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Abramson Cancer Center 
NCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Gastric Cancer - April 2002
National Cancer Institute®
Ultima Vez Modificado: 1 de abril del 2002
Table of Contents
1
UI - 10950081
AU - Testino G; Valentini M; Cornaggia M
TI -
Helicobacter pylori and gastric cancer.
SO - Am J Gastroenterol 2000 Aug;95(8):2131-3
2
UI - 11197247
AU - Xia HH; Talley NJ
TI -
Apoptosis in gastric epithelium induced by helicobacter pylori
infection: implications in gastric carcinogenesis.
SO - Am J Gastroenterol 2001 Jan;96(1):16-26
AD - Department of Medicine, The University of Sydney, Nepean Hospital,
Penrith, NSW, Australia.
OBJECTIVES: Helicobacter pylori is an identified carcinogen for gastric
cancer, however, the underlying mechanisms remain to be defined. In this
review, we sought to elucidate the role of apoptosis in gastric
carcinogenesis, to determine the influence of H. pylori infection on
apoptosis, and finally to provide insights into the mechanisms by which
H. pylori may lead to gastric carcinogenesis. METHODS: A broad-based
MEDLINE and Current Contents literature search was performed to identify
infection, apoptosis, cell proliferation, gastric carcinoma, oncogenes,
and tumor suppressor genes, as well as the products of these genes.
Abstracts from recent major conferences that provided adequate
additional data were also included. RESULTS: Apoptotic cells are rare in
the glandular neck region (the generative cell zone) of normal gastric
mucosa. With progression of atrophic gastritis, the generative cell zone
shifts downward and a relatively large number of apoptotic cells occur.
In intestinalized glands, both apoptotic cells and proliferative cells
are present in deeper portions of the glands, corresponding to the
generative zone. A higher frequency of apoptosis has been observed in
gastric dysplasia than in coexisting gastric carcinomas, whereas the
number of proliferative cells is significantly higher in gastric
carcinoma than in dysplasia. Upregulation of oncogene bcl-2 in
premalignant lesions and "downregulation" of the gene after malignant
change is probably a common event. Accumulation of p53 protein is first
detected in dysplasia, although mutation of the pS3 gene may occur in
intestinal metaplasia. H. pylori infection induces apoptosis in gastric
epithelial cells, which returns to normal after eradication of the
infection. Numerous molecules produced by H. pylori including cytotoxin
(VacA), lipopolysaccharide, monochloramine, and nitric oxide may
directly induce apoptosis. Moreover, H. pylori-stimulated host
inflammatory/immune responses lead to release of a large amount of
cytokines. Cytokines produced by type 1 T helper cells, such as
TNF-alpha and IFN-gamma, markedly potentiate apoptosis. Gastric cell
proliferation is significantly higher in patients with H. pylori
infection than in normal controls, and eradication of the infection
leads to a reduction in cell proliferation. Apoptosis and cell
proliferation are also increased in precancerous lesions such as gastric
atrophy, intestinal metaplasia, and dysplasia in the presence of H.
pylori infection. However, H. pylori-induced apoptosis may no longer be
cell cycle-dependent in these lesions because of the occurrence of
alterations and mutations of apoptosis-regulating genes, resulting in a
loss of balance between apoptosis and cell proliferation. CONCLUSIONS:
It is hypothesized that H. pylori-induced apoptosis may play a key role
in gastric carcinogenesis by increasing cell proliferation and/or
resulting in gastric atrophy.
3
UI - 11686031
AU - Aiba K
TI -
Upper gastrointestinal tumors.
SO - Cancer Chemother Biol Response Modif 2001;19():535-45
AD - Japanese Foundation for Cancer Research, Cancer Chemotherapy Center,
Kami-Ikebukuro 1-37-1, Toshima-ku, Tokyo 170-8455, Japan.
4
UI - 11875724
AU - Cuschieri A; Talbot IC; Weeden S; MRC Upper GI Cancer Working Party
TI -
Influence of pathological tumour variables on long-term survival in
resectable gastric cancer.
SO - Br J Cancer 2002 Mar 4;86(5):674-9
AD - Department of Surgery and Molecular Oncology, Ninewells Hospital and
Medical School, University of Dundee, Dundee DD1 9SY, UK.
a.cuschieri@dundee.ac.uk
Although tumour stage and nodal status are established prognostic
factors for resectable gastric cancer, the relative importance of other
pathological characteristics remains unclear. This study reports
univariate and multivariate analyses of the prognostic value of various
pathological and staging factors based on 324 patients entered into the
MRC randomised surgical trial for gastric cancer. In the univariate
analysis tumour stage, nodal status, UICC clinical stage, number of
involved nodes, WHO predominant type, mixed Lauren type, Ming type,
tumour differentiation, lymphocytic and tumour stromal eosinophilic
infiltration were all found to have a significant impact on survival
(logrank test, 5% level). In the multivariate analysis, UICC clinical
stage and eosinophilic infiltration were found to have a significant
influence. Risk of death increased for UICC stage II and III patients
(Hazard Ratio for stage II compared to stage I=2.0, 95% Confidence
Interval (CI) 1.4-2.9; Hazard Ratio for stage III compared to stage
I=3.5, 95% CI 2.5-4.8). Patients with numerous eosinophils had a lower
risk of death than those with none (Hazard Ratio=0.5, 95% CI 0.3-0.8).
This association between survival and eosinophilic infiltration merits
further study. Copyright 2002 Cancer Research UK
5
UI - 11875729
AU - Burgess DE; Woodman CB; Flavell KJ; Rowlands DC; Crocker J; Scott K;
TI -
Biddulph JP; Young LS; Murray PG
Low prevalence of Epstein-Barr virus in incident gastric adenocarcinomas
from the United Kingdom.
SO - Br J Cancer 2002 Mar 4;86(5):702-4
AD - Department of Pathology, Division of Cancer Studies, The Medical School,
University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Epstein-Barr virus has been associated with a proportion of typical
gastric adenocarcinomas. Here we report that the prevalence of
Epstein-Barr virus in gastric adenocarcinomas from the United Kingdom is
one of the lowest in the World. Gastric adenocarcinoma is another tumour
whose association with Epstein-Barr virus varies with the population
studied. Copyright 2002 Cancer Research UK
6
UI - 11875736
AU - Krieg A; Mahotka C; Krieg T; Grabsch H; Muller W; Takeno S; Suschek CV;
TI -
Heydthausen M; Gabbert HE; Gerharz CD
Expression of different survivin variants in gastric carcinomas: first
clues to a role of survivin-2B in tumour progression.
SO - Br J Cancer 2002 Mar 4;86(5):737-43
AD - Institute of Pathology, Heinrich Heine-University, Moorenstr 5, D-40225,
Duesseldorf, Germany.
Survivin is a novel member of the inhibitor of apoptosis family and
determines the susceptibility of tumour cells to pro-apoptotic stimuli.
Recently, we identified two novel alternative splice variants of
survivin, differing in their anti-apoptotic properties: whereas the
anti-apoptotic potential of survivin-DeltaEx3 is preserved, survivin-2B
has lost its anti-apoptotic potential and may act as a naturally
occurring antagonist of survivin. Because the in vivo expression of
these alternative splice variants has not been explored so far, we
analysed gastric carcinomas of different histological subtypes, grades
and stages. Since no antibodies are currently available to determine the
novel splice variants, quantitative reverse transcriptase polymerase
chain reaction was performed, using RNA samples obtained from 30
different gastric carcinomas. Polymerase chain reactions products were
quantified by densitometric evaluation. We found that all gastric
carcinomas, irrespective of their histological types, grades or stages,
express survivin-DeltaEx3, survivin-2B and survivin, the latter being
the dominant transcript. Comparing the disease stages I+II with III+IV,
expression of survivin and survivin-DeltaEx3 remained unchanged. In
contrast, a significant (P=0.033) stage-dependent decrease in the
expression of survivin-2B became evident. Our study demonstrates for the
first time the expression of alternative splice variants in gastric
carcinomas and provides a first clue to a role of survivin-2B in tumour
progression. Copyright 2002 Cancer Research UK
7
UI - 11891177
AU - Kang GH; Lee S; Kim WH; Lee HW; Kim JC; Rhyu MG; Ro JY
TI -
Epstein-barr virus-positive gastric carcinoma demonstrates frequent
aberrant methylation of multiple genes and constitutes CpG island
methylator phenotype-positive gastric carcinoma.
SO - Am J Pathol 2002 Mar;160(3):787-94
AD - Department of Pathology, Seoul NationalUniversity College of Medicine
and Cancer Research Institute, Seoul, Korea. ghkang@snu.ac.kr
CpG island methylation is an important mechanism for inactivating the
genes involved in tumorigenesis. Gastric carcinoma (GC) is one of the
tumors that exhibits a high frequency of aberrant CpG island
methylation. There have been many reports suggesting a close link
between Epstein-Barr virus (EBV) and the development of GC. However,
little is known about the oncogenic mechanism of EBV in gastric
carcinogenesis. Twenty-one cases of EBV-positive GC and 56 cases of
EBV-negative GC were examined for aberrant DNA methylation of the CpG
islands of 19 genes or loci and the differences in the methylation
frequency between EBV-positive and -negative GCs were investigated to
determine a role of aberrant methylation in EBV-related gastric
carcinogenesis. The average number of methylated genes or loci was
higher in EBV-positive GCs than in EBV-negative GCs (13.4 versus 7.8,
respectively, P < 0.001). EBV-positive GCs showed methylation in at
least 10 CpG islands (52.6% of the tested genes), whereas 62.5% of
EBV-negative GCs showed methylation in <10 CpG islands. THBS1, APC, p16,
14-3-3 sigma, MINT1, and MINT25 were methylated at a frequency >90% in
EBV-positive GCs. The methylation frequency difference in the respective
CpG islands between EBV-positive and -negative GCs was statistically
significant (P < 0.05). Among these genes or loci, the methylation
frequency of p16 in the EBV-positive GCs was more than three times
higher than in the EBV-negative GCs. The PTEN, RASSF1A, GSTP1, MGMT, and
MINT2 were methylated in EBV-positive GCs at a frequency of more than
three times that of the EBV-negative GCs. These results demonstrate a
relationship between EBV and aberrant methylation in GC and suggest that
aberrant methylation may be an important mechanism of EBV-related
gastric carcinogenesis.
8
UI - 11906123
AU - Kim H; Takashima S; Kaminou T; Hayashi S; Nishida N; Matsuoka T;
TI -
Nakamura K; Yamada R
Clinical studies on the visualization of gastric lesions using virtual
CT endoscopy.
SO - Osaka City Med J 2001 Dec;47(2):115-26
AD - Department of Radiology, Osaka City University Medical School, Osaka,
Japan.
OBJECTIVE: We evaluated the clinical usefulness of virtual CT
gastroendoscopy (VCTGE). METHODS: The subjects were 124 patients with
endoscopically identified gastric lesions. VCTGE images were obtained
using a GE-Navigator. We evaluated VCTGE in the visualization of gastric
lesions for their presence and morphology. RESULTS: The detection rate
of all gastric lesions by VCTGE was 76% (94 of 124 patients). The
smallest detectable early gastric cancer was II c measuring 10 x 8 mm.
The detection rates of each gastric lesion by VCTGE were 73% in early
gastric cancer, and 90% in advanced gastric cancer. VCTGE imaging in the
advanced gastric cancer was good in 12 (30%), fair in 25 (60%) and poor
in 4 (10%). VCTGE imaging in early gastric cancer was good in 20 (46%),
fair in 12 (27%) and poor in 12 (27%). The significance P level was
0.005 between the evaluation of the imaging of advanced and early
gastric cancer. CONCLUSIONS: VCTGE visualized the characteristics of
diverse gastric lesions and was considered useful for the detection and
the diagnosis of these lesions.
9
UI - 10049413
AU - Kolve M; Fischbach W; Greiner A; Wilms K
TI -
Differences in endoscopic and clinicopathological features of primary
and secondary gastric non-Hodgkin's lymphoma. German Gastrointestinal
Lymphoma Study Group.
SO - Gastrointest Endosc 1999 Mar;49(3 Pt 1):307-15
AD - Medizinische Poliklinik, University of Wurzburg, Germany.
BACKGROUND: Lymphomatous neoplasia of the stomach is initially seen
either as primary gastric B-cell lymphoma of the mucosa-associated
lymphoid tissue (MALT) or as nodal non-Hodgkin s lymphoma (NHL)
secondarily involving the GI tract. One hundred seventy-six patients
with primary gastric NHL (low grade, n = 65; high grade, n = 111) and 29
with secondary gastric NHL (low grade, n = 19; high grade, n = 10) were
studied to evaluate whether differences in pathogenesis are associated
with distinct clinical and endoscopic features. METHODS: Clinical
features, tumor size, localization, and growth pattern were analyzed by
means of esophagogastroduodenoscopy; grading was determined with
histologic examination. RESULTS: The analysis of various clinical
symptoms and endoscopic findings revealed a relationship between the
occurrence of abdominal pain, vomiting, and unifocal growth pattern with
an affiliation to the group with primary gastric NHL (p < 0.001),
whereas tumor localization in the gastric fundus was predominantly found
in secondary gastric NHL (p < 0.001). An equation has been generated
that may help to predict affiliation to primary or secondary gastric NHL
with an accuracy of 96%. CONCLUSIONS: Our results indicate that careful
pretreatment analysis of clinical and endoscopic findings may be helpful
in the diagnosis of primary or secondary gastric involvement by NHL,
although reliable discrimination still requires histologic verification.
10
UI - 10882989
AU - Tursi A
TI -
Difficulties in differentiating endoscopically primary from secondary
gastric non-Hodgkin's lymphoma.
SO - Gastrointest Endosc 2000 Jul;52(1):146-8
11
UI - 11484286
AU - Belchev B
TI -
[Esophagojejunostomy after Roux following gastrectomy for cancer of the
stomach]
SO - Khirurgiia (Sofiia) 2000;56(2):36-7
Not big number of cases (17) operated for cardia cancer are subject of
retrospective analyzing. Ezophagoejunoanastomosis by termino-lateral
plastic, type of Roux is realized in more of cases (9). Termino-terminal
junction and this after proximal gastric resection performed on hand,
are subject of discussion.
12
UI - 11852408
AU - Huntsman D; Carneiro F; Lewis F; MacLeod P; Hayashi A; Monaghan K; Maung
TI -
R; Seruca R; Jackson C; Caldas C
[Prophylactic gastrectomy in patients with deleterious E-cadherin gene
mutation]
SO - Gastroenterol Clin Biol 2001 Oct;25(10):931-2
AD - Hopital Europeen Georges-Pompidou, Paris, France.
13
UI - 11902529
AU - Du MQ; Isaccson PG
TI -
Gastric MALT lymphoma: from aetiology to treatment.
SO - Lancet Oncol 2002 Feb;3(2):97-104
AD - Department of Histopathology, Royal Free and University College Medical
School, University College London, UK. m.du@ucl.ac.uk
The development of gastric mucosa-associated lymphoid tissue (MALT)
lymphoma is dependent on Helicobacter pylori infection. Bacterial
colonisation of the gastric mucosa triggers lymphoid infiltration and
the formation of acquired MALT. The bacterial infection induces and
sustains an actively proliferating B-cell population through direct
(autoantigen) and indirect (intratumoral T cells specific for H. pylori)
immunological stimulation. Moreover, the bacterial infection provokes a
neutrophilic response, which causes the release of oxygen free radicals.
These reactive species may promote the acquisition of genetic
abnormalities and malignant transformation of reactive B cells. A
transformed clone carrying the translocation t(1;18)(q21;q21) forms a
MALT lymphoma, the growth of which is independent of H. pylori and will
not respond to bacterial eradication. Malignant clones without
t(11;18)(q21;q21), but with other genetic abnormalities, such as trisomy
3 or microsatellite instability, depend critically on immune stimulation
mediated by H. pylori for their clonal expansion. In the early stages,
the tumour can be successfully treated by eradication of the bacterium,
whereas at later stages the tumour may escape its growth dependency
through acquisition of additional genetic abnormalities such as
t(1;14)(p22;q32) and t(1;2)(p22,p12) involving the BCL-10 gene. Finally,
further genetic abnormalities, such as inactivation of the tumour
suppressor genes, p53 and p16, can lead to high-grade transformation.
Detection of these abnormalities may help with the clinical management
of patients with gastric MALT lymphoma.
14
UI - 11896205
AU - Laghi L; Ranzani GN; Bianchi P; Mori A; Heinimann K; Orbetegli O; Spaudo
TI -
MR; Luinetti O; Francisconi S; Roncalli M; Solcia E; Malesci A
Frameshift mutations of human gastrin receptor gene (hGARE) in
gastrointestinal cancers with microsatellite instability.
SO - Lab Invest 2002 Mar;82(3):265-71
AD - Division of Gastroenterology, Istituto Clinico Humanitas, Rozzano-Milan,
Italy.
Gastrointestinal tumors with DNA mismatch repair (MMR) defects show
microsatellite instability (MSI) and harbor frameshift mutations in
coding mononucleotide repeats of cancer-related genes (targets). We
assessed MSI status in 233 sporadic gastrointestinal tumors. We
classified as MSI-H (high-frequency microsatellite instability) 15 (10%)
of 150 colorectal cancers and 13 (16%) of 83 gastric cancers. We
searched for frameshift mutations in a coding poly(T)(8) tract within
the gastrin receptor gene (hGARE), which has a potential role in
gastrointestinal carcinogenesis. To this purpose, we screened 43
unstable tumors (including 15 hereditary nonpolyposis colorectal cancer
cases previously classified as MSI-H), 98 stable tumors, as well as 3
MMR-deficient and 4 MMR-proficient gastrointestinal cancer cell lines.
We found mutations in 8 (19%) of the 43 MSI-H tumors but in none of the
98 stable cancers. hGARE mutation frequency was similar in gastric (23%)
and colorectal cancers, including sporadic (13%) and hereditary (20%)
cases. All mutated tumors proved to harbor frameshift mutations in other
cancer-related genes that are considered as targets in MSI
tumorigenesis. The MMR-deficient and gastrin-sensitive LoVo colorectal
cancer cells also showed a hGARE heterozygous frameshift mutation, but
expressed only the mutated allele. All detected mutations can be
predicted to generate a truncated protein carrying amino acid changes.
On the basis of genetic findings, we propose hGARE as a new candidate
target gene in MSI tumorigenesis. Functional studies are warranted to
elucidate the mechanism by which the hGARE mutation might contribute to
gastrointestinal carcinogenesis.
15
UI - 11896207
AU - Kang YH; Lee HS; Kim WH
TI -
Promoter methylation and silencing of PTEN in gastric carcinoma.
SO - Lab Invest 2002 Mar;82(3):285-91
AD - Cancer Research Institute, Seoul National University College of Medicine
and BK21 Project for Medicine, Dentistry and Pharmacy, Seoul, Korea.
The PTEN/MMAC1/TEP1 gene (phosphatase and tensin homolog deleted on
chromosome 10/mutated in multiple advanced cancers/TGF-beta regulated
and epithelial cell enriched phosphatase 1), which regulates the
signaling pathways of Akt, is a novel tumor suppressor gene implicated
in multiple cancers. Because a number of tumor suppressor genes are
known to be silenced by aberrant promoter methylation, we examined the
methylation status of the 5' CpG islands of PTEN using
methylation-specific PCR. The altered expression of PTEN in 310 gastric
carcinomas was analyzed by immunohistochemical staining using
tissue-array and clinicopathologic profiles related to PTEN expression
were characterized. Of 310 consecutive gastric carcinomas, 62 cases
(20%) showed expression loss of PTEN. Altered PTEN expression was
significantly associated with tumor depth and size, lymphatic invasion,
advanced stage, pTNM stage, and patient survival (p < 0.001). The
promoter methylation frequency of PTEN was found to be present in 26
(39%) of 66 cases examined, and 19 (73%) of 26 gastric cancer tissues
showing promoter methylation exhibited the loss of PTEN expression.
Abnormalities in the expression of PTEN significantly correlated with
promoter methylation (p < 0.001). In conclusion, silencing of the PTEN
gene occurs frequently in gastric carcinoma and aberrant promoter
methylation is a major mechanism of silencing of the PTEN gene. The
abnormalities of the PTEN gene are associated with tumor progression,
metastasis, and survival.
16
UI - 11695220
AU - Kikuchi S; Matsuzaki H; Kurita A; Kobayashi N; Shimao H; Sakakibara Y;
TI -
Sato K; Kakita A
Tumor volume as an indicator of nodal status in advanced gastric
carcinoma.
SO - In Vivo 2001 Jul-Aug;15(4):295-8
AD - Department of Surgery, School of Medicine, Kitasato University, 1-15-1,
Kitasato, Sagamihara-shi, Kanagawa 228, Japan.
BACKGROUND: The significance of tumor volume as an indicator of lymph
node metastasis in advanced gastric cancer remains to be clarified.
MATERIALS AND METHODS: Tumor volume was measured from continuous tissue
sections taken from 60 patients with advanced gastric cancer (34 males
and 26 females, aged 35 to 81 years; average 57.3 years) using a
computer generated surface rendering method. The tumor volume and
conventional clinicopathological factors were then analyzed with respect
to the prevalence of lymph node metastasis. RESULTS: Lymph node
metastasis was detected in 26 patients (43%). Of 28 patients with a
tumor > or = 2000 mm3, lymph node metastasis was observed in 17 patients
(61%): n1, 12 patients; n2, 3 patients; n3, 2 patients. Of 32 patients
with a tumor < 2000 mm3, lymph node metastasis was observed in 9
patients (28%): n1, 6 patients; n2, 3 patients. A significant difference
was found in the prevalence of lymph node metastasis between the two
groups (p = 0.011). Furthermore, only tumor volume was an independent
variable associated with lymph node metastasis according to logistic
regression analysis (p = 0.013, odds ratio: 0.253, 95% confidence
interval: 0.086-0.747). CONCLUSION: Tumor volume appears to be an
important indicator of lymph node metastasis in advanced gastric cancer.
However, this factor cannot be used to introduce the option of limited
lymphadenectomy for such patients.
17
UI - 11788899
AU - Saitoh T; Mine T; Katoh M
TI -
Up-regulation of WNT8B mRNA in human gastric cancer.
SO - Int J Oncol 2002 Feb;20(2):343-8
AD - Genetics and Cell Biology Section, Genetics Division, National Cancer
Center Research Institute, Tokyo 104-0045, Japan.
WNT - beta-catenin - TCF signaling pathway is activated by Xenopus wnt-8
(Xwnt-8) during Xenopus early development, and dysregulated activation
of beta-catenin - TCF signaling pathway in mammalian cells leads to
carcinogenesis. We have previously cloned and characterized human WNT8A,
one of human orthologues of Xwnt-8. Here, we cloned and characterized
human WNT8B by using bioinformatics, cDNA-PCR, and RACE. WNT8B gene of
about 23-kb in size consisted of six exons, and encoded a 351-amino-acid
polypeptide with the N-terminal signal peptide and two N-linked
glycosylation sites. C-terminal region of WNT8B, WNT8A, WNT2, and WNT2B
were longer than that of other human WNTs. Thirty-five nucleotide
changes between WNT8B isolated by us and WNT8B isolated by another group
resulted in Gly230Ala and Arg284Leu amino-acid substitutions. Gly230 and
Arg284 of WNT8B were conserved in WNT8A. Gly230-Arg284 WNT8B allele was
also identified in human genome draft sequences AL133352.10,
AL359759.18, and human EST BF732616. These results indicate that the
Gly230-Arg284 WNT8B cDNA isolated in this study is derived from the more
common WNT8B allele. WNT8B mRNAs of 4.4- and 3.5-kb in size were weakly
detected in a colorectal cancer cell line SW480, but were undetectable
in any normal human tissues by using Northern blot analyses. WNT8B was
significantly up-regulated in gastric cancer cell lines KATO-III
(signet-ring cell carcinoma) and MKN45 (poorly differentiated
adenocarcinoma), and also in 5 out of 10 cases of primary gastric
cancer. WNT8B might play key roles in gastric cancer through activation
of the beta-catenin - TCF signaling pathway.
18
UI - 11865368
AU - Ichikura T; Morita D; Uchida T; Okura E; Majima T; Ogawa T; Mochizuki H
TI -
Sentinel node concept in gastric carcinoma.
SO - World J Surg 2002 Mar;26(3):318-22
AD - Department of Surgery I, National Defense Medical College Hospital, 3-2
Namiki, Tokorozawa 359-8513, Japan.
To assess the applicability of the sentinel node concept to gastric
carcinoma. The location of metastatic lymph nodes was analyzed
retrospectively in 119 patients with gastric carcinoma in whom
metastasis was limited to one or two nodes. Intraoperative lymphatic
mapping was attempted in 62 patients using indocyanine green injected
endoscopically into the gastric submucosa adjacent to the tumor.
Metastatic lymph nodes were distributed beyond the perigastric area in
4% of patients with a single node involved. The positive node was
located along the greater curvature in 21% of the patients with a tumor
on the lesser curvature. Two patients had a metastatic node totally
occupied by cancer tissue. In 16% of patients with two nodes involved, a
positive node was located on both the lesser and greater curvatures.
Lymphatic mapping was successful in all subjects. A larger number and
wider distribution of green-stained nodes were observed in patients
injected with 8 ml of indocyanine green solution than in those injected
with 4 ml. No metastasis was observed in any nodes in 47 (96%) of the 49
patients who had no metastasis in green nodes. In one patient showing
metastasis in non-green nodes without metastasis in green nodes, the
positive nodes were totally occupied by cancer tissue. Our results
showed the complexity of lymphatic streams within and from the stomach.
Lymphatic mapping using indocyanine green can be a tool for identifying
sentinel nodes in gastric carcinoma although lymph nodes occupied by
cancer tissue may not be detected by this technique.
19
UI - 11865369
AU - Hyung WJ; Noh SH; Yoo CH; Huh JH; Shin DW; Lah KH; Lee JH; Choi SH; Min
TI -
JS
Prognostic significance of metastatic lymph node ratio in T3 gastric
cancer.
SO - World J Surg 2002 Mar;26(3):323-9
AD - Department of Surgery, Yonsei University College of Medicine, 134
Shinchon-dong, Seodaemun-ku, 120-752 Seoul, Korea.
The fifth International Union Against Cancer tumor node metastasis (UICC
TNM) classification, based on the number of metastatic lymph nodes (LN),
has proved to be a reliable and objective method for predicting the
prognosis of patients with gastric cancer. However, the prognosis of
patients with T3 gastric cancer is still heterogeneous. This study was
carried out to investigate the validity of metastatic LN ratio as a
prognostic factor in T3 gastric cancer. A retrospective analysis was
performed on a total of 833 patients that had either T3N1M0 (n = 504) or
T3N2M0 (n = 329) gastric cancer by the fifth UICC classification. A
preliminary analysis revealed the cutoff values for T3N1M0 to be 10% and
for T3N2M0 to be 25%. The mean metastatic LN ratio was 9.0% for T3N1M0
cancer and 26.9% for T3N2M0 cancer. For the T3N1M0 stage, the patients
who showed less than 10% of the metastatic LN ratio were grouped as
N1-low with the others grouped as N1-high. For the T3N2M0 stage group,
those who had less than 25% of the metastatic LN ratio were grouped as
N2-low, the remainder as N2-high. The metastatic LN ratio decreased in
proportion to the extent of lymphadenectomy and it increased in relation
to the increasing scale of the fourth N classification. The rates of
recurrence were significantly different according to the metastatic LN
ratio in N1 and N2 classification of the fifth UICC classification (p <
0.05). The 5-year survival rates after gastrectomy decreased
significantly by increasing the metastatic LN ratio in both T3N1M0
cancers (p =0.0026) and T3N2M0 cancers (p = 0.0057). The metastatic LN
ratio was an independent risk factor for recurrence and poor prognosis.
Our data suggest that the metastatic LN ratio is a significant
prognostic factor for T3 gastric cancer. Furthermore, the application of
the metastatic LN ratio can provide information not only about the
extent of LN metastasis but also about the extent of lymphadenectomy in
T3 gastric cancer.
20
UI - 11865370
AU - Nogueira C; Silva AS; Santos JN; Silva AG; Ferreira J; Matos E; Vilaca H
TI -
Early gastric cancer: ten years of experience.
SO - World J Surg 2002 Mar;26(3):330-4
AD - Surgery Department, Surgery 1, Hospital Geral de Santo Antonio, Largo
Prof. Abel Salazar, 4000 Oporto, Portugal. carlosnog2001@yahoo.com
Gastric cancer is a disease in which the main treatment is surgical
extirpation. The modifications introduced in the surgical treatment over
the last decades were accompanied by a clear increase of survival, which
reaches global values of 61% at 5 years in Japan. One of the reasons
that contribute to this improvement is early diagnosis of the lesions.
In the period between January 1, 1990 and December 31, 1999 662 patients
with gastric adenocarcinoma were treated in the Service of Surgery 1 of
our hospital; 110 were refused surgical treatment. Of the resected
patients, 91 (21.4%) were classified as early gastric cancer according
to the definition of the Japanese Society of Digestive Endoscopy. There
were 30 women and 61 men, with a median age of 60.2 +/- 15 years; 3
patients had a preoperative diagnosis of gastric ulcer; 2 others were
operated without recent histology; and 1 patient was urgently resected
for a bleeding ulcer. In all the remaining patients biopsy confirmed the
presence of cancer (89%) or serious dysplasia (4.6%). The lesions had
been distributed essentially in the medium 1/3 (48.3%) and distal 1/3 of
the stomach. Subtotal gastrectomy was accomplished in 48 patients, total
gastrectomy in 40, total desgastrogastrectomy in 3, and in 9 patients
the surgery involved the spleen (8 patients) and the spleen and tail of
the pancreas in 1 patient. Lymphadenectomy was not performed in 5
patients, lymph nodes by the first lymph node barrier were removed in 25
patients and by the second barrier in 61 patients (67%). Median tumor
size was 26 +/- 1.8 mm. The lesion reached the mucosa in 46 patients and
the mucosa and submucosa in 45. In 6 patients the removed lymph nodes
were microscopically invaded (6.7%). Five patients died (5.7%). The
median follow-up of the patients is 41 +/- 26 months; 7 patients died
(8.1%) during this period; 4 died unequivocally of disease progression.
The median survival of patients was 85% at 5 years and 80% at 10 years.
In our series, survival was affected by the presence of invaded lymph
nodes, not by the penetration in depth of the lesion or the size of the
tumor.
21
UI - 11911346
AU - Sato Y; Iwafuchi M; Ueki J; Yoshimura A; Mochizuki T; Motoyama H;
TI -
Sugimura K; Honma T; Narisawa R; Ichida T; Asakura H; Van T
Gastric carcinoid tumors without autoimmune gastritis in Japan: a
relationship with Helicobacter pylori infection.
SO - Dig Dis Sci 2002 Mar;47(3):579-85
AD - Third Department of Internal Medicine, Faculty of Health Science,
Niigata University School of Medicine, Japan.
In Japan, most cases of gastric carcinoid tumor (GCT) are unassociated
with either autoimmune gastritis (AIG) showing type-A chronic atrophic
gastritis (CAG-A) or Zollinger-Ellison syndrome (ZES). However, the
pathogenesis of this tumor remains unknown. Recent studies have
determined that Helicobacter pylori infection induces gastric carcinoid
in Mongolian gerbils and that H. pylori lipopolysaccharide exerts a
mitogenic effect on ECL cells. We examined five patients with
histologically diagnosed GCT, 40 patients with H. pylori-positive
gastric ulcer (Hp+GU), 24 patients with H. pylori-positive duodenal
ulcer (Hp+DU), and 12 patients with AIG showing CAG-A topographically.
We compared the prevalence of H. pylori infection, and the levels of
gastrin and pepsinogen (PG) in the serum of patients with GCT with those
of patients with Hp+GU, or Hp+DU, and AIG. We also investigated the
histological characteristics of the tumor and the gastric corpus mucosa
in the GCT patients. The levels of serum gastrin and PG I and II were
measured using an RIA kit. In all five (100%) patients with GCT, H.
pylori infection was present, without any evidence of AIG or ZES. The
serum levels of gastrin in the GCT patients were higher than those in
either Hp+GU or Hp+DU patients and lower than those in the AIG patients.
In contrast, serum PG I levels and the PG I/II ratio were lower in the
GCT group than in the Hp+GU or Hp+DU groups. Histologically, all GCTs
were ECL cell tumors and peritumoral corporal mucosal atrophy was
observed in four of the five patients with GCT. In conclusions, H.
pylori infection and hypergastrinemia were found in the patients with
GCT without AIG. This finding suggests that H. pylori infection may
induce corporal mucosal atrophy and hypergastrinemia that can produce a
GCT with time.
22
UI - 11565793
AU - Sinha P; Poland J; Schnolzer M; Celis JE; Lage H
TI -
Characterization of the differential protein expression associated with
thermoresistance in human gastric carcinoma cell lines.
SO - Electrophoresis 2001 Aug;22(14):2990-3000
AD - Institut fur Laboratoriumsmedizin und Pathobiochemie,
Universitatsklinikum Charite, Berlin, Germany. pranav.sinha@charite.de
Resistance to chemotherapeutic agents is one of the major problems faced
during palliative therapy of tumor cells. Thus, chemotherapy is
frequently combined with other modes of therapy such as radiation
therapy and/or hyperthermia. Tumor cells respond to heat stress with
development of thermotolerance and the interactions between chemo- and
thermoresistance phenomena are not clearly understood. In this paper, we
analyze the differential protein expression in vitro in human stomach
cancer cells, their chemoresistant and thermoresistant counterparts
using proteomics. The immediate aim was to identify sets of proteins
that may lead to the development of thermoresistance. Based on these
results, we aim to develop functional tests and methods for the
modulation of thermoresistance and chemoresistance phenomena that may
assist the therapy of inoperable cancers.
23
UI - 11869324
AU - Flett ME; Lim MN; Bruce D; Campbell SH; Park KG
TI -
Prognostic value of laparoscopic ultrasound in patients with
gastro-esophageal cancer.
SO - Dis Esophagus 2001;14(3-4):223-6
AD - Department of Surgery, Aberdeen Royal Infirmary, Foresterhill, Aberdeen,
UK.
Forty-four patients with gastro-esophageal tumors regarded as resectable
by conventional staging underwent laparoscopic ultrasonography (LUS).
Following LUS, seven were found to be irresectable and were managed by
palliative therapies. Thirty-seven patients proceeded to surgical
exploration and 36 were resected (R0 80%, R1 11%, and R2 9%). All
patients were reviewed until death or for a minimum of 24 months.
Patients undergoing resection had a 62% 1-year survival (median 17
months; confidence intervals, CI 6-28). LUS defined nodal status
indicated a trend toward prolonged survival in the node-negative group,
median 22 months (CI 5-39), compared with 13 months (CI 6-20) in the
node-positive group. Disease-free survival was greater in LUS
node-negative patients at 29 months (CI 23-35) compared with
node-positive patients at 13 months (CI 5-21) P=0.0083. LUS staging
allows prediction of the likelihood of recurrence of gastro-esophageal
malignancies. This may prove useful for the appropriate allocation of
patients to primary and adjuvant therapies.
24
UI - 11054376
AU - Fischbach W; Dragosics B; Kolve-Goebeler ME; Ohmann C; Greiner A; Yang
TI -
Q; Bohm S; Verreet P; Horstmann O; Busch M; Duhmke E; Muller-Hermelink
HK; Wilms K; Allinger S; Bauer P; Bauer S; Bender A; Brandstatter G;
Chott A; Dittrich C; Erhart K; Eysselt D; Ellersdorfer H; Ferlitsch A;
Fridrik MA; Gartner A; Hausmaninger M; Hinterberger W; Hugel K; Ilsinger
P; Jonaus K; Judmaier G; Karner J; Kerstan E; Knoflach P; Lenz K;
Kandutsch A; Lobmeyer M; Michlmeier H; Mach H; Marosi C; Ohlinger W;
Oprean H; Pointer H; Pont J; Salabon H; Samec HJ; Ulsperger A; Wimmer A;
Wewalka F
Primary gastric B-cell lymphoma: results of a prospective multicenter
study. The German-Austrian Gastrointestinal Lymphoma Study Group.
SO - Gastroenterology 2000 Nov;119(5):1191-202
AD - Medizinische Klinik II, Klinikum Aschaffenburg, Aschaffenburg, Germany.
BACKGROUND & AIMS: Appropriate management of primary gastric lymphoma is
controversial. This prospective, multicenter study aimed to evaluate the
accuracy of endoscopic biopsy diagnosis and clinical staging procedures
and assess a treatment strategy based on Helicobacter pylori status and
tumor stage and grade. METHODS: Of 266 patients with primary gastric
B-cell lymphoma, 236 with stages EI (n = 151) or EII (n = 85) were
included in an intention-to-treat analysis. Patients with H.
pylori-positive stage EI low-grade lymphoma underwent eradication
therapy. Nonresponders and patients with stage EII low-grade lymphoma
underwent gastric surgery. Depending on the residual tumor status and
predefined risk factors, patients received either radiotherapy or no
further treatment. Patients with high-grade lymphoma underwent surgery
and chemotherapy at stages EI/EII, complemented by radiation in case of
incomplete resection. RESULTS: Endoscopic-bioptic typing and grading and
clinical staging were accurate to 73% and 70%, respectively, based on
the histopathology of resected specimens. The overall 2-year survival
rates for low-grade lymphoma did not differ in the risk-adjusted
treatment groups, ranging from 89% to 96%. In high-grade lymphoma,
patients with complete resection or microscopic tumor residuals had
significantly better survival rates (88% for EI and 83% for EII) than
those with macroscopic tumor residues (53%; P < 0.001). CONCLUSIONS:
There is a considerable need for improvement in clinical diagnostic and
staging procedures, especially with a view toward nonsurgical treatment.
With the exception of eradication therapy in H. pylori-positive
low-grade lymphoma of stage EI and the subgroup of locally advanced
high-grade lymphoma, resection remains the treatment of choice. However,
because there is an increasing trend toward stomach-conserving therapy,
a randomized trial comparing cure of disease and quality of life with
surgical and conservative treatment is needed.
25
UI - 11885923
AU - Jedrychowski W; Popiela T; Steindorf K; Tobiasz-Adamczyk B; Kulig J;
TI -
Penar A; Wahrendorf J
Nutrient intake patterns in gastric and colorectal cancers.
SO - Int J Occup Med Environ Health 2001;14(4):391-5
AD - Collegium Medicum, Jagiellonian University, Cracow, Poland.
myjedryc@cyf-kr.edu.pl
The purpose of the study was to present the dietary risk pattern in
gastric and colorectal cancers, using the same methodological approach
in a parallel hospital-based case-control study. In all, 180 cases of
colorectal cancer and 80 cases of stomach cancer, confirmed
histopathologically, were enrolled from the University Hospital in
Cracow. A high intake of carbohydrates was associated with an increased
risk of colorectal cancer (OR = 2.45). For stomach cancer, a moderate
consumption of carbohydrates markedly increased relative risk (OR =
4.29), while a high intake of carbohydrates increased the risk by 8.73.
The patterns of dietary risk factors related to intake of fats were
definitively different in both cancer sites. The higher fat consumption
was not associated with the higher risk of stomach cancer. A medium
intake of fats increased the risk of colorectal cancer by 1.96 and that
above 83 g/day by 2.20. In colorectal cancer, the significant protective
effect of retinol, carotene and vitamin C has been evidenced, however,
only carotene and vitamin E were inversely correlated with stomach
cancer.
26
UI - 11888878
AU - Yasuda K; Inomata M; Fujii K; Shiraishi N; Adachi Y; Kitano S
TI -
Superficially spreading cancer of the stomach.
SO - Ann Surg Oncol 2002 Mar;9(2):192-6
AD - Department of Surgery I, Oita Medical University, Oita, Japan.
kyasuda@oita-med.ac.jp
BACKGROUND: Superficially spreading cancer (SSC) of the stomach is rare
and extends widely along the mucosa or submucosa of the stomach. This
study was conducted to clarify the clinicopathologic characteristics and
prognosis of patients with SSC. METHODS: SSC was defined as a tumor
invading the mucosa or submucosa and measuring > or =5 cm in size. The
clinicopathologic findings and outcomes of 36 patients with SSC were
compared with those of 300 patients with early gastric cancer (EGC)
measuring < or =5 cm and 271 with advanced gastric cancer measuring > or
=5 cm. RESULTS: SSC was significantly different from ordinary EGC in
tumor size, frequency of lymph node metastasis, lymphatic invasion,
venous invasion, and stage II, III, and IV disease. The frequency of
serosal invasion, lymph node metastasis, and lymphatic and venous
invasions in cases of SSC was significantly lower than with advanced
gastric cancer. Although tumor size of SSC evaluated before operation
was smaller than that on the resected specimen, the 10-year survival
rate was not different between SSC and ordinary EGC. CONCLUSIONS: SSC
was characterized by high frequency of lymp
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