helicobacter pylori and risk of gastric cancer and ... filehypothesis hp gastritis risk of cancer...
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Falk Symposium 149Highlights in
Gastrointestinal OncologyBerlin, October 1-2, 2005
Helicobacter pylori and risk ofgastric cancer and lymphoma
W. FischbachAschaffenburg, Germany
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Helicobacter pylori
Peptic ulcer
MALT lymphoma gastric cancer
dyspepsiaExtragastricdiseases
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Helicobacter pyloriis a crucial factor in the pathogenesis
of gastric cancer
Helicobacter pyloriis a group I carcinogene
WHO 1994
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Helicobacter pylori and gastric cancerEvidence for an association
• Epidemiology• Induction of gastritis, atrophy, IM• Ascorbin acid• Hyperproliferation• O2-radicals, NO• Hypochlorhydria, hypergastrinemia• Animal studies• Observational studies• Interventional studies
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Hp and risk of gastric cancerMetaanalysis of prospective case-control-studies
Danesh, Aliment Pharmacol Ther
Further increase of risk by 1.6 in case of cagA +Huang, Gastroenterology 2003
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Population based case-control study
More than 2/3 of non-cardia cancerare attributable to Helicobacter pylori
Ekstrom, Gastroenterology 2001
Hp and risk of gastric cancer
case-control study with rigorous exclusion criteria
OR of non-cardia cancer:3.7 18.3 for any Hp5.7 28.4 for CagA +
Brenner, Am J Epidemiol 2004
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Hp and risk of gastric cancerFamilial cancer risk and Hp
German Health and Nutrition Survey1351 male and female, age 30-74 years
0
10
20
30
40
50
60
70
%
familial cancer no cancer
Hp prevalence
Brenner et al., Gastroenterology 2000
Hp is an independent risik factor(RR 2.7)
Familial risk of gastric cancer:due to intrafamilial clustering
of Hp infection ?
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Familial cancer risk and Hp
Hp cagA positive individuals with a family historyof gastric cancer have
8-fold increased risk for gastric cancer16-fold increased risk for non-cardia cancer
Independent risk factors
BackgroundFamilial history of gastric cancer:
Is it a consequence of a clustering of Hp infectionor are Hp and familial history independent risk factors ?
Brenner, Cancer 2000
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Gastric cancerGenetic disposition and Hp
Hypothesis
Hp Gastritis
risk gastritisrisk of cancer
Genetic disposition
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Cytokine genetic polymorphismsare associated with an increased risik for
gastric cancer(Machado, Gastroenterology 2003)
• Proinflammatory IL-1 polymorphisms are associated withmore severe inflammation and increased prevalence of IM andatrophic gastritis. ATA haplotype carriers of IL-10 werecolonized by more virulent Hp strains(Rad et al., Gut 2004)
• Genetic polymorphisms in IL-8, IL-10, and TNF-alphaplay a role in gastric carcinogenesis in the Chinese population(Lu et al., Carcinogenesis 2005)
• IL-1B polymorphisms may predispose to gastric cancer in theChinese pand Korean population(Yang et al., Cancer Lett 2004; Chang et al., Int J Cancer 2005)
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Host genetics Hp strains
risk gastritis phenotype
gastric cancer
Environmental and dietary factors
Hp and risk of gastric cancer
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Helicobacter pylori and gastric cancerEvidence for an association
• Epidemiology• Induction of gastritis, atrophy, IM• Ascorbin acid• Hyperproliferation• O2-radicals, NO• Hypochlorhydria, hypergastrinemia• Animal studies• Observational studies• Interventional studies
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Hp and gastric cancerUemura et al., N Engl J Med 2001
patients with gastric/duodenal ulcer, gastral hyperplasia, NUDn = 1526
endoscopc-bioptic survey over 7.8 years (1-10,6)
Hp +n=1246
Hp -n=280
cancer in 2,9% cancer in 0%Hp -Hp +
p < 0,001
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Hp and gastric cancerUemura et al., N Engl J Med 2001
Cancer risk was associated with:
severe atrophyCorpus dominant gastritis
intestinal metaplasia
Hp positive patients
2,9 %NUD4,7%
Hplasia2,2%
Uv3,4%
Ud0 %
cancer risk
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Hp and gastric cancerChemopreventive study
Correa et al., J Natl Cancer Inst 2000
Columbia: high prevalence of cancer and of multifocal atrophy/IM
randomisation
Hp eradication Beta-Caroten Ascorbin acid
Comparison of histologies before and after 6 years:significant reduction of atrophy/IM
combination not superior to monotherapy
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Hp eradication for prevention ofgastric cancer in a high risk area
Wong BCY et al., JAMA 2004
GASTRO UPDATE 2005 Oberer GI-Trakt 145/1
prospective randomised placebo controlledpopulation-based interventional study in
1630 healthy Hp infected individuals from aChinese region with high cancer incidence
n = 988initially no precancerous lesions
(atrophy, IM, dysplasia)
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Hp eradication for prevention ofgastric cancer in a high risk area
Wong BCY et al., JAMA 2004
GASTRO UPDATE 2005 Oberer GI-Trakt 145/2
primary study aim:Is there a difference in the incidence of
gastric cancer between eradication and placeboduring a 7.5-years follow-up ?
Gastric carcinomaeradication n = 7placebo n = 11p 0,33
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Hp eradication for prevention ofgastric cancer in a high risk area
Wong BCY et al., JAMA 2004
GASTRO UPDATE 2005 Oberer GI-Trakt 145/3
secondary study aim:Is there a difference between individuals
with / without precancerous lesionsin the eradication and control group ?
Gastric carcinoma
eradication n = 0placebo n = 6p 0,02
no precancerous lesions
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Gastric carcinogenesisnormal gastric mucosa
chronic-active gastritis
atrophic gastritis
intestinal metaplasia
dysplasia
carcinoma
Hp Hp
? point of no return
?
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Prevalence of Hp and gastric cancerin long-living elderly in JapanMasaya Kawade et al., J Gastroenterol Hepatol 2004
0
10
20
30
40
50
60
%
65-74 75-84 > 85
Hp seropositivity
02468
1012
%
65-74 75-84 > 85
Prevalence
gastric cancer colon cancer
* **
The lower prevalence of gastric cancer in the elderlymay be due to disappearance of Hp colonization
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Host genetics Hp strains
risk gastritis phenotype
gastric cancer
Environmental and dietary factors
Hp and risk of gastric cancer
Hp genotypinghost genotyping
selective early prophylactic Hp eradication
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Gastric cancer originating frombone marrow-derived cells and Hp
Houghton J, et al., Science 2004
• Bone marrow-derived cells (BMDCs) are frequentlyrecruited to sites of inflammation
• Hp infection of mice induced population of the stomachwith BMDCs.
• Subsequently, these cells progressed through metaplasiaand dysplasia to cancer
• Epithelial cancers can originate from BMDCs after Hpinduced gastritis.New aspects of host and exogene factors interactions withpotential implications on carcinogenesis
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Helicobacter pylori
Peptic ulcer
MALT lymphoma gastric cancer
dyspepsiaExtragastricdiseases
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Hp eradication forgastric cancer prophylaxis ?
Hp eradication should be performedin cases of• EMR or subtotal surgical resection ofhigh grade dysplasia or gastric cancer
• familial clustering of gastric cancer• risk gastritis
(predominant corpus gastritis, atrophy, IM)• young patient (< 40 years ?)
• patient´s desire
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Helicobacter pylori
Peptic ulcer
MALT lymphoma gastric cancer
dyspepsiaExtragastricdiseases
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Helicobacter pylori and MALT-lymphoma
aetiopathogenetic roleof Hp for MALT-lymphoma
molecularbiologicalfindings
epidemiologicaldata
animalstudies
morphologicaldata
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Helicobacter pylori and gastric MALT lymphoma
Morphological data
Lymphoid follicles in gastric mucosa represent animmune response to Campylobacter pylori. Thisacquired lymphoid tissue has characteristics of MALT.(Wyatt 1988; Stolte 1989)
Successful treatment of Hp is followed by regressionof MALT(Stolte 1992)
Hp infection is present in 92% of 110 patients withgastric MALT lymphoma(Wotherspoon 1991)
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Helicobacter pylori and gastric MALT lymphoma
Epidemiological data
The incidence of gastric MALT lymphoma depends onthe rate of Hp infection(Doglioni, Lancet 1992)
Case-control-study:Hp leads to a 6-fold risk for gastric MALT lymphoma.Hp infection preceeds the development for gastriclymphoma.(Parsonnet, NEJM 1994)
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Helicobacter pylori and gastric MALT lymphoma
Molecularbiological data
The growth of tumor cells from low grade gastricMALT lymphoma can be stimulated by Hp
The neoplastic B cells are not immuneresponsive to Hpbut lymphoma proliferation is mediated bycontact-dependent Hp specific T cells
Hp dependent T cell activation B cell proliferationmonoclonal selection
(Hussel, Lancet 1993, J Pathol 1996)
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Helicobacter pylori and gastric MALT lymphoma
Hp induces acquisition of lymphoid tisuein the gastric mucosa:Condition for the developmentof gastric MALT lymphoma
Hp represents an antigenic stimulus forthe lymphoma growth:Progression of gastric MALT lymphoma
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HELICOBACTER PYLORI ERADICATION INLOW GRADE GASTRIC MALT - LYMPHOMA
Wotherspoon et al., Lancet 1993
“Hp eradicationshould be the first choice of treatment “
6 patients with low grade gastric B-cell-lymphomaof MALT-type
Hp eradication
regression of lymphoma: 5/6 cases
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Helicobacter pylori eradicationin low grade gastric MALT-lymphoma
of stage I
lymphoma regression in 70 - 80%
(literature)
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What is the long-term outcome afterexclusive Hp eradication therapy ?
Are lymphoma regressions long lasting ?
Does it offer a real chance of cure ?
How often do relapse, progressionor high grade transformation occur ?
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CR62 (65%)
MRD15 (16%)
PR9 (10%)
NC7 (7%)
PD1 (1%)
?1 (1%)
Hp eradication
n = 95
Follow-up49,5 (12-89 mo)
Fischbach et al., Gut 2004;53:34-37
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Long-term outcomeafter Helicobacter pylori eradication therapy
Conclusions
The majority of patients havea favourable long-term outcome.
Hp eradication offers a real chance of cure
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Are there any predictors forlymphoma regression
after successful eradication of Hp ?
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Hp associated gastritisreactive benign disease
malignancy
Hp
dependent
geneticchanges
Marginal zone B celllymphoma of MALTt(1;14) < 5% Apoptose regulierendes BCL10
t(11;18) -t(11;18) +
DLBCLt(11;18) -
numerous genetic changes
high gradetransformation
de novo
mostly singleclonal abnormality
Hp eradicationfailure
(definition?)
Hp eradicationresponsive
Hp induces andSustains an acttive
ProliferatingB-cell population
Hp attracts andactivates neutrophils
Release
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Translocation t(11;18) and regression ofgastric MALT-lymphoma after Hp eradication
Liu et al., Gastroenterology 2002
46
1 0 1
17
26
4
16
05
101520253035404550
I >II I >II
t(11;18) -t(11;18) +
completeregression
noregression
t(11;18) positive MALT-lymphoma do not/rarelyrespond to Hp eradication therapy:
predictor of treatment failure ?
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Minimal residual low-gradegastric MALT-type lymphoma aftereradication of Helicobacter pylori
Fischbach W, Goebeler-Kolve ME, Starostik P,Greiner A, Müller-Hermelink HK
Lancet 2002; 360:547-548
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Fischbach et al., Lancet 2002
No relapseNo lymphoma dissemination
No high grade transformation
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MRD after successful eradication of H. pyloriExperience from a clinical series
of the EGILS group (Fischbach W, DDW 2005, submiited)
Follow-up42,2 (2–144 months)
PD n = 6 (6%)
MRD n = 67 (62%)
Hp eradicationafter 12 months:
MRD
Low grade gastricMALT lymphoma
stage In = 108
CR n = 35 (32%)
local progression: n=5high grade lymphoma n=1
Favourable naturalcourse of disease
in 95%
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It is justifiable topostpone oncological treatment
in patients with MRDafter successful eradication of Hp
A watch-and-wait strategy isa valid approach to manage MRD
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Therapy of early gastric lymphoma
MALT
Hp eradicationif Hp-, progression
or relapse:RTx (surgery)
MRD:watch-and-wait
RTx (surgery)
CTx
large B-cell-ly
CTx + RTx( surgery + CTx)
((Hp eradication))
CTx + RTx(surgery + CTx)
CTx + RTx
stage
I 1/2
II 1/2
III / IV