene expression by cDNA array provides us with an overview of key factors that may involved in GC, and may aid the study of GC carcinogenesis and provide molecular targets for diagnosis and therapy. The precise relationship between the altered genes and gastric carcinogenesis is a matter for further investigation.
UI - 12174361
AU - Yao XX; Yin L; Sun ZC
TI - The expression of hTERT mRNA and cellular immunity in gastric cancer and precancerosis.
SO - World J Gastroenterol 2002 Aug;8(4):586-90
AD - Department of Digestive Medicine, the 2nd Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China. firstname.lastname@example.org
AIM: To observe the expression of Human telomerase reverse transcriptase (hTERT) in gastric carcinomas and precancerosis lesions, to evaluate the immune state of such patients, and to then study the clinical significance of hTERT and immune state for the diagnosis, treatment and prognosis of gastric cancer.METHODS: In situ hybridization was used to detect the expression of hTERT mRNA in 116 endoscopic of gastric mucosa. Analyzed tissue samples were as follows: 30 cases of chronic superficial gastritis (CSG), 44 of precancerosis lesions (including 27 of chronic atrophic gastritis, 8 of adenomatous polyp and 9 of gastric ulcer) and 42 of gastric cancer (GC). In addition, the T lymphocyte subsets (CD3(+), CD4(+), CD8(+), CD4(+)/CD8(+)) and natural killer cells (NK) in peripheral blood were determined by flow cytometric analysis (FCM) in 30 cases of CSG, 27 of precancerosis (chronic atrophic gastritis, CAG), and 42 of GC. The data were compared with those of normal control (NC).RESULTS:The detected positive rate of hTERT varied as follows: 86 % (36/42) in GC, 36 % (16/44) in precancerosis lesions and 0 % (0/30) in CSG. The expression of hTERT mRNA was not associated with patient gender, tumor location, macroscopic type, lymph node metastasis, or degree of differentiation. It was found that the CD3(+), CD4(+) of the CSG group were lower than that of NC (P<0.05). Meanwhile, the T lymphocyte subsets (CD3(+), CD4(+), CD4(+)/CD8(+) ratio) and NK cells of CAG were remarkably lower than that of NC and CSG groups (P<0.05-0.01). Values of T cells and NK cells of the GC group were significantly abnormal when compared with the CAG group (P<0.05-0.01). Furthermore, with tumor progression, the function of T cells was weakened gradually.CONCLUSION: The expression of telomerase may be a crucial step in gastric carcinogenesis and increased hTERT mRNA may serve as a novel marker for diagnosis of GC. The immune state of patients with GC and precancerosis was somewhat depressed, which indicates the importance of cellular immunological assays in cancer patients.
UI - 12174363
AU - Ren J; Dong L; Xu CB; Pan BR
TI - The role of KDR in the interactions between human gastric carcinoma cell and vascular endothelial cell.
SO - World J Gastroenterol 2002 Aug;8(4):596-601
AD - Department of Oncological Radiotherapy,First Hospital,Xi'an Jiaotong University Xi'an 710061,Shaanxi Province, China. email@example.com
AIM:To study the interactions between human gastric carcinoma cell (HGCC) and human vascular endothelial cell (HVEC), and the role of KDR in these interactions. METHODS:Antisense oligodexynucleotide(ASODN) specific to KDR gene was devised and added to the culture medium of HGCC and HVEC. After the action of ASODN, the proliferation of two cells was measured by MTT method. The role of KDR in regulating the proliferation of two kinds of cells was known through observing the effect of ASODN on them. The conditioned mediums (CMs) of HGCC and HVEC were prepared. The CM of one kind of cell was added acting on the other kind of cell, then the cell proliferation was measured by MTT. After the action of ASODN or CM, the cellular expression of KDR gene was detected with in situ hybridization (ISH) for mRNA level and with immunohistochemical staining for protein level. ABC -ELISA was used to detect hVEGF in the CMs of two cells. RESULTS: KDR ASODN could specifically inhibit the proliferation of HGCC and HVEC significantly. The growth inhibitory rate amounted to 55.35 % and 54.83 %, respectively (P<0.01). HGCC and HVEC could secret a certain level of hVEGF(92.06+/-1.69 ng/L, 77.70+/-8.04 ng/L). The CM of HGCC could significantly stimulate the growth(2.70+/-0.01 times) and KDR gene expression of HVEC(P<0.01) while the CM of HVEC could significantly inhibit the growth(52.97+/-0.01 %) and KDR gene expression of HGCC (P<0.01). CONCLUSION: KDR plays a key role in regulating the proliferation of HGCC and HVEC. There exist complicated interactions between HGCC and HVEC. HGCC can significantly stimulate the growth of HVEC while HVEC can significantly inhibit the growth of HGCC. KDR is involved in the interactions between them.
UI - 12174364
AU - Ren J; Dong L; Xu CB; Pan BR
TI - Expression of sphingosine kinase gene in the interactions between human gastric carcinoma cell and vascular endothelial cell.
SO - World J Gastroenterol 2002 Aug;8(4):602-7
AD - Department of Oncological Radiotherapy, First Hospital,Xi'an Jiaotong University Xi'an 710061, Shaanxi Province, China. firstname.lastname@example.org
AIM: To study the interactions between human gastric carcinoma cell (HGCC) and human vascular endothelial cell (HVEC), and if the expression of sphingosine kinase(SPK) gene was involved in these interactions. METHODS: The specific inhibitor to SPK, dimethyl sphingosine (DMS), was added acting on HGCC and HVEC, then the cell proliferation was measured by MTT. The conditioned mediums (CMs) of HGCC and HVEC were prepared. The CM of one kind of cell was added to the other kind of cell, and the cell proliferation was measured by MTT. After the action of CM, the cellular expression of SPK gene in mRNA level was detected with in situ hybridization(ISH). RESULTS: DMS could almost completely inhibit the proliferation of HGCC and HVEC. The growth inhibitory rates could amount to 97.21 %, 83.42 %, respectively (P<0.01). The CM of HGCC could stimulate the growth of HVEC (2.70+/-0.01, P<0.01) while the CM of HVEC could inhibit the growth of HGCC (52.97+/-0.01 %, P<0.01). There was no significant change in the mRNA level of SPK gene in one kind of cell after the action of the CM of the other kind of cell. CONCLUSION: SPK plays a key role in regulating the proliferation of HGCC and HVEC. There exist complicated interactions between HGCC and HVEC. HGCC can significantly stimulate the growth of HVEC while HVEC can significantly inhibit the growth of HGCC. The expression of SPK gene is not involved in the interactions.
UI - 12193861
AU - Calli Demirkan N; Tuncyurek M; Ugur Ertan E; Bulent Alkanat M; Icoz G
TI - [Correlation of histological classifications of gastric carcinomas with location and prognosis]
SO - Gastroenterol Clin Biol 2002 Jun-Jul;26(6-7):610-5
AD - Service d'Anatomie Pathologique, CHU du Pamukkale, Denizli, Turquie. email@example.com
AIM: To evaluate the prognostic impact of different histological classifications of gastric adenocarcinoma. METHODS: Between 1993-2000, 94 patients with gastric adenocarcinoma were studied. Tumors were classified according to TNM staging, WHO, Lauren and Goseki classifications. Twenty five patients (27%) had a proximal tumor and 69 (73%) a distal tumor. Intestinal type according to Lauren were more often observed among the proximal carcinomas (19/25) than in distal ones (32/69) (P=0.01). According to Goseki, lymph node metastasis were less frequently found in group III (5/13) than in other groups (64/81) (P=0.033). The mean follow-up was 23 months. Survical was not influenced by WHO, Lauren, and Goseki classifications. Survival significantly varied according to the different groups of the TNM classification. The proximal location of the tumor was associated with poorer prognosis than distal location (P=0.0373). Number of metastatic lymph nodes, invasion of perineurium, and vascular invasion had significant prognostic value in proximal carcinomas. CONCLUSION: The results of this study suggest that gastric carcinomas should be divided into proximal and distal tumors using the Goseki classification in addition to the Lauren classification because the Goseki classification recognizes tumor groups with different dissemination routes.
UI - 12204060
AU - Yoo J; Park SY; Robinson RA; Kang SJ; Ahn WS; Kang CS
TI - ras Gene mutations and expression of Ras signal transduction mediators in gastric adenocarcinomas.
SO - Arch Pathol Lab Med 2002 Sep;126(9):1096-100
AD - Department of Pathology, St Vincent's Hospital, Catholic University, Suwon, Kyungkido, South Korea.
OBJECTIVE: To investigate ras gene alteration in human gastric adenocarcinomas and its potential relationship to ras signal transduction mediators. DESIGN: Genomic DNA from 104 gastric tumors were analyzed by sequencing of polymerase chain reaction-amplified products for the presence of ras mutations. All the samples were further investigated with the use of immunohistochemical analysis for ERK1 and ERK2. SETTING: Tertiary care teaching hospital. PATIENTS: Seventy patients from a Korean population and 34 from a Midwestern US population composed of white Americans and African Americans. RESULTS: Fifteen tumors (14%) were positive for either H-ras or K-ras mutation: 9 (13%) of 70 Korean patients and 6 (18%) of 34 US patients. Seven (78%) of the 9 mutated tumors from Korean patients and all 6 (100%) from the US patients were intestinal-type lesions. Either ERK1 and/or ERK2 was overexpressed in 68 samples (65%). No association was established between ras mutations and overexpression of ERK1/2. However, the correlation between ERK1/2 and progression (early vs late) was statistically significant (P =.007). CONCLUSIONS: These data suggest that ras mutations are uncommon in gastric adenocarcinomas and that differing racial and/or geographic mechanisms may not underlie ras gene alteration. Most ras mutations were, however, observed in the group of intestinal-type samples, supporting the different genetic mechanisms of carcinogenesis between the intestinal- and diffuse-type tumors. It is noteworthy that enhanced ERK1/2 activity could be one of the characteristics of tumor invasiveness in gastric cancers.
UI - 12210063
AU - Oue N; Motoshita J; Yokozaki H; Hayashi K; Tahara E; Taniyama K;
TI - Matsusaki K; Yasui W Distinct promoter hypermethylation of p16INK4a, CDH1, and RAR-beta in intestinal, diffuse-adherent, and diffuse-scattered type gastric carcinomas.
SO - J Pathol 2002 Sep;198(1):55-9
AD - Department of Molecular Pathology, Hiroshima University Graduate School of Biomedical Sciences, Hiroshima, Japan.
Hypermethylation of CpG islands in gene promoters is associated with silencing of various tumour suppressor genes. Recent studies of colorectal and gastric carcinomas have defined a CpG island methylator phenotype (CIMP), which involves the targeting of multiple genes by promoter hypermethylation. In this study, methylation-specific polymerase chain reaction (PCR) was performed to study methylation of CpG islands in the promoters of the p16(INK4a), cadherin 1 (CDH1), and retinoic acid receptor-beta (RAR-beta) genes in 45 gastric carcinomas and to investigate whether CDH1 and RAR-beta promoter hypermethylation is associated with CIMP-positive gastric carcinoma. CpG island hypermethylation of the p16(INK4a), CDH1, and RAR-beta promoters was detected in 12 (27%), 26 (58%), and 24 (53%) of the 45 gastric carcinomas, respectively. Hypermethylation of the p16(INK4a) promoter was more common in intestinal type than in diffuse type gastric carcinomas (p = 0.0023; Fisher's exact test) and was inversely associated with p53 mutations (p = 0.0225; Fisher's exact test). However, CDH1 and RAR-beta promoter hypermethylation was observed more frequently in diffuse-scattered type gastric carcinoma than in other types (intestinal and diffuse-adherent types) (p = 0.0175 and p = 0.0335, respectively; Fisher's exact test) and was not associated with p53 mutation status. Moreover, hypermethylation of the CDH1 and RAR-beta promoters occurred concordantly (p < 0.0001; Fisher's exact test). These results suggest that at least two types of promoter methylation status are involved in the development of the intestinal (p16(INK4a) promoter hypermethylation) and diffuse-scattered types (CDH1 and RAR-beta promoter hypermethylation) of gastric carcinoma. Copyright 2002 John Wiley & Sons, Ltd.
UI - 1550997
AU - Becker N; Rittgen W
TI - Fitting cancer mortality data with cumulative damage models.
SO - Math Biosci 1992 Feb;108(1):57-73
AD - Department of Epidemiology, German Cancer Research Center, Heidelberg.
Cumulative damage models conceive the epidemiologically observed aspects of carcinogenesis as some kind of total balance over a complex biological process and suggest that this total balance might behave as a wear-and-tear process. The essential concepts of this mechanistic model are exposure to a carcinogenically damaging environment and resistance of a host system against those damages. Intensity of exposure and magnitude of host resistance are the parameters to be assessed. The paper describes (1) the statistical methods for fitting this model to birth cohort data; (2) for which cancer sites the model provides acceptable fits and for which it does not; and (3) how model extensions provide improvements in the goodness of fit. It is shown that from a theoretical viewpoint the consideration of extra-Poisson variation is needed for descriptive epidemiological applications. The practical examples indicate that the present version of the model provides acceptable fits for only a few cancer sites and that refinements are needed in the majority of sites. However, plausible model extensions suggest considerable improvements of goodness of fit.
UI - 1634304
AU - Kliewer EV
TI - Influence of migrants on regional variations of stomach and colon cancer mortality in the Western United States.
SO - Int J Epidemiol 1992 Jun;21(3):442-9
AD - National Centre for Epidemiology and Population Health, Australian National University, Canberra, ACT.
In order to examine the impact of migrants on regional variations in stomach and colon cancer, standardized mortality ratios (SMRs) were calculated for the total, nonmigrant (born and dying in same state), and migrant (born out of state) White residents of each of the 11 western states in the United States (US). The SMRs were derived from the National Center for Health Statistics' Mortality Detail Files for 1979-1981 and the 1980 Census Public Use Microdata 5-Percent Sample tapes. Migrants in the western US accounted for 79% of all stomach and colon cancer deaths. There was no consistent relationship between the SMRs of migrants and nonmigrants, with the migrant SMRs being higher in some states and lower in others. As a consequence of this differential impact, and their substantial numbers, migrants obscured the underlying regional patterns of mortality risk observed in the nonmigrants. The states of high or low risk were more contiguous in the analysis based on nonmigrants than the total population, and the interstate ranges in mortality were greater for nonmigrants. In areas with high in-migration, mortality atlases based on the total population may give an inaccurate portrayal of regional mortality risks, and spurious correlations may arise between the distributions of diseases and environmental characteristics of the regions. Regional mortality patterns of nonmigrants may more precisely reflect the factors which are influencing these cancers and thus provide a greater potential in providing clues to their aetiologies.
UI - 8082950
AU - Lee WC; Lin RS
TI - Interactions between birth cohort and urbanization on gastric cancer mortality in Taiwan.
SO - Int J Epidemiol 1994 Apr;23(2):252-60
AD - Institute of Public Health, College of Medicine, National Taiwan University, Taipei, Republic of China.
Birth-cohort analysis is of particular importance for gastric cancer since migrant studies have indicated that early life experiences play a dominant role in the occurrence of the disease. However, none of the birth-cohort analyses conducted in various countries have provided information on variation in the birth-cohort phenomenon. To examine the interaction of birth cohort and urbanization, mortality data for gastric cancer between 1971 and 1990 in differentially urbanized areas in Taiwan were analysed. Traditional birth-cohort analysis and age-period-cohort (APC) analysis were employed in the study. The identification problem inherent in the APC analysis was circumvented by the 'individual record' method. Grading of the degree of urbanization of each township and district in Taiwan was based on an urbanization index derived from several demographic and socioeconomic variables. The birth-cohort effects diffused from urban to rural areas after fitting the APC model. In the older generations, born before 1910, the relative risks of gastric cancer were higher in urban areas than in rural ones, but in recent generations, i.e. those born after 1916-1922, the reverse was true. The age curves of gastric cancer mortality emerged as almost straight lines when plotted on a double logarithmic scale. Sex ratios increased with age up to age 60 and then remained constant. The spread of the birth-cohort effects suggested that dietary factors, e.g. dietary habits and food processing practices, in the early life of the population play an important role in the occurrence of gastric cancer.(ABSTRACT TRUNCATED AT 250 WORDS)
UI - 10348814
AU - Higham AD; Bishop LA; Dimaline R; Blackmore CG; Dobbins AC; Varro A;
TI - Thompson DG; Dockray GJ Mutations of RegIalpha are associated with enterochromaffin-like cell tumor development in patients with hypergastrinemia.
SO - Gastroenterology 1999 Jun;116(6):1310-8
AD - The Physiological Laboratory, University of Liverpool, Liverpool, England.
BACKGROUND & AIMS: The RegIalpha gene (Reg) encodes a secretory protein proposed to regulate islet beta-cell and gastric mucous cell growth. Reg is expressed in rat gastric enterochromaffin-like (ECL) cells. The aim of this study was to examine Reg expression in human corpus and to determine the identity of Reg in ECL cell carcinoid tumors in hypergastrinemic patients. METHODS: Reg messenger RNA (mRNA) abundance was quantified by Northern blot in extracts of gastric corpus from patients with and without ECL cell tumors and in AR4-2J cells stimulated by gastrin; cellular origins were determined by immunocytochemistry. Mutations of Reg were determined by reverse-transcription polymerase chain reaction, cloning, and sequencing, and the mutated protein was expressed in HIT-T15 cells. RESULTS: Reg mRNA abundance was increased approximately threefold in the corpus of hypergastrinemic patients compared with controls, and was enriched in 3 of 7 ECL cell carcinoid tumors but not in non-endocrine cell gastric polyps. In AR4-2J cells, gastrin stimulated Reg mRNA abundance; this was eliminated by the gastrin/cholecystokinin B antagonist L-740,093 (10(-9) mol/L). Immunocytochemistry indicated that Reg was located in both chief cells and ECL cells in human corpus. Mutations of Reg were identified in 3 of 5 patients with ECL cell carcinoid tumors; in 2 cases, mutation of the initiator methionine residue led to exclusion of the protein from the secretory pathway. CONCLUSIONS: Gastrin regulates Reg mRNA abundance in human corpus. Mutations of Reg that prevent secretion are associated with ECL cell carcinoids, suggesting a function as an autocrine or paracrine tumor suppressor.
UI - 11941977
AU - Wu MS; Lee CW; Sheu JC; Shun CT; Wang HP; Hong RL; Lee WJ; Lin JT
TI - Alterations of BAT-26 identify a subset of gastric cancer with distinct clinicopathologic features and better postoperative prognosis.
SO - Hepatogastroenterology 2002 Jan-Feb;49(43):285-9
AD - Department of Internal Medicine, National Taiwan University Hospital, No. 7 Chun-Shan S. Rd., Taipei, Taiwan.
BACKGROUND/AIMS: Gastrointestinal tumors with microsatellite instability represent a replication error-positive phenotype. BAT-26, a repeat of 26 deoxyadenosine localized in intron 5 of hMSH2 gene, has been reported as a reliable indicator of replication error phenotype in colorectal cancers. This study investigated whether BAT-26 is a useful marker for a mutator phenotype with distinct clinicopathologic features in gastric cancer. METHODOLOGY: One hundred and nineteen gastric cancer tissues and matched non-tumor tissue were examined by polymerase chain reactions with electrophoresis for 9 dinucleotide microsatellites and BAT-26, and frameshift mutations of transforming growth factor-beta type II receptor. The relation between BAT-26 alterations and relevant clinicopathological or genetic parameters were analyzed. RESULTS: Gastric cancer with BAT-26 alterations was highly correlated with multiple microsatellite alterations (> or = 3 loci) and frameshift mutations of transforming growth factor-beta type II receptor, and predominantly showed antral location, intestinal histologic subtype, advanced stage, a higher rate of Helicobacter pylori infection, a better postoperative survival and less lymph node metastasis. CONCLUSIONS: These results show testing of BAT-26 alterations is a convenient and rapid screening method for identifying a subset of gastric cancer with a mutator phenotype and better prognosis.
UI - 12167575
AU - Shimoyama S; Yasuda H; Mafune K; Kaminishi M
TI - Indications of a minimized scope of lymphadenectomy for submucosal gastric cancer.
SO - Ann Surg Oncol 2002 Aug;9(7):625-31
AD - Department of Gastrointestinal Surgery, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. firstname.lastname@example.org
BACKGROUND: A recent trend for less invasive surgery has increased consideration for a minimized scope of lymphadenectomy for submucosal cancer; however, feasibility criteria have not been precisely established. METHODS: Patterns and sites of nodal involvement were retrospectively investigated in 294 patients with solitary submucosal gastric cancer in association with other clinicopathologic characteristics, including pre- and intraoperative evaluations of cancer depth (cT) and nodal involvement (cN). RESULTS: Among the early (cT1) and node-negative (cN0) cancer, intestinal (< or =1.5 cm) and diffuse types (< or =1.0 cm) of submucosal cancer showed low incidences of nodal involvement (3%) confined to the first tier. When the cancer exceeded these cutoff diameters, positive nodes of the second tier were confined to three priority stations (left gastric, common hepatic, and celiac arteries) at an incidence of 2.3%. Perigastric and preferential dissection of these three node stations (modified D2 dissection) showed survival benefits identical to those of a conventional D2 dissection. CONCLUSIONS: When submucosal cancer is evaluated as cT1cN0, a virtually sufficient minimized scope of lymphadenectomy is a D1 dissection for that within the cutoff diameter and a modified D2 dissection for that exceeding the cutoff diameter. These two types of dissection can even cover the infrequently observed node-positive stations and can realize no residual disease at surgery.
UI - 12045710
AU - Skacel M; Paris PL; Pettay JD; Tsiftsakis EK; Tubbs RR; Casey G; Hsi ED
TI - Diffuse large B-cell lymphoma of the stomach: assessment of microsatellite instability, allelic imbalance, and trisomy of chromosomes 3, 12, and 18.
SO - Diagn Mol Pathol 2002 Jun;11(2):75-82
AD - Department of Clinical Pathology, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Several types of genetic aberrations including microsatellite instability (MSI), allelic imbalance (AI), and chromosomal trisomies have been reported in low-grade (LG) mucosa-associated lymphoid tissue (MALT)-type gastric lymphomas. Presence of such genetic alterations could be a discriminator between de novo large cell lymphoma and high-grade (HG) MALT-type lymphoma. We investigated 17 primary gastric large B-cell lymphomas with and without features of MALT-type lymphoma for MSI, AI, and presence of trisomy of chromosomes 3, 12, and 18. We studied resection specimens from 17 primary gastric extranodal diffuse large B-cell lymphomas. Cases classified as HG MALT-type lymphoma, based on either the presence of LG MALT-type lymphoma component in the background (L/H MALT) or large cell lymphoepithelial lesions (HG MALT), and diffuse large B-cell lymphoma (DLBCL-NOS) when no features of MALT were present. MSI was analyzed using fluorescently labeled polymerase chain reaction primers (D3S11, D6S262, D3S1261, D3S1262, D3S1265). Paired tumor and normal DNA samples were amplified, and PCR products were analyzed on a DNA sequencer (ABI PRISM 373XL) with GeneScan (Applied Biosystems, Foster City, CA). MSI was defined as a gain of a novel-length allele compared with the corresponding normal tissue. AI was assessed at locus 3q27 (D3S1262 and D3S1265). The cases were analyzed for the presence of trisomy of chromosomes 3, 12, and 18 using interphase fluorescence in situ hybridization. MSI was detected in 4 out of 15 (27%) cases from which DNA was amplifiable with all primers and all MALT-type lymphomas. In two cases (13%), MSI was present at two loci sufficient to be classified as high-frequency MSI (MSI-H); this was seen exclusively in HG MALT lymphomas (P = 0.04). In the remaining two cases, MSI was detected at a single locus (low-frequency MSI). Allelic imbalance at the locus D3S1262 was detected in 4 out of 17 (24%) cases. It occurred more commonly in stage IE lymphomas when compared with higher stages (P = 0.03), regardless of lymphoma subtype. Trisomy 12 was detected in 3 out of 17 cases (18%) exclusively in stage IE lymphomas (P = 0.08). MSI was uncommon and was found exclusively in MALT-type lymphomas. MSI-H was even less common but occurred in HG MALT lymphomas only. Allelic imbalance at 3q27 (D3S1262) and trisomy 12 were found more commonly in low-stage disease. The latter two findings are in concordance with the recent suggestion that the published variation in gain of chromosomal material in high-grade gastric lymphomas may be related to stage rather than to the subtype of lymphoma. Because of the relatively low frequency of MSI in the high-grade B-cell lymphomas of the stomach, this feature cannot be used to reliably discriminate between the histologic types of extranodal diffuse large B-cell lymphoma.
UI - 12216071
AU - Yabuta T; Shinmura K; Tani M; Yamaguchi S; Yoshimura K; Katai H;
TI - Nakajima T; Mochiki E; Tsujinaka T; Takami M; Hirose K; Yamaguchi A; Takenoshita S; Yokota J E-cadherin gene variants in gastric cancer families whose probands are diagnosed with diffuse gastric cancer.
SO - Int J Cancer 2002 Oct 10;101(5):434-41
AD - Biology Division, National Cancer Center Research Institute, Tokyo, Japan.
To identify germline E-cadherin mutations responsible for the predisposition to diffuse gastric cancer (DGC) among the Japanese, we screened 17 patients with familial aggregation of gastric cancer by sequencing analysis. All the patients were diagnosed with DGC and had at least 1 sibling with gastric cancer. Two novel E-cadherin gene variants were detected. One was detected in 1 patient only and associated with an amino acid substitution (Val/Met) at codon 832 in the region essential for binding to beta-catenin. The M832 variant was detected not only in the proband but also in 2 other gastric cancer patients in the family. Immunohistochemical analysis of gastric cancer tissue from the proband revealed that E-cadherin expression was markedly reduced and beta-catenin expression was also reduced in cancer cells. However, no significant difference in the activity of beta-catenin binding was detected between the M832 variant and V832 wild-type E-cadherin in immunofluorescence and immunoprecipitation/Western blot analyses. The other was detected in 5 patients and was located in the splice donor site (IVS1+6T/C); however, RT-PCR analysis indicated that the IVS+6C variant did not cause an aberrant splicing. Thus, the M832 variant could be a germline mutation causative of familial aggregation of DGC, although further functional studies are needed to understand the pathogenic significance of this variant. Copyright 2002 Wiley-Liss, Inc.
UI - 12216076
AU - Chang YW; Han YS; Lee DK; Kim HJ; Lim HS; Moon JS; Dong SH; Kim BH; Lee
TI - JI; Chang R Role of Helicobacter pylori infection among offspring or siblings of gastric cancer patients.
SO - Int J Cancer 2002 Oct 10;101(5):469-74
AD - Department of Gastroenterology, Kyung Hee University College of Medicine, Seoul, Korea.
A positive family history is an increased risk factor for gastric cancer within family members, and one of the possible causes of this is the intrafamilial clustering of Helicobacter pylori infection. Our study examined the prevalence of H. pylori infection, serum antibodies to CagA and VacA and atrophic gastritis and/or intestinal metaplasia in the offspring or siblings of gastric cancer patients. A total of 726 subjects included 300 relatives of 300 separate gastric cancer patients and 426 controls. All subjects underwent upper gastrointestinal endoscopic examination with a rapid urease test. Blood samples were obtained to test for the presence of serum antibodies to the CagA and VacA proteins of H. pylori. The prevalence of H. pylori infection was higher in relatives of cancer patients (75.3%) than in controls (60.1%), and the adjusted odds ratio was 2.1 (95% CI 1.5-2.9). When either siblings or 2 or more family members were gastric cancer patients, the prevalence of H. pylori infection was much higher compared to the prevalence in controls. There was no specific relationship between CagA and VacA, and H. pylori infection. Atrophic gastritis and/or intestinal metaplasia were more frequently found in H. pylori-infected relatives of cancer patients (26.1%) than in H. pylori-infected controls (12.9%). These results strongly support a role for H. pylori infection in familial aggregation of gastric cancer. The prophylactic eradication of H. pylori infection in the offspring or siblings of gastric cancer patients may be clinically beneficial. Copyright 2002 Wiley-Liss, Inc.
UI - 11956652
AU - Aratanechemuge Y; Komiya T; Moteki H; Katsuzaki H; Imai K; Hibasami H
TI - Selective induction of apoptosis by ar-turmerone isolated from turmeric (Curcuma longa L) in two human leukemia cell lines, but not in human stomach cancer cell line.
SO - Int J Mol Med 2002 May;9(5):481-4
AD - Faculty of Bioresources, Mie University, Tsu-city, Mie 514-0001, Japan.
We have investigated the effects of ar-turmerone isolated from turmeric (Curcuma longa L) on DNA of human leukemia cell lines, Molt 4B, HL-60 and stomach cancer KATO III cells. It was found that selective induction of apoptosis by ar-turmerone was observed in human leukemia Molt 4B and HL-60 cells, but not in human stomach cancer KATO III cells. Morphological changes showing apoptotic bodies were observed in the human HL-60 and Molt 4B cells treated with ar-turmerone. The fragmentation of DNA by ar-turmerone to oligonucleosomal-sized fragments that is a characteristic of apoptosis was observed to be concentration- and time-dependent in Molt 4B and HL-60 cells, but not in KATO III cells. The data of the present study show that the suppression by ar-turmerone of growth of these leukemia cell lines results from the induction of apoptosis by this compound.
UI - 11956659
AU - Saitoh T; Mine T; Katoh M
TI - Frequent up-regulation of WNT5A mRNA in primary gastric cancer.
SO - Int J Mol Med 2002 May;9(5):515-9
AD - Genetics and Cell Biology Section, Genetics Division, National Cancer Center Research Institute, Tsukuji 5-chome, Chuo-ku, Tokyo 104-0045, Japan.
WNT signal is transduced to the beta-catenin - TCF pathway, the JNK pathway, or the Ca2+-releasing pathway through seven-transmembrane-type WNT receptors encoded by Frizzled genes (FZD1-FZD10). We have previously cloned and characterized human WNT2B/WNT13, WNT3, WNT3A, WNT5B, WNT6, WNT7B, WNT8A, WNT8B, WNT10A, WNT10B, WNT11, WNT14, and WNT14B/WNT15 by using bioinformatics, cDNA-library screening, and cDNA-PCR. Here, we investigated expression of human WNT5A mRNA in various normal tissues, 66 primary tumors derived from various tissues, and 15 human cancer cell lines. WNT5A mRNA was relatively highly expressed in salivary gland, bladder, uterus, placenta, and fetal kidney. Up-regulation of WNT5A mRNA was detected in 5 out of 8 cases of primary gastric cancer, 5 out of 18 cases of primary colorectal tumors, and in 2 out of 7 cases of primary uterus tumors by using matched tumor/normal expression array analysis. Up-regulation of WNT5A mRNA was also detected in 7 out of 10 other cases of primary gastric cancer by using cDNA-PCR. Although low-level expression of WNT5A mRNA was detected in gastric cancer cell line MKN45, WNT5A mRNA was almost undetectable in gastric cancer cell lines OKAJIMA, TMK1, MKN7, MKN28, MKN74, and KATO-III. Compared with frequent up-regulation of WNT5A mRNA in primary gastric cancer, expression levels of WNT5A mRNA in 7 gastric cancer cell lines were significantly lower than that in normal stomach. Frequent up-regulation of WNT5A mRNA in human primary gastric cancer might be due to cancer-stromal interaction.
UI - 11972882
AU - Perri F; Piepoli A; Quitadamo M; Quarticelli M; Merla A; Bisceglia M
TI - HLA-DQA1 and -DQB1 genes and Helicobacter pylori infection in Italian patients with gastric adenocarcinoma.
SO - Tissue Antigens 2002 Jan;59(1):55-7
AD - Department of Internal Medicine, Gastroenterology Unit, Casa Sollievo della Sofferenza Hospital, I.R.C.C.S., San Giovanni Rotondo, Italy. email@example.com
Both HLA-DQA1 and -DQB1 genes and Helicobacter pylori infection have been linked to gastric cancer. The aim of this work was to determine if HLA-DQA1 and -DQB1 alleles are presented at altered frequency in Italian patients with gastric adenocarcinoma and H. pylori infection. Oligotyping for HLA-DQA1 and -DQB1 and H. pylori serology was performed for 50 patients with gastric adenocarcinoma and compared with 80 patients with colonic adenocarcinoma and 179 healthy subjects. H. pylori infection was present in 76% of gastric cancer patients, 77.5% of colonic cancer patients, and 72% of controls. The prevalence of infection was not significantly different in the three groups of subjects sorted according to their HLA-DQA1 or -DQB1 status. Apart from HLA-DQA1* 0201, which was less common in patients with colonic carcinoma than controls, no other HLA-DQA1 and no HLA-DQB1 allele were present at altered frequency in patients with gastric or colonic cancer. Neither anatomical location and histological type of cancer nor the presence of lymph node or distant metastases were significantly associated with specific HLA-DQA1 or -DQB1 alleles or H. pylori infection. Both HLA-DQA1 and -DQB1 genes have a minor, if any, role in H. pylori infection and gastric carcinogenesis.
UI - 12170283
AU - Diaz Plasencia JA; Yan-Quiroz EF; Burgos-Chavez OA; Santillan-Medina JP;
TI - Stewart-Vilela Guillen E; Rojas-Vergara AM [Prognostic significance of tumor size in the survival of patients with advanced gastric carcinoma]
SO - Rev Gastroenterol Peru 2001 Jan-Mar;21(1):21-9
AD - Departamento de Cirugia del Hospital Belen de Trujillo.
OBJECTIVES: To determine the prognostic significance of size tumor in the survival of patients with advanced gastric carcinoma. MATERIAL AND METHODS: This retrospective study evaluated 95 patients with advanced gastric adenocarcinoma with a diameter smaller than 7 centimeters (Group I) and 85 cases with lesions equal or greater than 7 centimeters (Group II) whom underwent radical gastrectomy with lymphadenectomy D0-D1 (n=148) or D2-D3-D4 (n=32) at Belen Hospital, Trujillo, Peru, between 1966 and 1998. RESULTS: The median age of the Group I and II was of 58.1 12.9 and 58.5 15.3 years, respectively. The patients of the group II had a lower level of seric hemoglobin (p=0.007) and more frequency of lesions Borrmann type II and IV (p= 0.003). Using the log-rank test, there was no statistically significant difference with relation to five-year survival between both groups using the multivariate analysis of Cox regression. There was not statistically significance difference between the size tumoral and the survival but there were independent factors statistically related with the survival: depth of invasion (p=0.017) and lymph nodes compromised (p=0.014). CONCLUSIONS: Clinically the size of the tumor was not a factor to take as parameter in the prediction of the actuarial survival in patients with advanced gastric cancer.
UI - 11235563
AU - Wang J; Ye F
TI - [Identification of a new molecular marker related to tumorigenesis of the stomach and small intestine]
SO - Zhonghua Zhong Liu Za Zhi 2000 Nov;22(6):460-2
AD - Central Laboratory, First Affiliated Hospital of Guangdong Medical College, Zhanjiang 524001, China.
OBJECTIVE: Screening and identification of molecular markers associated with tumorigenesis of the gastrointestinal tract. METHODS: Techniques of random amplified polymorphic DNA (RAPD), restriction fragment length polymorphism (RFLP), Southern blot and
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