Table of Contents
1
UI - 11751424
AU - Lin MT; Juan CY; Chang KJ; Chen WJ; Kuo ML
TI -
IL-6 inhibits apoptosis and retains oxidative DNA lesions in human
gastric cancer AGS cells through up-regulation of anti-apoptotic gene
mcl-1.
SO - Carcinogenesis 2001 Dec;22(12):1947-53
AD - Department of Surgery, National Taiwan Hospital, Taipei, Taiwan.
Apoptosis plays a critical role in maintaining genomic integrity by
selectively removing the most heavily damaged cells from the population.
Reactive oxygen species (ROS) and certain inflammatory cytokines are
always elevated during the human carcinogenic process. However, the
biological significance of the interplay between ROS and inflammatory
cytokine remains elusive. This study demonstrates that interleukin-6
(IL-6) effectively protects gastric cancer cells from the apoptosis
induced by hydrogen peroxide (H(2)O(2)). The cell death signaling JNK
pathway elicited by H(2)O(2) is also inhibited by IL-6. We further found
that Mcl-1, but not other Bcl-2 family members, was up-regulated by
IL-6, by a substantial level over 24 h. We further transfected a mcl-1
expression vector, pCMV-mcl-1, into the AGS cells, and successfully
obtained several mcl-1-overexpressing clones. Flow cytometric analysis
shows that these mcl-1-overexpressing AGS cells are more resistant to
the apoptosis induced by H(2)O(2) when compared with the neo control AGS
cells. Consistently, the activation of the JNK pathway induced by
H(2)O(2) is also blocked in mcl-1-overexpressed cells. These results
indicate that the anti-apoptotic effect of IL-6 is, at least in part,
due to the up-regulation of mcl-1. To our surprise, either IL-6 exposure
or mcl-1 overexpression fails to reduce the level of intracellular
peroxides in the AGS cells triggered by H(2)O(2). This study also
determined the level of 8-hydroxydeoxyguanosine (8-OH-dGua), an
indicator for oxidative DNA lesions in IL-6-treated or
mcl-1-overexpressed AGS cells after treatment with H(2)O(2). Notably,
our results indicate that a majority of the 8-OH-dGua is efficiently
removed in the AGS cells without IL-6 treatment, whereas only
approximately 50% of the 8-OH-dGua was repaired in the IL-6-treated AGS
cells after 24 h. Similarly, approximately 60-70% of the 8-OH-dGua also
failed to repair and was retained in the genomic DNA of the mcl-1
transfectants. Results in this study provide a novel mechanism by which
up-regulation of the Mcl-1 protein by IL-6 may enhance the
susceptibility to H(2)O(2)-induced oxidative DNA lesions by overriding
apoptosis.
2
UI - 11778557
AU - Wu H; Yang G; Dong Y
TI -
[APC gene expression in precancerous lesions of stomach examined by
light and electron microscopic in situ hybridization]
SO - Zhonghua Zhong Liu Za Zhi 2000 Jul;22(4):308-10
AD - Department of Pathology, Anhui Medical University, Hefei 230032, China.
OBJECTIVE: To study the significance of abnormal expression of APC gene
in gastric cancer and its precancerous lesions. METHODS: The expression
of APC gene was examined in 119 cases of precancerous lesions and 40
cases of gastric cancers by light and electron microscopic in situ
hybridization technique. RESULTS: 1. The positive rate of APC gene
expression in normal gastric mucosa, mild dysplasia, moderately severe
dysplasia, severe dysplasia and gastric cancer was 83.3%, 77.8%, 62.5%,
25.9%, and 6.7%-8.0%, respectively. 2. In 4 types of intestinal
metaplasia (IM), APC gene expressed much more frequently in colonic type
than in small intestinal type (P < 0.05), more frequently in incomplete
type of IM than in complete type (P > 0.05). The positive rate of
incomplete colonic type was the highest. 3. Under electron microscope,
the APC positive signals were located in the cytoplasm matrix of gastric
mucosa cells. They decreased gradually from normal parietal cells,
dysplasia cells to cancer cells till negative. CONCLUSION: Abnormal
expression of APC gene occurs mainly in precancerous lesion-severe
dysplasia. It is considered as an early event during gastric
carcinogenesis. Detecting APC gene in gastric mucosa helps predict the
trend of dyplasia to become malignant, and diagnose gastric cancer in
early stage.
3
UI - 11778558
AU - Chen Z; Zheng T; Chen J
TI -
[Evaluation of ten-year results of cancer prevention and treatment in
Changle City with high incidence of gastric cancer]
SO - Zhonghua Zhong Liu Za Zhi 2000 Jul;22(4):311-3
AD - Fujian Provincial Tumour Hospital, Fuzhou 350014, China.
OBJECTIVE: To evaluate the results of cancer prevention and treatment
over a 10-year period (1988-1997) in Changle City with high incidence of
gastric cancer. METHODS: The results were analysed with sick rate random
test, trend test, GM and Kaplan-Meier method with SAS statistical
software. RESULTS: During the ten years, the sick rate of malignant
tumors in male residents initially increased but then decreased. Gastric
cancer had a tendency to decline. There was no obvious change for
females. By short-term prediction, the sick rate of malignant tumors and
gastric cancer would decrease, and that of liver cancer remain steady.
The life expectancy of male residents increased 4.2 years and that of
female residents increased 1.8 years from 1988 to 1997 if cancer death
was ignored, but the increase was not significant if only deaths from
gastric and liver cancers were excluded. The 5-year survival rate of
gastric cancer and liver cancer increased 8.8% and 29.3% from 1988 to
1990, respectively. The cumulative risk rate of gastric cancer in males
was 3 times as high as that of females, and that of liver cancer in
males was 2.5 times as high as that of females. CONCLUSION: Sustained
measures of cancer prevention and treatment woult anticipate further
improvement of health status of Changle's residents in the years to
come.
4
UI - 11521798
AU - Raderer M; Osterreicher C; Machold K; Formanek M; Fiebiger W; Penz M;
TI -
Dragosics B; Chott A
Impaired response of gastric MALT-lymphoma to Helicobacter pylori
eradication in patients with autoimmune disease.
SO - Ann Oncol 2001 Jul;12(7):937-9
AD - Department of Internal Medicine I, University of Vienna, Austria.
markus.raderer@akh-wien.ac.at
BACKGROUND AND AIMS: Gastric MALT-lymphoma is thought to be related to
chronic antigenic stimulation provided by Helicobacter pylori (HP). As
clonal expansion of gastric B cells not related to HP has been
demonstrated in patients with autoimmune disease (AD), we have analysed
whether AD adversely influences response of MALT-lymphoma following
HP-eradication. PATIENTS AND METHODS: Retrospective analysis of all
patients with early stage gastric MALT-lymphoma treated with
HP-eradication was performed. The presence of AD was evaluated by
personal questioning for specific symptoms and serologically by analysis
of rheumatoid factor, antinuclear antibodies and thyroid autoantibodies.
RESULTS: A total of 22 patients were identified receiving only
antibiotic treatment for initial management, and six presented with an
autoimmune condition: three had Sjogren's syndrome, one polymyalgia
rheumatica, one autoimmune thyroiditis along with psoriasis, and one
patient had only autoimmune thyroiditis. Successful eradication of HP
was achieved in all patients, and 15 of 22 patients (68%) achieved
complete response of the lymphoma, while none out of the six patients
with an autoimmune disorder responded to HP-eradication. CONCLUSION:
Apart from questioning the role of HP in the development of lymphoma in
such patients, these results suggest that patients with autoimmune
disease might not be optimal candidates for HP-eradication even in case
of early stage lymphoma.
5
UI - 11577792
AU - Sun W; Haller DG
TI -
Recent advances in the treatment of gastric cancer.
SO - Drugs 2001;61(11):1545-51
AD - University of Pennsylvania Cancer Center, Philadelphia, Pennsylvania
19104, USA.
Gastric cancer is one of the most common cancers in the world. The
prognosis of the disease is poor, with only 40% of patients eligible to
undergo potentially curative surgery. Even for those patients who
undergo a complete resection, the rate of recurrence is very high.
Extensive studies of multidisciplinary adjuvant treatment have been
conducted seeking to improve the cure rates in the past two decades. The
benefit of D2 dissection is still controversial and is undergoing
prospective evaluation. Preliminary results from the United States
Gastrointestinal Intergroup study, a well designed trial, have shown
overall survival benefit of postoperative chemoradiation therapy.
Neoadjuvant chemotherapy or chemoradiation is under active study in
order to increase the number of patients to undergo potential curative
surgery. Although many chemotherapy regimens have been developed
recently, only modest clinical efficacy has been demonstrated for
advanced metastatic disease. So far, there is no single regimen
considered to be standard.
6
UI - 11815962
AU - Hyung WJ; Noh SH; Lee JH; Huh JJ; Lah KH; Choi SH; Min JS
TI -
Early gastric carcinoma with signet ring cell histology.
SO - Cancer 2002 Jan 1;94(1):78-83
AD - Department of Surgery, Yonsei University College of Medicine, Seoul,
Korea.
BACKGROUND: There has been much controversy surrounding the biologic
behavior and prognosis of early stage gastric signet ring cell carcinoma
(SRC). To clarify the biologic behavior of early stage gastric SRC
(early SRC), we compared the clinicopathologic features and prognosis of
early SRC with other histologic types. METHODS: A total of 933 patients
with early gastric carcinoma who had undergone gastrectomy from 1987 to
1995 were retrospectively analyzed. Among them, 263 patients with SRC
were compared to 670 patients with other histologic types. RESULTS:
Younger patients more often had SRC than non-SRC. Additionally, the
proportion of females was greater in SRC than in non-SRC. Signet ring
cell carcinoma had a larger proportion of mucosa-confined lesions and a
lower rate of lymph node metastasis than non-SRC. Even after stratifying
the clinicopathologic characteristics, SRC showed a lower rate of lymph
node metastasis than non-SRC. When the lymph node metastasis rate was
compared between SRC and undifferentiated histology other than SRC, SRC
demonstrated a lower lymph node metastasis rate. Multivariate analysis
showed that SRC histology was a negative independent risk factor for
lymph node metastasis in early gastric carcinoma. The prognosis of SRC
was significantly better than that of non-SRC (P = 0.0104). CONCLUSIONS:
Early gastric carcinoma with SRC is a distinct type of gastric carcinoma
in terms of clinicopathologic features and prognosis. The favorable
prognosis and lower rate of lymph node metastasis in early SRC suggest
that the patients with early gastric carcinoma with SRC could be
candidates for less invasive surgeries for an improved quality of life.
Copyright 2002 American Cancer Society.
7
UI - 11552717
AU - Chan WY; Chan EK; Chow JH
TI -
Epstein-Barr virus-associated gastric lymphomas are distinct from
mucosa-associated lymphoid tissue-type lymphomas: genetic abnormalities
of p53 gene.
SO - Diagn Mol Pathol 2001 Sep;10(3):153-60
AD - Department of Anatomical & Cellular Pathology, Chinese University of
Hong Kong, Prince of Wales Hospital, Shatin, NT. wingchan@cuhk.edu.hk
The authors studied 46 primary gastric lymphomas for expression of the
p53 gene by immunohistochemistry and screened for mutations in p53 exon
5-8 by polymerase chain reaction-single strand conformation
polymorphism. Twenty-five specimens cases were also analyzed for loss of
heterozygosity (LOH) of chromosomal region 17p12-13.1. In 36 lymphomas
negative for Epstein-Barr virus (EBV) infection, of which 29 were of
mucosa-associated lymphoid tissue (MALT) type, p53 genetic changes were
found in 47.2% but correlated poorly with overexpression. Only 20% of
the mutations involved exon 7. There were recurrent mutations of intron
7, intron 6, and exon 6. In contrast, the 10 EBV-positive cases, none of
MALT type, had a much higher rate of mutation, and all showed both p53
overexpression and p53 mutation and/or LOH, and 87.5% had mutations
involving exon 7. Four of these involved codon 242, not seen in the
EBV-negative group. Splicing mutations of intron 8 were seen in three
specimens, two involving the same nucleotide position. In four of five
specimens, LOH analysis identified microsatellite instability, allelic
loss, or both. The Helicobacter pylori infection rate in the
EBV-positive group (20%) was much lower than in the EBV-negative group
(91.7%). These differences between the two groups suggest involvement of
different carcinogens. Mutation of codon 242 has not been specifically
associated with other tumors and may represent a mutational hot spot in
the EBV-positive lymphomas.
8
UI - 11747229
AU - Gu M; Ghafari S; Nguyen PT; Lin F
TI -
Cytologic diagnosis of gastrointestinal stromal tumors of the stomach by
endoscopic ultrasound-guided fine-needle aspiration biopsy:
cytomorphologic and immunohistochemical study of 12 cases.
SO - Diagn Cytopathol 2001 Dec;25(6):343-50
AD - Department of Pathology, University of California Irvine Medical Center,
Orange, California 92868, USA. mgu@uci.edu
Gastrointestinal stromal tumor (GIST) is an uncommon tumor, which was
usually diagnosed by endoscopic biopsy or surgical resection. This study
evaluated the efficacy and accuracy of endoscopic ultrasound (EUS)
-guided fine-needle aspiration (FNA) biopsy in the diagnosis of GIST and
reported its cytomorphologic features. Twelve patients with gastric GIST
were diagnosed through EUS-guided FNA. Immediate on-site evaluation and
cytologic diagnoses were given in nine cases (75.0%) with an average of
three passes. Cell blocks provided diagnostic material in three cases
(25.0%). Spindle cells were present in the cytologic material in all
cases. Two patients had subsequent surgical resections.
Immunohistochemical (IHC) studies performed in cell blocks and two
surgical specimens all supported the original diagnoses. In the two
cases with surgical resections, IHC results in cell blocks were similar
to that in the resected specimens. This study demonstrated that when
combining smears and cell blocks, EUS-guided FNA is accurate and
efficient in the diagnosis of GIST. IHC reactivity in cell blocks
correlated with that of the main tumors. Copyright 2001 Wiley-Liss, Inc.
9
UI - 11769693
AU - Liu X; Wang Q; Ma J
TI -
[A case-control study on the risk factors of stomach cancer in Tianjin
city]
SO - Zhonghua Liu Xing Bing Xue Za Zhi 2001 Oct;22(5):362-4
AD - Department of Epidemiology, Tianjin Medical University, Tianjin 300070,
China.
OBJECTIVE: To explore the risk factors of stomach cancer in Tianjin.
METHODS: A matched case-controls study was carried out. A total number
of 189 patients with stomach cancer who were individually matched and
interviewed. RESULTS: Multivariate conditional logistic analysis showed
that stomach cancer was closely relate to the four factors: smoked food
(OR = 2.34, 95% CI: 1.60-4.98), cigarettes smoking (OR = 6.07, 95% CI:
1.26-7.16), heavy salt intake (OR = 1.95, 95% CI: 1.27-3.23) and
excessive intake of meats (OR = 1.46, 95% CI: 1.05-2.02) were risk
factors for stomach cancer. CONCLUSION: Frequent eating smoked food,
cigarettes smoking, heavy salt intake and over intake of meats were risk
factors for stomach cancer.
10
UI - 11775866
AU - Wang R; Fang D; Liu W; Luo Y
TI -
[Aberrant expression of MUC2 and MUC3 genes in gastric carcinoma and its
significance]
SO - Chin Med J (Engl) 2000 Jun;113(6):502-7
AD - Department of Gastroenterology, Southwest Hospital, Third Military
Medical University, Chongqing 400038, China.
OBJECTIVES: To explore the clinicopathological significance of the
expression of MUC2 (mucin 2) and MUC3 (mucin 3) genes in tissues of the
normal gastric mucosa, intestinal metaplasia (IM) and gastric carcinoma.
METHODS: MUC2 and MUC3 apomucins were detected by immunohistochemistry;
MUC2 and MUC3 mRNAs were detected by in situ hybridization. RESULTS: In
the normal stomach, antibody detecting MUC2 apomucin and oligonucleotide
probe detecting MUC2 mRNA were not reactive with mucus-producing cells
in the superficial epithelium and neck, which were weakly reactive with
antibody and probe detecting MUC3. In the duodenum, MUC2 apomucin and
mRNA were found at the peri- and supranuclear area of goblet cells, but
MUC3 apomucin and mRNA were at the cytoplasm of goblet cells and
columnar cells. MUC2 and MUC3 apomucins and its mRNAs were found in
85.2%, 88.9% and 31.6%; 57.1% of specimens of IM, 67.4%, 66.7% and
57.9%, 43.6% of specimens of gastric carcinoma. There were no
associations between expressions of MUC2 and MUC3 genes and different
types of IM. Patients with moderate/well differentiation had higher
proportion of MUC2 apomucin expression than those with poor
differentiation (P < 0.05), and patients with positive staining of MUC3
apomucin in the cancerous tissues had higher proportions of metastasis
of lymph nodes (P < 0.01), serosal invasion (P < 0.05) and clinical
stages III-IV (P < 0.05). CONCLUSIONS: MUC2 and MUC3 genes are mainly
expressed in the mucosa of the duodenum, and marked expression is seen
during the neoplastic transformation of stomach mucosa. MUC3 apomucin
might have a poor prognostic significance.
11
UI - 11774216
AU - Wang Q; Chen H; Bai J; Wang B; Wang K; Gao H; Wang Z; Wang S; Zhang Q;
TI -
Fu S
[Analysis of loss of heterozygosity on 19p in primary gastric cancer]
SO - Zhonghua Yi Xue Yi Chuan Xue Za Zhi 2001 Dec;18(6):459-61
AD - Laboratory of Medical Genetics, Harbin Medical University, Harbin
Heilongjian, 150086 P.R.China.
OBJECTIVE: To investigate the loss of heterozygosity (LOH) frequency of
microsatellite loci in primary gastric cancer samples and locate the
deleted regions on 19p in which might exist human gastric cancer related
genes. METHODS: The LOH of microsatellite loci on chromosome 19p was
analyzed using PCR-SSLP-silver stain method in 43 primary gastric
cancers and their paired normal tissues. RESULTS: In 43 primary gastric
tumors, LOH was detected on the site for D19S424(29.63%),
D19S216(11.53%), D19S406 (33.33%), D19S413(8.57%), D19S221(13.15%),
D19S226(8.00%), D19S411(6.45%), D19S883(6.89%), and D19S886(10.71%),
microsatellite instability (MSI) was found at the same time at locus
D19S886 (17.85%). CONCLUSION: The most common LOH occurrence at D19S406
and D19S424 might imply the existence of the potential genes related to
the tumorigenesis of gastric cancer in these loci.
12
UI - 11802535
AU - Chen TK; Wu CH; Lee CL; Lai YC; Yang SS; Tu TC
TI -
Endoscopic ultrasonography to study the causes of extragastric
compression mimicking gastric submucosal tumor.
SO - J Formos Med Assoc 2001 Nov;100(11):758-61
AD - Division of Gastroenterology, Department of Internal Medicine, Cathay
General Hospital, Taipei, Taiwan.
BACKGROUND AND PURPOSE: Many reports have confirmed that endoscopic
ultrasonography (EUS) can differentiate gastric submucosal tumor from
extragastric compression, but only a few specifically concentrated on
EUS in identifying the causes of external compression. MATERIALS AND
diagnose gastric submucosal tumor or external compression. We excluded
183 patients who had submucosal tumors and analyzed the remaining 55
patients with extragastric compression. Malignant causes of external
compression were proved by surgery or biopsy. Benign causes of external
compression were proved by other imaging examinations (abdominal
ultrasound, computerized tomography, angiography) or surgery. Patients
with external compression caused by normal organs were followed up with
repeated upper gastrointestinal endoscopy or EUS. RESULTS: The stomach
was compressed by normal extragastric organs in 32 patients (spleen 10,
splenic vessel 6, gall bladder 9, liver 3, pancreas 3, and intestine 1),
by benign pathologic lesions in 12 patients (liver cyst 7, liver
hemagioma 2, splenic cyst 1, pancreatic cyst 1, pancreatic cystadenoma
1) and by malignant tumors in 5 patients (hepatoma 1, liver metastasis
from colon cancer 2, pancreatic cystadenocarcinoma 1 and lymphoma of
spleen 1). In the remaining six patients, neither submucosal tumor nor
external compression was found during EUS examination and the external
compression was considered transient. CONCLUSION: When an extragastric
compression mimicking submucosal tumor is detected by upper
gastrointestinal endoscopy, EUS is indicated to identify the cause of
extragastric compression.
13
UI - 11808968
AU - Tendler DA
TI -
Malignant gastric outlet obstruction: bridging another divide.
SO - Am J Gastroenterol 2002 Jan;97(1):4-6
14
UI - 11578917
AU - Davis PA; Sano T
TI -
The difference in gastric cancer between Japan, USA and Europe: what are
the facts? what are the suggestions?
SO - Crit Rev Oncol Hematol 2001 Oct;40(1):77-94
AD - Imperial College School of Medicine, St. Mary's Hospital, London, UK.
In Japan the survival rate for gastric cancer has steadily improved over
the last 30 years whilst that in the West has remained static and
inferior. In this review three hypotheses are examined to explain the
difference. There is little evidence to suggest genetic differences,
which might result in a less aggressive cancer in Japan. Recently there
has been a rise in the proportion of cancers of the gastro-oesophageal
junction in the West and this has not been seen in Japan. The comparison
of survival data from these two regions is problematic with different
staging systems and a stage migration effect. The established surgical
treatment of gastric cancer in Japan is radical gastrectomy and regional
lymphadenectomy and this has been proposed as a superior treatment to
the standard gastrectomy common in the West. The results for survival
benefit however, have not been reproduced in randomized clinical trials.
The heterogeneity of adjuvant and neoadjuvant treatment regimens in
Japan and the West has led to difficulties in the interpretation of
their effects. There is considerable scope for future collaboration
between clinicians in the West and Japan.
15
UI - 11807778
AU - Hiyama T; Haruma K; Kitadai Y; Masuda H; Miyamoto M; Tanaka S; Yoshihara
TI -
M; Shimamoto F; Chayama K
K-ras mutation in helicobacter pylori-associated chronic gastritis in
patients with and without gastric cancer.
SO - Int J Cancer 2002 Feb 10;97(5):562-6
AD - First Department of Internal Medicine, Hiroshima University School of
Medicine, Hiroshima, Japan.
Mutations of an oncogene, K-ras, are associated with the development and
progression of many types of human cancer. To elucidate the significance
of K-ras mutations in gastric carcinogenesis, we examined K-ras
mutations in gastric cancers and in Helicobacter pylori-associated
chronic gastritis (H. pylori-CG), which is associated with an increased
risk for the gastric cancer development. Specimens of gastric cancer and
H. pylori-CG were obtained from 64 gastric cancer patients with H.
pylori-CG, 99 cancer-free H. pylori-CG patients and 30 H.
pylori-negative healthy subjects. K-ras mutations were examined by
polymerase chain reaction-single strand conformation polymorphism
(PCR-SSCP), followed by DNA sequencing analysis. K-ras mutations were
detected in 4 of 48 (8.3%) gastric cancers, in 10 of 163 (6.1%) H.
pylori-CG and none of the 30 H. pylori-negative healthy subjects. In the
gastric cancer patients, mutated K-ras was detected in differentiated
type cancers but not in any of the undifferentiated type cancers. K-ras
mutations in H. pylori-CG were significantly more frequent in gastric
cancer patients than in cancer-free patients (10.9% vs. 3.0%, p =
0.044). In addition, K-ras mutations in H. pylori-CG were significantly
more frequent in patients with K-ras mutated gastric cancer than in
patients with K-ras unmutated gastric cancer (50.0% vs. 3.7%, p =
0.037). These data suggest that the genetic mechanism(s) of
carcinogenesis differs between the differentiated type and the
undifferentiated type of gastric cancer and that K-ras mutations may be
involved in the early stages of gastric carcinogenesis of the
differentiated type. Copyright 2001 Wiley-Liss, Inc.
16
UI - 11807799
AU - Yatsuya H; Toyoshima H; Mizoue T; Kondo T; Tamakoshi K; Hori Y; Tokui N;
TI -
Hoshiyama Y; Kikuchi S; Sakata K; Hayakawa N; Tamakoshi A; Ohno Y;
Yoshimura T
Family history and the risk of stomach cancer death in Japan:
differences by age and gender.
SO - Int J Cancer 2002 Feb 10;97(5):688-94
AD - Department of Public Health/ Health Information Dynamics, Field of
Social Life Science, Program in Health and Community Medicine, Nagoya
University Graduate School of Medicine, Nagoya, Japan.
h828@med.nagoya-u.ac.jp
Familial aggregation of stomach cancer has long been observed. The
effect on disease risk of family history and its magnitude according to
the type of affected relatives, however, is not well known. We conducted
a prospective analysis using the JACC study (Japan Collaborative Cohort
Study For Evaluation of Cancer Risk, sponsored by Monbusho) data. During
the follow-up period, 662 stomach cancer deaths were documented. A
positive history of stomach cancer in one or more first-degree relatives
was associated with a significantly increased risk of death from the
disease in both men (RR 1.60; 95% CI 1.11-2.31) and women (RR 2.47; 95%
CI 1.50-4.06). In the subanalysis stratified by age, the association
between positive family history and stomach cancer was stronger in the
age group from 40-59 (RR 2.62; 95% CI 1.34-5.11 for men and RR 5.88; 95%
CI 2.70-12.82 for women) than in the age group from 60-79 (RR 1.31; 95%
CI 0.84-2.05 for men and RR 1.44; 95% CI 0.72-2.88 for women). In the
age group from 40-59, men with father's history and women with mother's
and sister's history of the disease had a significantly increased risk
(RR 3.14; 95% CI 1.51-6.55, RR 10.46; 95% CI 4.54-24.12, RR 13.39; 95%
CI 3.89-46.12, respectively). When 2 or more family members were
affected, the increment in the risk was prominent especially in women
(RR 9.45; 95% CI 4.46-20.05). These results suggest the existence of a
certain subtype of stomach cancer that is inherited more often by women
from one generation to the next in gender-influenced fashion. Any
preventive strategy should take into account the degree of individual
susceptibility. Copyright 2001 Wiley-Liss, Inc.
17
UI - 11722818
AU - Casado Martin F; Dominguez-Diez A; Rodriguez Sanjuan J; Lopez Useros A;
TI -
Cabrera Garcia M; Moreno Muzas C; Palomar Fontanet R;
Fernandez-Escalante C; Gomez Fleitas M
[Surgery of early gastric cancer. Twenty-five year experience]
SO - Gastroenterol Hepatol 2001 Nov;24(9):427-32
AD - Instituto de Patologia Digestiva, Hospital Universitario Marques de
Valdecilla, Santander, Cantabria, Spain.
AIM: To study the influence of the depth of parietal invasion
(mucosal-submucosal), the presence or absence of ganglionic invasion and
type of gastrectomy performed (subtotal or total) on survival in
patients with early gastric cancer. STUDY DESIGN: Longitudinal
study.Patients: A clinical-pathologic study of 101 patients who
underwent surgery for early gastric cancer was performed. Probability of
survival was estimated using the Kaplan-Meier and logrank tests and
multivariate analysis was performed using the Cox test. RESULTS: Mucosal
involvement was found in 46 patients (45.5%) and submucosal involvement
in 55 patients (54.5%). The presence of ganglionic metastases was
greater in tumors reaching the submucosa (14 [25.5%]) than in those
limited to the mucosa (4 [8.7%]). Partial gastrectomy was performed
according to tumor location in 84 patients (83.2%), total gastrectomy
was performed in 16 patients (15.8%) and 1 wedge resection was
performed. The mean postoperative follow-up was 84.04 55.89 months
(range: 2-264). Comparison of survival in patients with tumors limited
to the mucosal or submucosal layers revealed a p-value of 0.06 (NS).
Comparison of survival in patients with metastases and in those without
metastases revealed a p-value of < 0.0001. Comparison of survival
between patients who underwent total gastrectomy and those who underwent
partial gastrectomy showed a p-value of 0.38 (NS). Postoperative
mortality was nil. Overall survival at 5 years was 79.24% and at 10
years was 68.14%. Multivariate analysis revealed that ganglionic
involvement and depth of parietal invasion influenced survival.
CONCLUSIONS: Survival is influenced by ganglionic involvement but not by
submucosal invasion. Partial gastrectomy may be an appropriate procedure
since survival is similar to that associated with total gastrectomy.
18
UI - 11724680
AU - Jones RG; Trowbridge DB; Go MF
TI -
Helicobacter pylori infection in peptic ulcer disease and gastric
malignancy.
SO - Front Biosci 2001 Dec 1;6():E213-26
AD - Gastrointestinal Section, VA Salt Lake City Health Care System and the
Division of Gastroenterology, University of Utah School of Medicine,
Salt Lake City, Utah 84148, USA.
Helicobacter pylori infection is the world's most common chronic
infection in humans and is the cause of most gastritis cases. This
infection is accepted as the etiology of the majority of peptic ulcers.
It has been implicated as a significant contributing factor in the
development of gastric malignancy--both gastric MALT lymphoma and
gastric adenocarcinoma. Both endoscopic and non-endoscopic tests are
available for accurate diagnosis of the infection. Several multi-drug
regimens are useful for effective eradication of the infection.
Strategies have been developed for managing patients with gastric MALT
lymphoma. Criteria to identify populations with increased risk for
gastric malignancy are being developed. H. pylori induces gastritis; it
is also involved in both apoptosis and cellular proliferation. The role
of H. pylori infection in the pathogenesis of premalignant lesions,
altered gastric acid secretion, and significant clinical presentations
is the subject of numerous studies worldwide.
19
UI - 11798530
AU - Qiao W; Hu J; Wu K
TI -
[The relationship between vac A genotype of Helicobacter pylori clinical
isolate and gastric cancer and precancer]
SO - Zhonghua Nei Ke Za Zhi 2000 Nov;39(11):729-31
AD - Department of Gastroenterology, First Hospital, Xi'an Jiaotong
University, Xi'an 710063, China.
OBJECTIVE: To analyze the relationship between vac A genotype of
Helicobacter pylori (Hp) and gastric cancer and precancer in Xi'an area.
METHODS: To establish the stock of Hp clinical isolates and perform vac
A gene typing of Hp isolates by PCR. RESULTS: 192 Hp clinical strains
are isolated from the antrum of 259 patients. In them, type s1 is 174
strains (90.6%); s2 is 18 stains (9.4%). Type m1 and m2 is 99 (51.6%)
and 93 (48.4%) respectively. All strains are s1 or s2 and m1 or m2. In
gastric cancer group, the expression of type s1 is 94.5% and s1a is more
than s1b (P < 0.05). There is no difference between type m1 and m2. In
gastritis group, type s1 is 89.8%, s1a is almost equal to s1b and no
difference between m1 and m2. CONCLUSION: Type s1 is the main expression
in both gastric cancer group and gastritis group. Expression of type s1a
is higher than s1b. We can't determine it is a malignant index of
gastrointestinal diseases. We need to research it extensively.
20
UI - 11782383
AU - Hippo Y; Taniguchi H; Tsutsumi S; Machida N; Chong JM; Fukayama M;
TI -
Kodama T; Aburatani H
Global gene expression analysis of gastric cancer by oligonucleotide
microarrays.
SO - Cancer Res 2002 Jan 1;62(1):233-40
AD - Genome Science Division, The University of Tokyo, Tokyo 153-8904, Japan.
To gain molecular understanding of carcinogenesis, progression, and
diversity of gastric cancer, 22 primary human advanced gastric cancer
tissues and 8 noncancerous gastric tissues were analyzed by high-density
oligonucleotide microarray in this study. Based on expression analysis
of approximately 6800 genes, a two-way clustering algorithm successfully
distinguished cancer tissues from noncancerous tissues. Subsequently,
genes that were differentially expressed in cancer and noncancerous
tissues were identified; 162 and 129 genes were highly expressed (P <
0.05) >2.5-fold in cancer tissues and noncancerous tissues,
respectively. In cancer tissues, genes related to cell cycle, growth
factor, cell motility, cell adhesion, and matrix remodeling were highly
expressed. In noncancerous tissues, genes related to
gastrointestinal-specific function and immune response were highly
expressed. Furthermore, we identified several genes associated with
lymph node metastasis including Oct-2 or histological types including
Liver-Intestine Cadherin. These results provide not only a new molecular
basis for understanding biological properties of gastric cancer, but
also useful resources for future development of therapeutic targets and
diagnostic markers for gastric cancer.
21
UI - 11802218
AU - Kim HJ; Chang WK; Kim MK; Lee SS; Choi BY
TI -
Dietary factors and gastric cancer in Korea: a case-control study.
SO - Int J Cancer 2002 Feb 1;97(4):531-5
AD - Department of Preventive Medicine, Hanyang University College of
Medicine, Seoul, Korea.
To assess gastric cancer (GC) risk in relation to dietary intake in
Korea, a case-control study was performed. Trained dietitians
interviewed 136 patients diagnosed with GC, and the same number of
controls were selected by matching sex, age and hospital. A significant
decrease in GC risk was observed with increased intake of Baiechu kimchi
(prepared with salted Chinese cabbage and red pepper, etc.), Baiechu
kimchi-stew, garlic, mushroom and soybean milk. On the contrary, a
significant increase in the risk of GC was observed with increased
intake of cooked rice with bean, charcoal grilled beef, pollack soup,
Kkakduki (a kind of kimchi prepared with salted radish and red pepper,
etc.), Dongchimi (a kind of kimchi prepared with radish and a large
quantity of salt water) and cooked spinach. In food groups, increased
intake of soybean products was associated with decreased risk of GC.
Intake of citrus fruits rather than total fruits was shown to have a
protective effect on the risk of GC, but was not significant. In this
study, intake of total vegetables was shown to have a protective effect,
whereas high nitrate-containing vegetables increased the risk of GC. In
conclusion, our study suggests that the risk of GC decreased with high
consumption of fresh vegetables and fruits, whereas high consumption of
foods rich in nitrate and carcinogenic substances produced during the
cooking process increased the risk of GC. Copyright 2001 Wiley-Liss,
Inc.
22
UI - 11714113
AU - Abnet CC; Qiao YL; Mark SD; Dong ZW; Taylor PR; Dawsey SM
TI -
Prospective study of tooth loss and incident esophageal and gastric
cancers in China.
SO - Cancer Causes Control 2001 Nov;12(9):847-54
AD - Cancer Prevention Studies Branch, Division of Clinical Sciences,
National Cancer Institute, Bethesda, MD 20892-7058, USA.
abnetc@mail.nih.gov
OBJECTIVE: To determine the association between tooth loss and the risk
of developing esophageal squamous cell carcinoma, gastric cardia
adenocarcinoma, or gastric non-cardia adenocarcinoma in a prospective
study. METHODS: Cox proportional hazards regression was used to examine
these associations in a 28,868-person cohort followed prospectively for
5.25 years. The baseline questionnaire included questions regarding
tooth loss, and individuals reporting lost teeth had their teeth counted
by study personnel. The analytic cohort included 620 esophagus, 431
gastric cardia, and 102 gastric non-cardia cancer cases. RESULTS: Tooth
loss was associated with a significantly elevated risk of developing all
three cancers. When examined as median splits, tooth loss was associated
with a relative risk (RR) (95% confidence interval, CI) of 1.3 (1.1-1.6)
in the esophagus, 1.3 (1.0-1.6) in the gastric cardia, and 1.8 (1.1-3.0)
in the gastric non-cardia. Further analysis demonstrated that this
increased risk was most strongly associated with the loss of the first
few teeth and was primarily confined to the younger members of our
cohort. CONCLUSIONS: In this cohort tooth loss increased the risk of
developing upper gastrointestinal cancer. We hypothesize that this may
be related to alterations in oral bacterial flora and subsequent
increases in the in-vivo production of carcinogens such as nitrosamines.
23
UI - 11785203
AU - Gabrys K; Nowicka J; Medras E; Pabisek D; Mazur G; Jelen M
TI -
[Haematologic changes in gastritic cancer]
SO - Pol Tyg Lek 1995;50(1-35):809-11
AD - Katedra i Klinika Hematologii i Chorob Rozrostowych, Wroclaw.
Haematologic disturbances in 13 cases of gastric cancer are described.
All the patients had anemia of different origin. Increased leukocytosis
was observed in half of the cases, leukaemia reaction in one third.
Haemolysis was present in 50% of cases. Thrombocytopenia coexisted most
frequently with disseminated intravascular coagulation in 4 patients.
Bone metastases were visualised as osteolytic foci with radiological
methods or increased capture of isotopic marker in the bones under
scintigraphic examination. Under the microscope neoplastic metastases
were found in bone marrow smears of 5 patients. All patients displayed
symptoms of gastric ulcer disease acute or chronic phase. In some cases
only repeated gastroscopic examination and mucosa biopsy was the only
way to confirm cancer. In other cases the diagnosis was made after the
histopathologic examination of the resected stomach, in still others by
a section.
24
UI - 11756228
AU - Ebert MP; Fei G; Kahmann S; Muller O; Yu J; Sung JJ; Malfertheiner P
TI -
Increased beta-catenin mRNA levels and mutational alterations of the APC
and beta-catenin gene are present in intestinal-type gastric cancer.
SO - Carcinogenesis 2002 Jan;23(1):87-91
AD - Department of Gastroenterology, Hepatology and Infectious Diseases,
Otto-von-Guericke University, D-39120 Magdeburg, Germany .
Beta-catenin is critical for intercellular adhesion and also plays a
role as a transcription activating protein in the Wnt signalling
pathway. Increased protein levels and mutation of the beta-catenin gene
have been demonstrated in various cancers; however, the role of
beta-catenin in gastric cancer remains largely unknown. Using gastric
cancer tissues and normal adjacent gastric mucosa obtained from 20
patients with gastric cancer (eight diffuse-type, 12 intestinal-type)
undergoing gastric resection or endoscopy, we assessed the expression of
beta-catenin by immunohistochemistry and quantitative PCR analysis.
Furthermore, the tumour suppressor gene APC, which down-regulates the
beta-catenin levels was analysed for mutations. Overall mRNA levels of
beta-catenin were significantly increased in the tumour samples compared
with the matched normal gastric mucosa (P < 0.05). Increased
beta-catenin mRNA levels were significantly more frequent in
intestinal-type gastric cancers as compared to diffuse-type gastric
cancers (P < 0.01). Six out of 20 tumours exhibited >6-fold increased
beta-catenin mRNA levels as compared with normal mucosa. APC gene
mutations were found in four cases. A beta-catenin gene mutation was
identified only in one intestinal-type gastric cancer exhibiting a
massive overexpression of beta-catenin mRNA in the tumour. In
intestinal-type gastric cancers beta-catenin mRNA levels are greatly
enhanced. APC and beta-catenin gene mutations are also present primarily
in intestinal-type gastric cancers. These findings support the
hypothesis that in intestinal-type gastric cancers the accumulation of
beta-catenin protein may result from impaired degradation of the
beta-catenin protein due to alterations of the beta-catenin and APC
genes, as well as from enhanced beta-catenin transcription which is
present in the great majority of intestinal-type gastric cancers.
25
UI - 11745702
AU - Nabais S; Carneiro F; Nogueira AM; Machado JC; Seruca R; Sobrinho-Simoes
TI -
M
Re. 'Cellular phenotypes of differentiated-type adenocarcinomas and
precancerous lesions of the stomach are dependent on the genetic
pathways'.
SO - J Pathol 2001 Dec;195(5):636-7
26
UI - 11801910
AU - Park MS; Kim KW; Yu JS; Kim MJ; Yoon SW; Chung KW; Lee JT; Yoo HS
TI -
Radiologic findings of gastrointestinal tract involvement in
hepatocellular carcinoma.
SO - J Comput Assist Tomogr 2002 Jan-Feb;26(1):95-101
AD - Department of Diagnostic Radiology and Research Institute of
Radiological Science, Yonsei University College of Medicine, Seoul,
South Korea.
PURPOSE: The purpose of this work was to evaluate the radiologic
findings of gastrointestinal (GI) tract involvement in hepatocellular
carcinoma (HCC) and to discuss mechanisms of spread. METHOD: Eighteen
patients with histologically proven GI tract metastasis in HCC for 4.5
years underwent CT and five also underwent upper GI (UGI) series. The
cases were classified according to the mode of spread, based on the
radiologic findings. RESULTS: The involved portion of the GI tract was
the stomach (n = 11), duodenum (n = 4), and colon (n = 4). The mode of
spread was direct invasion from a contiguous primary tumor (n = 12),
hematogenous metastasis (n = 3), peritoneal seeding (n = 1), and
undetermined (n = 2). In cases of direct invasion from contiguous
primary tumors, CT revealed GI tract invasion directly from bulky
hepatic masses (n = 9) or daughter masses at the portion of the bowel
wall contiguous to the hepatic masses (n = 3). In cases of hematogenous
spread, CT revealed an intramural mass in the stomach and duodenum (n =
2) or a diffuse thickening of the wall of the stomach (n = 1). In the
case of peritoneal seeding, CT revealed multiple small nodules in the
right paracolic gutter, omentum, and mesentery with invasion to the
colon. CONCLUSION: GI tract involvement in HCC shows various radiologic
findings according to the mode of spread, but the most common finding is
direct invasion of the stomach, duodenum, or colon from contiguous
primary tumor.
27
UI - 11211858
AU - Hoption Cann SA; van Netten JP; van Netten C
TI -
MALT lymphomas and Helicobacter pylori?
SO - Gut 2001 Feb;48(2):283
28
UI - 9424909
AU - Polkowski W; Ciechanski A; Wallner G; Dabrowski A; Pawlowski A;
TI -
Chibowski D; Misiuna P
[Stomach and esophageal neoplasm. Changes over 16 years in clinical
materials]
SO - Wiad Lek 1997;50 Suppl 1 Pt 2():388-93
AD - Kliniki Chirurgii Ogolnej II Katedry Chirurgii, Akademii Medycznej w
Lublinie.
Increasing prevalence of adenocarcinoma of the esophagus and
esophago-gastric junction has been reported. The aim of the study was to
determine whether this phenomenon is reflected in the cohort of patients
referred for surgery to our institution. Clinical and pathological
records of patients with adenocarcinoma of the stomach (n = 433) or
gastro-esophageal junction (n = 302), and squamous cell carcinoma of the
esophagus (n = 266) were reviewed from 1981 to 1996. Yearly prevalence
of carcinoma of the gastric cardia in comparison to carcinoma of (a more
distal) stomach has not changed, ranging 19-46%. From 1981 to 1984 out
of 58 gastric resections, 14 (24%) total gastrectomies were done,
whereas from 1993 to 1996 total gastrectomies were performed in 104 out
of 138 (75%) patients with gastric cancer (p < 0.001). In the first 4
years of the study period adenocarcinoma of the cardia and/or esophagus
was found in 19% of all patients with esophageal and junctional tumors,
while in the last 4 years,-in 30%. Resection rates for gastric and
cardiac cancers have not changed significantly, 75-100% and 21-65%
respectively. Resection rate for carcinoma of the esophagus increased
from 50% (17/34) to 79% (53/67) (p = 0.006, test chi2). Increasing rate
of total gastrectomies can be explained by a trend towards more proximal
localisation of the primary gastric tumors and/or clinical application
of Lauren classification for the choice of operative procedure. Higher
resection rate for carcinoma of the esophagus is a result of increasing
experience of the surgical team, improvement in preoperative staging,
new palliative modalities, and application of preoperative
chemo-/radiotherapy.
29
UI - 11595470
AU - Farthing MJ; Fitzgerald R; Zhang ZW
TI -
Acid, helicobacter and immunity: a new paradigm for oesophagogastric
cancer.
SO - J Physiol Paris 2001 Jan-Dec;95(1-6):423-7
AD - Faculty of Medicine, University of Glasgow, 12, Southpark Terrace,
Glasgow GL12 8LG, UK. m.farthing@clinmed.gla.ac.uk
Epidemiological evidence has clearly shown a highly significant
relationship between Helicobacter pylori infection and the development
of duodenal ulcer and distal gastric adenocarcinoma. Despite H. pylori
being a common aetiological factor for both disorders, the two disease
phenotypes are virtually mutually exclusive. This indicates that the
host response to infection has a pivotal role in determining outcome;
these disease phenotypes relate to the effect of infection on gastric
acid secretion, duodenal ulcer being closely related to sustained acid
secretion whereas gastric cancer follows gastric atrophy and impaired
gastric acid secretion. Cancer at the oesophageal junction and that
associated with Barrett's oesophagus is now the most rapidly increasing
tumour in the gastrointestinal tract. The challenge for the next
millennium, therefore, is to try and develop methods for identifying
patients at risk of developing oesophagogastric cancer. A common feature
in the pathogenesis of both gastric and oesophageal adenoc
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