Plenary Session 1
Prevalence - Incidence
Etiology - Origins

 Plenary Session 2
Genetic & Cell changes

 Plenary Session 3
Clinical features - Obesity
Imaging

 Plenary Session 4
Endoscopic diagnosis (1)

 Plenary Session 5
Endoscopic diagnosis (2) - Dysplasia

 Plenary Session 6
Histology - Immuno-histology

 Plenary Session 7
PPIs & Chemoprevention (1)

 Plenary Session 8
PPIs & Chemoprevention (2)

 Plenary Session 9
Endoscopic treatments of Barrett's esophagus (1)

 Plenary Session 10
Endoscopic treatments of Barrett's esophagus (2) - Dysplasia

 Plenary Session 11
Surgical treatments of Barrett's esophagus

 Plenary Session 12
Surveillance
Reversal of Barrett's esophagus

 Plenary Session 13
Progression to adenocarcinoma - Markers

 Plenary Session 14
Prevalence - Incidence of adenocarcinoma

 Plenary Session 15
Treatments of adenocarcinomas (1)

 Plenary Session 16
Treatments of adenocarcinomas (2)

 Plenary Session 17
Natural history

Sunday, August 29, 7:00 - 9:20 a.m. - Amphitheater

Prevalence - Incidence
Etiology - Origins

Chairs: N.J. Shaheen (Chapel Hill) - R.C. Fitzgerald (Cambridge)
Discussants: P.T. Chandrasoma (Los Angeles) - H.B. El Serag (Houston)

1

What is the prevalence of BE and possible associated risk factors in a general population?
   

. Should variations in histologic criteria be considered as a factor of variation? R.E. Sampliner (Tucson)
2 What is the accepted prevalence rate of BE among racial minorities?
J. Abrams (New York)
3 Can the reasons for the epidemic rate of rising incidence of BE be specified? B.C. Jacobson (Boston)
4 How do different histologic criteria for Barrett's mucosa affect the prevalence rates of BE in different populations? R.H. Riddell (Toronto)
   

. Why is Barrett's mucosa so uncommon in the East Asia?
5 Is there a proven association between dietary patterns, life style, and the development of BE and adenocarcinoma? L. Murray (Belfast)
6 In Barrett's patients, does the influence of metabolic changes induced by adipocytokins and the apparently strong association existing between obesity, central adiposity and BE lead us to reconsider some  aspects of the natural history of BE, or only of GERD? J.H. Rubenstein (Ann Arbor)
7 Can it be assessed that the absence of H pylori increases the risk of GERD and, hence, the risk of BE?
8 What role do sensory abnormalities play in the pathogenesis?
A. Lund-Krarup (Aalborg)
9 What can we tell about the etiology of Barrett's esophagus from experimental testing of the esophagus with multi-modal sensory testing?
A.M. Drewes (Aalborg)
10 What are the ways of detecting cellular oxidative stress?
   

. What can be expected from expression of stress response proteins as a screening tool for BE? G.A. Prasad (Rochester)
11 Does Barrett’s esophagus really develop in adulthood? K. Roark (Chicago)
12 Is there a clear understanding of the sequence normal, squamous epithelium and apoptosis-resistant metaplastic epithelium?
   

. What is the evidence that esophageal squamous epithelium is more susceptible to acid injury in patients with Barrett's esophagus than in those with GERD without BE? R.C. Fitzgerald (Cambridge, UK)
13 What is the role of DGER in the development of BE? J.E. Richter (Philadelphia)
14 Do reflux patterns (long vs short episodes) influence the pathogenesis of BE and dysplasia?  R.Tutuian (Bern)
15 What is the difference in cellular oxidative stress induced by acute or chronic exposure to bile acids? G.J. Jenkins (Swansea)
16 What is the current understanding of the role of DNA damaging induced by bile acids in the development of BE? K. Dvorak (Tucson)
17 May post-prandial enlargement of the acid pocket be considered as a factor for the development of BE? H.P. Parkman (Philadelphia)
18 What are the features of the regulation of anti-apoptotic pathways? P. Lao-Sirieix (Cambridge)
19 What are the implications for clinical practice of T-cell-related mucosal CMPs (Combinatorial molecular Protein patterns) in Barrett's epithelium? P. Konturek (Erlangen)
20 Can proteomic analysis help in understanding the pathogenic mechanisms involved in BE? A.C. Chang (Ann Arbor)

     


Sunday, August 29, 9:40 a.m. - 12:00 p.m. - Amphitheater

Genetic & Cell changes

Chairs: N.S. Buttar (Rochester, MN) - D.G. Beer (Ann Arbor)
Discussants: R.C. Fitzgerald (Cambridge, UK)  - C.C. Maley (Philadelphia)

1

Is there a specific genetic code predictive of BE to be considered as a useful tool in epidemiological studies? R.F. Souza (Dallas)
2 Are there serum biomarkers that can diagnose patients with Barrett's esophagus? S.J. Meltzer (Baltimore)
3 Is there a genetic profile, predisposing to a strong pro-inflammatory host response, associated with BE? D. Fang (Chongqing)
4 Is chromosomal instability the main cause of genomic instability in Barrett's esophagus?
   

. How can it be identified? K.K. Wang (Rochester, MN)
5 What is the role of developmental signaling pathways in the mechanisms by which GERD may induce esophageal expression of Cdx (Caudal homeobox) genes that mediate the development of Barrett's metaplasia? G. Freschi (Florence)
6 What are the model systems likely to show the impact of acid and bile exposure on gene expression of the esophagus in vivo? G. Triadafilopoulos (Stanford)
7 Can a relationship between genetic clonal diversity and risk for malignant transformation be shown? C.C. Maley (Philadelphia)
8 What are the limitations of currently available Barrett's cell lines?
J. Wang (St Louis)
9 How is clonal diversity in Barrett's esophagus recognized? A.C. Chang (Ann Arbor)

10 Rather than genetic homogeneity, is clonal diversity of valuable predictive value for progression of BE to adenocarcinoma? What clinical implications could be expected? N.S. Buttar (Rochester – MN)
11 How can the clonality study by individual crypt dissection demonstrate that Barrett's epithelium heterogeneity results from multiple independent clones? H. Barr (Gloucester)

12 What is the order of clonal expansion in Barrett's esophagus? C.C. Maley (Philadelphia)
13 What lessons can be learned from the in-vivo models about the influence of environmental factors on the cellular phenotype(s) in non-neoplastic Barrett’s cell lines and the pathogenesis of malignant transformation ? K.M. Das (New Brunswick)
14 What insight into the molecular process of BE can be expected by applying peptide arrays to clinical samples of metaplastic mucosa? P. Schneider (Zurich)
15 Can active cell-signaling pathways in BE be delineated? K.K. Krisnadath (Amsterdam)
16 What are the characteristics of Barrett's cell lines related to proliferation and apoptosis? R.F. Souza (Dallas)
17 With the help of the new robotic whole-cell imaging technology, what can be shown by the evaluation of changes in T-cell-related mucosal CMPs (Combinatorial Molecular Protein patterns)
18 Are there tissue biomarkers that can stratify risk for future neoplasia in Barrett's esophagus? S.J. Meltzer (Baltimore)
19 Is there one transcription factor that shows a significant increase in the progression from Barrett's metaplasia to adenocarcinoma? C. Tselepis (Birmingham)
20 Is there an order in proteomic changes associated with neoplastic progression?

     

Sunday, August 29, 1:15 - 3:35 p.m. - Amphitheater

Clinical features - Obesity
Imaging

Chairs: I.J.S. Cook (Sydney)  - J.E. Richter (Philadelphia)
Discussants: C.L. Canon (Birmingham, AL) - B.C. Jacobson (Boston)

1

Can Barrett's esophagus  be considered as an adaptative defense against reflux? R.C. Orlando (Chapel Hill)
2 What is the difference in the prevalence and severity of metabolic syndrome in patients with GERD or BE?
3 Do particular clinical factors influence the development and extent of BE? E.M.M. Quigley (Cork)
4
 What is the symptom profile in patients with BE? R. Tutuian (Bern)
5 What is the respective influence of BMI and body fat distribution on the development of BE? B.C. Jacobson (Boston)
6 Is BMI of value for predicting BE development in GERD patients? I.J.S. Cook (Sydney)
7

Can it be said that central obesity may worsen acid reflux leading to BE?
   

. If so, by what mechanism? J. Lenglinger (Vienna)

8 What is the impact of pro-inflammatory adipocytokines and metabolic syndrome on the development of Barrett's mucosa? J.H. Rubenstein (Ann Arbor)
9 What is the relationship between pro-inflammatory markers and the length of BE? J.V. Reynolds (Dublin)
10 Can it be correctly stated that abdominal fat is metabolically active by regulation of tumor necrosis factor, expression of Cox-2 and interleukin-1? P.C. Konturek (Erlangen)

11 May body fat distribution in men, where visceral obesity is more common, be an explanation for the higher incidence of BE in this population?
12 Does BMI induce a difference in healing erosive esophagitis or Barrett's epithelium? B.C. Jacobson (Boston)
13 Is it likely that intra-abdominal fat is a risk marker of GERD, BE, and adenocarcinoma?
   

. What are the means by which obesity may (also) promote carcinogenesis in Barrett's patients? M. Cicala (Rome)  
14 Considering the effect of adiponectin in cell apoptosis and proliferation, can the role played by abdominal fat in the development of carcinogenesis be specified?
15 Does surgery for obesity result in better control of GERD and risk of malignancy in BE? R.W. McCallum (El Paso)
   

Imaging
16 What is the role of double-contrast esophagography in the diagnosis and screening for BE in patients with reflux symptoms? M.S. Levine (Philadelphia)
17 What can be expected from real-time cross-sectional images of the esophagus for the detection of patients with BE? R.M. Gore (Evanston)
18 Can PET/CT differentiate BE from other benign esophageal disorders?
19 What is the value of the three dimensional image processing scintigraphy in the diagnosis of BE? A. Wuttge-Hannig (Munich)
20 What criteria can be expected from High Resolution Endoluminal Sonography for the diagnosis of BE? J. H. Hwang (Seattle) 

     


Sunday, August 29, 4:25 - 6:45 p.m. - Amphitheater

Endoscopic diagnosis (1)

Chairs: H. Inoue (Yokohama) - R.E. Sampliner (Tucson)
Discussants: J. Horwhat (Washington)  - G. Triadafilopoulos (Stanford)

1

What is the most consistent landmark for the endoscopic diagnosis of BE? N. Ishimura (Shimane)
   

.  What are the best markers of the distal extent of endoscopic BE by use of standard equipment? (gastric folds, hiatus, palisade vessels)

2 Is the diagnosis of ultra-short segment Barrett's mucosa beneficial for patient care? H.D. Appelman (Ann Arbor)
3 What is the value of the Prague C & M criteria for standardization of the endoscopic grading of BE and its progression over time? R. Penagini (Milan)
4 What are the means of detecting focal islands of SIM not visible at conventional endoscopy? G.W. Falk (Cleveland)
5 What is the sensitivity-specificity of the endoscopic diagnosis of BE? R.K.H. Wong (Washington)
6 May the accuracy of MCE (Magnification endoscopy) with indigo carmine dye staining allow for prediction of histological detection of HGD and, thus avoid biopsies in Barrett's patients? M. Muto (Kyoto)

7 Should the non-reproducibility of endoscopic staining techniques by all endoscopists restrict its use for detection of SIM and dysplasia in BE? R.E. Sampliner (Tucson)
8 What can be expected from the novel devices to assess reflux at the hypopharynx level without the need for manometry or endoscopy? I.F. Herrmann (Rome)
9 Should non-sedated ultrathin endoscopy be recommended for screening BE in the office setting? R. Tutuian (Bern)
10 Is capsule endoscopy an accurate enough tool for screening BE in clinical practice? L. Gerson (Stanford)
11 What are the reasons for the poor sensitivity and specificity of esophageal capsule endoscopy in the detection of BE? Th. Ponchon (Lyons)
12 Should string capsule endoscopy, allowing controlled movement within the esophagus, have better accuracy in the diagnosis of BE? F.C. Ramirez (Phenix)
13 Should two-headed camera esophageal capsule be currently part of the endoscopic armamentarium for screening Barrett's patients? H.C. Wolfsen (Jacksonville)
14 What attitude should be adopted when there are no visible abnormalities in a patient? J. Horwhat (Washington)
15 What is the correlation between NBI patterns with histological findings?P.D. Siersema (Utrecht)

16 What are the limitations still to be considered in endoscopy with NBI? H. Inoue (Yokohama)
17 What can be expected from Magnifying Endoscopy associated with NBI for the detection of SIM in Barrett's mucosa? C.J. Lightdale (New York)

18 Can the classification of "mucosal morphology", as allowed by NBI, help in interpretation of magnifying endoscopy?M. Muto (Kyoto)
19 Can association of NBI with High-Resolution Endoscopy lead to a change in the current practice of random biopsies in Barrett's patients? K.R. DeVault (Jacksonville)
20 Can NBI be considered as a tool for routine clinical practice? G. Freschi (Florence)

     


Monday, August 30, 7:00 - 9:20 a.m. - Amphitheater

Endoscopic diagnosis (2) - Dysplasia

Chairs: R. Lambert (Lyons) - G.W. Falk (Cleveland)
Discussants: R. Chuttani (Boston) - L. Messerini (Florence)

   

LGD
1

What is the comparative value of immunostaining for p16, p53, and cytoplasmic protein (Rab11a) immunoreactivity in the histologic assessment of dysplasia in Barrett's patients? J. Hart (Chicago) 

2 What is the sensitivity-specificity of balloon cytology in detecting LGD? H.H. Wang (Boston)

3 In spite of the promising value of flow cytometry in detecting aneuploidy of G2/tetraploidy on cytological specimens, do cost and restricted availability of this technique represent true limitation to its wide clinical use? Q. Huang (Boston)
4 What is unstable aneuploidy? Is it a marker for neoplastic progression?A.M. Bellizzi (Boston)

5 Can biopsies accurately identify dysplasia in the presence of reflux esophagitis?
   

. What are the criteria that allow differentiating inflammatory or regenerative changes from dysplasia? G. De Hertog (Leuven)
   

. What are the alternatives to flow cytometry to determine DNA abnormalities in cell cycle?
6 How should extent of dysplasia be histologically defined? A. Srivastava (Lebanon)
   

. How should precise distinction between "focal" and "diffuse" dysplasia be made?
7 What are the differences between the main categorization systems used for grading dysplasia in BE? (Inflammatory bowel disease dysplasia morphology group - Vienna classification system) R.H. Riddell (Toronto)
8 May the known extension of LGD fields beyond those of HGD, as well as their larger surface areas, be an explanation for characterization of LGD as a significant risk factor for development of carcinoma in Barrett's patients? N.S. Buttar (Rochester, MN)
9 What is the sensibility-specificity of in vivo cellular imaging using Confocal Endomicroscopy and "optical biopsies" for the detection of dysplasia in Barrett's mucosa? T.Wang (Ann Arbor)

10 What is the value of protoporphyrin fluorescence for the accurate detection of LGD? H.C. Wolfsen (Jacksonville)
11 What is the value of acetic acid application for selection of areas for biopsy? A. Hoffman (Mainz)
12 Does the high sensitivity-specificity of AMACR (Alpha Methyl CoAracunase) immuno-staining give this technique a place of choice for detection of dysplasia?
13 What can be expected from the endoscopic detection of dysplasia using 5-ALA sensitization and illumination with blue light? L.F. Johnson (Birmingham- AL)
14 What is the technique that allows for best selection of biopsies and endoscopic diagnosis of dysplasia? M.D. Saunders (Seattle)
    HGD
15

What are the criteria to differentiate inflammatory or regenerative changes from dysplasia?
16

What are the patterns to be considered in Magnification Chromo-Endoscopy as specific for HGD? A. Hoffman (Mainz)
17 Does resolution currently existing in Optical Coherence Tomography and tissue spectroscopy warrant the use of this tool for identification of HGD in Barrett's patients? J.H. Hwang (Seattle)

18

Does NBI securely allow for targeted biopsies using fewer samples to detect advanced dysplasia?

   

. Can diagnosis of HGD without staining by NBI with magnification be considered as a reliable? H.C. Wolfsen (Jacksonville)
19 Does addition to NBI of High Resolution Endoscopy and Auto Fluorescence Imaging allow for better detection of HGD and lowering of false positive results?
20

Is extent of HGD clearly related to the progression of Barrett's mucosa to adenocarcinoma? N.S. Buttar (Rochester, MN)

     


Monday, August 30, 9:40 a.m. - 12:00 p.m. - Amphitheater

Histology - Immuno-histology

Chairs: M. Vieth (Bayreuth) - R. Odze (Boston)
Discussants: G. De Hertog (Leuven) - R.H. Riddell (Toronto)

1

Is the histological presence of IM to be definitely included in the definition of BE? H. Barr (Gloucester)
   

. The AGA Chicago workshop
   

. The BSG guidelines
2 Can IM at the esophagus be reliably distinguished from cardiac mucosa? M. Upton (Seattle)
3 What is the distribution of IM in the proximal or distal edge of Barrett's epithelium, and should it influence the biopsy protocol? P.T. Chandrasoma (Los Angeles)
4 Is there evidence for a role for the esophageal submucosal glands in the origin of BE? R.C. Orlando (Chapel Hill)
5 Is there, in 2010, a consensus on the definition of BE?
   

. Why is the lower boarder of the longitudinal vessels ignored by Western gastroenterologists as the end of tubular esophagus, when it is such a critical landmark in Japan? D. Armstrong (Hamilton)
6 In GERD patients who do not develop Barrett's esophagus, does squamous epithelium differ from those who develop BE? G. De Hertog (Leuven)
7 What are the genetic abnormalities existing in the histologically normal esophageal squamous epithelium in BE and adenocarcinoma?
   

. Are these genetic abnormalities in the squamous epithelium or in the underlying stroma? C.C. Maley (Philadelphia)
8 Is cardiac mucosa always abnormal and metaplastic? M. Vieth (Bayreuth)
   

. Can it progress to dysplasia and adenocarcinoma?
9 What is the significance of microscopic foci of SIM at the GEJ? E. Wiley (Chicago)
10 Is new monoclonal antibody Das-1 (mAb Das – 1) likeky to help in recognizing esophageal IM? K.M. Das (New Brunswick)  
11 Is there a consensus on the characteristic features predictors of the presence of non-dysplastic SIM? A. Bennett (Cleveland)
12 What is the frequency of cells showing a similarity with intestinal goblet cells on biopsies, and their influence on false diagnosis of Barrett's metaplasia? M. Younes (Houston)
13 Can prevalence of SIM at endoscopically normal GEJ be specified? P.K. Chandrasoma (Los Angeles)
14 How to avoid erroneous diagnosis in patients with short segment Barrett's epithelium and hiatal hernia? M. Conio (Genoa)
15 Are systematic four-quadrant biopsies the safest way to detect Barrett's epithelium? J.J. Going (Glasgow)
16 Due to the patchy nature of Barrett's epithelium, what are the challenges in documenting the presence of IM in a CLE segment? V. Sharma (Gilbert)
   

. What is the optimal biopsy protocol to be considered for accurate detection of IM?
17

According to the non homogenous histology of Barrett's epithelium with all 3 types of metaplasia being present in the same patient, what is the best procedure for biopsy sampling and the adequate number feasible in the current clinical environment? J. Abrams (New York)
   

. Is it possible to specify the potential barriers that may impede adherence to practice guidelines for biopsy sampling?
    Immuno-histology
18 Can the exact role of biomarkers for the diagnosis of BE be defined?
M. Younes (Houston)
19 What is the value of molecular markers (cdx-2, muc-2, CK7/20) for identification of patients predisposed to the development of BE? A. Taddei (Florence)
20 Can the CK patterns show differences between CLE and normal cardiac mucosa? R.D. Odze (Boston)

     


Monday, August 30, 1:15 - 3:35 p.m. - Amphitheater

PPIs & Chemoprevention (1)

Chairs: C. Scarpignato (Parma) - D. Sifrim (London)
Discussants: M. Cicala (Rome) - R.H. Hunt (Hamilton) - K.R. DeVault (Jacksonville)

1

Are esophageal defense mechanisms different in Barrett's esophagus? R.W. McCallum (El Paso)
2 What is the effect of 5-HT4 agonists on esophageal EGF secretion in patients with GERD and BE? A. Taddei (Florence)
3 What is the effect of lubriprostone (Amitizia) on chloride channels agents or mucus protection factors in the esophagus? J. Saroziek (Kansas City)
4 In view of the high levels of toxin-producing Campylobacter species found in Barrett's patients, should prophylactic use of antibiotics be considered?
J.F. Dillon (Dundee)

5 Is pre-endoscopy use of PPIs to be avoided, owing to their capacity of healing macroscopic lesions and thus removing useful prognostic markers? R.H. Hunt (Hamilton)
6 Can prior use of PPI therapy be considered as a predictor of shorter length of BE? R.E. Sampliner (Tucson)
7 What is the link between presence of unconjugated bile acids (deoxycholic acid) and the deleterious effect of refluxate in patients taking PPIs? K. Dvorak (Tucson)
8 Should Baclofen be added to PPIs to address non-acid & bile reflux factors ? D. Sifrim (London)
9 In patients on PPI therapy, what is the threshold for adequate suppression of esophageal acid exposure as expected from pH monitoring? J.E. Richter (Philadelphia)
10 Should we still advocate a trial of a PPI to diagnose GERD? R. Tutuian  (Bern)
11 What are the effects of PPI therapy on the length of Barrett's mucosa and on the development of squamous islands? P.O. Katz (Philadelphia)
12 In consideration of the abnormalities in cancer biomarkers that may be observed, should squamous islands developed in Barrett's patients after prolonged use of PPIs, synonymous of incomplete healing, be submitted to especially attentive follow-up? H.S. Garewal (Tucson)
13 What are the effects of PPIs on stabilization of epithelial cell proliferation, reduction of cell cycle abnormalities, and hyperplasia of the basal cell layer? M. Vieth (Bayreuth)
14 As suggested by studies of macroscopic markers in Barrett's patients, should effect of PPI therapy be mediated by anti-inflammatory effects rather than an effect on proliferation?
15 Can PPI therapy achieve normalization of esophageal pH in Barrett's patients? G. Triadafilopoulos (Stanford)
16 Are there factors that can help to predict persistent low intra-esophageal pH in these patients? P.D. Siersema (Utrecht)
17 Are different effects of PPI therapy to be expected in relation to the predominant phenotype of cellular proliferation in Barrett's epithelium? N. Ishimura (Shimane)
18 Can the reasons why PPIs do not bring acid secretion under control in some patients be specified? D.O. Castell (Charleston)
19 What is the respective value of Symptom Index (SI), Symptom Sensibility Index (SSI) and Symptom Association probability (SAP) for the interpretation of the causality of symptoms and their potential response to medical treatment? J.E. Richter (Philadelphia)
20 Can correlation between use of PPIs and development of dysplasia be considered? V. Nilton Felix (San Paulo)

     


Monday, August 30, 4:25 - 6:45 p.m. - Amphitheater

PPIs & Chemoprevention (2)

Chairs: D.O. Castell (Charleston) - J.R. Malagelada (Barcelona)
Discussants: M. Wolfe (Boston) - D.A. Peura (Charlottesville) 

1

What can be expected from pH monitoring in patients with atypical symptoms and normal endoscopy who do not respond to PPI therapy? P.O. Katz (Philadelphia)
2 Should 48 hour acid reflux monitoring be strongly recommended in patients on PPIs with persisting GERD symptoms? J.E. Richter (Philadelphia)
3 Should use of a wireless system with recording of off- and on- therapy testing be recommended in patients with normal endoscopy that do not respond to PPI therapy?  R. Penagini (Milan)
4 Are there clear therapeutic implications to be expected from impedance testing in symptomatic patients non responsive to PPI therapy? D. Pohl (Zurich)
5 What can be currently expected from bile acid reflux testing? H.S. Garewal (Tucson)
6 Are patients with dyspepsia less responsive to PPI therapy? E. Savarino (Genoa)
7 In non-responder patients with extra-esophageal symptoms, is double-dose PPIs followed by pH monitoring the most cost-effective means to determine the role of GERD in worsening symptoms?
   

. The hugely different effects of double-dose vs BID C. Rees (Winston Salem)
8 Is low response to PPIs a challenge for the treatment of NERD patients or of those classified as "functional heartburn" patients?
   

. Should pathogenesis of symptoms be reevaluated in these cases? F. Pace (Milan)
9 What can be anticipated from novel PPI formulation in patients who cannot be adequately treated with once-daily therapy, or for maintenance of healing in patients with severe erosive esophagitis? D.O. Castell (Charleston)
10 What is to be expected from the "dual-release delivery" action of newly developed PPIs? D.A. Peura (Charlottesville)
11 How should issues regarding long-term use of PPIs (hip fractures, C-difficile infection, pneumonia, fundic gland polyps) be considered? S. Herzig (Boston)
12 Should prokinetic agents such as dopaminergic antagonists be considered as a valuable addition to the treatment of Barrett's patients? T. Kamiya (Nagoya)
13 Is there an effect of obesity on symptom resolution in GERD and Barrett's patients treated with PPIs? A. Rastogi (Kansas City)
14 Should PPI dose be altered in obese patients? C. Scarpignato (Parma)
15 How can PPI therapy be tailored to individual needs in a cost-effective manner?
16 What is the role of Baclofen, an agent that blocks TLESR, in the treatment of Barrett's esophagus? R.K.H. Wong (Washington)
17 What is the compared effect of PPIs on Nocturnal Acid Breakthrough (NAB)? D. Armstrong (Hamilton)
18 Compared to PPIs given at bed time, what are the advantages of the low overnight gastric and esophageal acidity observed with the immediate-release omeprazole (OME-IR)?

19 Is combination of PPIs with anti-inflammatory drugs (NSAIDS) and aspirin to be considered as the future of chemoprevention in BE? P. Bechi (Florence)
20 What can be expected from new PPIs currently under investigation on prolonged plasma concentration of drug and intake regardless of meal timing? R.H. Hunt (Hamilton)

     


Tuesday, August 31, 7:00 - 9:20 a.m.- Amphitheater

Endoscopic treatments of Barrett's esophagus (1)

Chairs: Th. Ponchon (Lyons) - C.J. Lightdale (New York)
Discussants: H. Barr (Gloucester) - V. Sharma (Gilbert)

1

In 2010, what are the current indications and results of the endoscopic treatments of BE? M.D. Saunders (Seattle)
2 What are the results of the endo-luminal plication procedures in GERD? S.J.M. Kraemer (Redmont)
3 May endoscopic ablation therapies induce formation of cells undergoing differentiation, and more susceptible to genomic damage? K. Dvorak (Kansas City)
4 Given the low risk for cancer development, should endoscopic ablation be undertaken in non-dysplastic Barrett's patients? K.K. Wang (Rochester, MN)
5 What can be expected from banding without resection in short-segment BE? E. Diaz-Cervantes (Mexico)
6 What is the mechanism of regression following this technique? E. Diaz-Cervantes (Mexico)
7 How should complete ablation of Barrett's mucosa be defined? M. Upton (Seattle)
8
What is the recurrence rate of IM after Argon Plasma Coagulation?
   

. Is length of mucosa a pivotal factor? R. Ferraris (Turin)
9 Can the factors for recurrence of IM be defined?
10 How to ascertain the absence of buried glands under the neosquamous epithelium and the correlative risk of malignant progression, as shown by biomarkers? A. Das (Scottsdale)
11 Is the combination of APC with antireflux surgery, a good means to enhance late results? L. Bonavina (Milan)
12 Are there still indications for YAG laser thermal therapy in Barrett's esophagus?B.F. Overholt (Knoxville)

13 What differences can be shown in the long-term surveillance of patients having undergone MPEC or APC with apparently complete ablation of Barrett's mucosa?  G.A. Prasad (Rochester, MN)
14 What can be expected from genetic biomarkers as predictors of resistance to PDT? S.Meltzer (Baltimore)
15 Following PDT, has outcome of buried columnar glands been evaluated? G.Y. Lauwers (Boston)
   

. Does it influence the risk of adenocarcinoma? 
16 At the time of ablation, what are the means to determine completeness of the procedure? H.C. Wolfsen (Jacksonville)
17 Can the rate of incompletely ablated Barrett's epithelium, as shown by increased expression of cancer-associated biomarkers, be evaluated? V. Sharma (Gilbert)
18 Are there currently available data likely to allow for statistical comparison of MPEC-APC-PDT for ablation of BE and their impact on carcinoma development? K.K. Krisnadath (Amsterdam)
19 Should recurrence rate after PDT lead to the assumption that novel genetic alterations may have developed in these patients? N.S. Buttar (Rochester, MN)
20 Following PDT, can persistence of genetic abnormalities in residual Barrett's mucosa, leading to metachronous lesions, be rated? S.J. Spechler (Dallas)


     


Tuesday, August 31, 9:40 a.m. - 12:00 p.m. - Amphitheater

Endoscopic treatments of Barrett's esophagus (2) - Dysplasia

Chairs: B.F. Overholt (Knoxville) - W.M. Weinstein (Los Angeles)   
Discussants: H.D. Appelman (Ann Arbor) - K.K. Wang (Rochester,MN)

1

What are the results of cryotherapy in dog models? B.D. Greenwald (Baltimore)
2 What are the current indications for cryotherapy in patients with BE? S.J. Sontag (Chicago)
3 What are the criteria that determine the mean number of cryotherapy sessions and total length of treatment? J. Horwhat (Washington)
   

. Is PPI therapy concomitant to cryotherapy mandatory?
4 Can the late results of cryotherapy in Barrett's patients be evaluated? J. Dumot (Cleveland)
5 What are the current indications for a balloon-based Radio-Frequency Ablation device? M.B. Saunders (Seattle)
6 What is the efficiency of RFA for elimination of IM? B.F. Overholt (Knoxville)
7 Does the impossibility of histological analysis of the burned tissues represent a drawback for the RFA procedure?
8 Do the difficulties of full contact of the balloon with the area located immediately above the EGJ represent a limitation to the RFA technique?D.S. Utley (Sunnyvale)
9 Compared to other thermal ablation modalities, what is the rate of development of sub-squamous glandular mucosa following RFA? R. Chuttani (Boston)
10 What is expected from future technical developments of the RFA technology (automated process) to optimally size the ablation balloon? C.J. Lightdale (New York)
11 Is evaluation of the respective rates of IM foci left under regenerated squamous epithelium following the various ablation procedures (thermal-mechanical-chemical-photodynamic) possible in 2010? B.F. Overholt (Knoxville)
12 What are the comparative adverse effects of the diverse ablation procedures?
13 Is the potential rate of recurrence of Barrett's epithelium following ablation currently known?
   

. What are the reasons for variability in published results? M. Upton (Seattle)
14 Following treatment, should expression of cancer-associated biomarkers be systematically checked in Barrett's patients? B. McKenna (Ann Arbor)
    Treatments of dysplasia
15 Given the low risk for cancer development, should LGD be treated at all? H.D. Appelman (Ann Arbor)
16 What is the effect of continuous therapy with PPIs compared to intermittent prescription on the rate of progression of BE to HGD and adenocarcinoma? H.M. Shields (Boston)
17 What are the current indications for PDT in ablation of HGD? K.K. Wang (Rochester,MN)
   

.Can long-term efficacy of PDT ablation of HGD in Barrett's patients be specified?
18 Can the role of RFA in ablating dysplasia be currently evaluated? N.J. Shaheen (Chapel Hill)
   

. What are the results of the late evaluation (2010) of RFA for treating dysplasia?
19 Is NBI a valuable help for targeted mucosectomy for HGD or intra-mucosal carcinoma? I. Waxman (Chicago)
20 Can a clear advantage of endoscopic treatments vs surgery be demonstrated in patients with HGD?
   

. Can the results of long-term studies be applied to general clinical practice? G.A. Prasad (Rochester-MN)


     


Tuesday, August 31, 1:15 - 3:35 p.m. - Waterfront I-II

Surgical treatments of Barrett's esophagus

Chairs: D.H. Birkett (Boston) -  J.A. Salo (Helsinki)
Discussants: L.L. Swanstrom (Portland) - R.P. Tatum (Seattle)

1

How long should medical treatment be continued before antireflux surgery? P. Parise (Pisa)
2 Can esophagography differentiate Barrett's esophagus from early carcinoma?   I. Laufer (Philadelphia)
3 What is the effect of the various AR procedures on the LES? R. Rosati (Milan)
4 What are the consequences of an impaired esophageal motility on the choice of the surgical technique? K.S. Dua (Milwaukee)
5 What are the indications of transthoracic Nissen fundoplication? J.M. Collard (Brussels)
6 Should highly selective vagotomy be added to antireflux surgery? R.P. Tatum (Los Angeles)
7 What are the indications for duodenal switch in Barrett's patients? I.Braghetto (Santiago)
8 What information can be expected from preoperative High Resolution Manometry for the choice between various techniques? C.P. Gyawali (St Louis)
9 What is the rate of occurrence of vagal damage after antireflux surgery?
10 Should gastric emptying be routinely assessed before considering a fundoplication? R.W. McCallum (El Paso)
11 What can be expected from gastric electrical stimulation in the treatment of post-vagotomy gastroparesis occurring after Nissen fundoplication? I. Sarosiek (Kansas City)
12 Can complete regression of BE after successful Anti-Reflux Surgery be assessed? L. Bonavina (Milan)
13 Can ARS be considered as reducing or potentially eliminating the risk of malignant progression? C. Pellegrini (Seattle)
14 Should systematic pre-operative endoscopy be performed in all patients undergoing bariatric surgery to detect asymptomatic reflux lesions that could affect the type of surgery performed?  B.C. Jacobson  (Boston)
15 What is the effect of pre-operative existence of diffuse non-GERD symptoms (bloating, abdominal crampy pain, IBS) on the results of surgery? H. Van der Walt (Pretoria)   
16 Are there radiographic findings that ascertain the existence of a shortened esophagus, and what is the consequence on the surgical strategy? C.L. Canon (Birmingham, AL)
17 What are the indications and long-term outcome of the Collis modification of fundoplication? A. Badaloni (Buenos Aires)
18 In 2010, what is the role of robotic technology in ARS? E. Hazebroek (Utrecht)
19 Should the choice of the type of fundoplication still be the matter of discussion? A. Del Genio (Naples)
20 When should surgery be proposed to young patients with chronic GERD or BE? P. Omelanczuk  (Mendoza)

     


Tuesday, August 31, 4:25 - 6:45 p.m. - Cityview I

Surveillance
Reversal of Barrett's esophagus

Chairs: J. Hart (Chicago) - R. Shaker  (Milwaukee)
Discussants: A. Maitra (Baltimore) - P.D. Siersema (Utrecht)

1

According to potential sampling errors, should decision of surveillance be based upon the presence of IM at endoscopy? C.P. Caygill (London)
2

As the majority of cases of BE remain unrecognized in the general population, how can surveillance studies be conducted? J. Theisen (Munich)
3 Following treatment, what should be the right follow-up of patients in whom squamous epithelium stains normally with a variety of biomarkers, thus witnessing complete ablation of the Barrett's mucosa? K. Dvorak (Tucson)
4 What is the long-term follow-up of surgery in Barrett's esophagus with no dysplasia vs radio-frequency ablation?G. Triadafilopoulos (Stanford)
5 Should LSBE and SSBE be included in the same surveillance program? R.E. Sampliner (Tucson)
6 According to the various proposed guidelines, what surveillance interval should be recommended in Barrett's patients with no evidence of dysplasia? V. Nilton Felix (San Paulo)
7 Is a clear distinction between prevalent and incident dysplasia mandatory to avoid bias in the study of surveillance cohorts? J.L. Hornick (Boston)
8 Given the potential transient evolution of LGD, should its diagnosis continue to drive the frequency of surveillance endoscopy? R.C. Fitzgerald (Cambridge)
9 What is the value of the OESO topographic grid to define the landmarks of Barrett's mucosa? R. Ferraris (Turin)  
10 Can anatomic changes following fundoplication hinder appropriate esophageal sampling during surveillance endoscopy? C.P. WU (Seattle)

11 According to the various guidelines for endoscopic surveillance of Barrett's patients, can a program for adequate biopsy sampling be specified? J. Abrams (New York) 
   

. What are the barriers that may impede adherence to these guidelines?
   

. Since PPIs may stimulate squamous metaplasia in BE, what is the preferred biopsy protocol for surveillance of Barrett's patients treated with PPIs? 
12 What is the value of tissue spectroscopy and Optical Coherence Tomography in the surveillance of Barrett's patients?
   

. Do the various broad-field optical enhancement technologies, aimed at improving the efficiency of  detection of dysplasia, lead to drastic modification of surveillance protocols? 

13 Should Radio Frequency Ablation, allowing for lengthening of surveillance intervals by down-staging or eliminating Barrett's mucosa, be considered as a valuable tool for reduction of health care costs? A. Das (Scottsdale)
14 For screening and surveillance of Barrett's patients, should unsedated small-caliber endoscopy be a valuable choice to reduce costs and risks associated with sedation? B.A. Jobe (Pittsburgh)
15 In spite of its low accuracy, can capsule endoscopy be considered in 2010 as a cost-effective alternative for BE screening? P.D. Siersema (Utrecht)
16 Considering the variability of data concerning cancer incidence in patients with Barrett's esophagus, and as most cases of adenocarcinoma are diagnosed at entry, should cost-effectiveness of intensive biopsy protocols to assess the degree of dysplasia be questioned? S. Nandurkar (Melbourne)
17 For surveillance of Barrett's patients, are there valuable utility scores for the evaluation of quality of life and the management of cost-effectiveness analyses? D. Provenzale (Durham)
   

. Have screening and surveillance proven impact on the outcome of BE?
18 Are there convincing data that support regression of BE? B.K. Oelschlager (Seattle)
   

. What information can be expected from biomarkers in "reversed" Barrett's esophagus?

19 Do genetic abnormalities persist after successful regression? A. Maitra (Baltimore)
20 What clear risk stratification should be considered in 2010 to develop appropriate surveillance strategies? G.W. Falk (Cleveland)

     


Tuesday, August 31, 1:15 - 3:35 p.m. - Amphitheater

Progression to adenocarcinoma - Markers

Chairs: R.K. Mittal (San Diego) - S.J. Meltzer(Baltimore)
Discussants: L.B. Gerson (Stanford) - P. Rabinovitch (Seattle) - J. Zhang (Xian)

    Progression to adenocarcinoma
1

In GERD patients, is progression to BE a necessary step towards development of adenocarcinoma? A. Maitra (Baltimore)
2 In progression of HGD to adenocarcinoma, are the mechanisms of acid and nitric oxide induced DNA damage in esophageal cells currently known? R.C. Fitzgerald (Cambridge)
3 What is the role of acid and bile salts in neoplastic progression in cell lines?  K.M. Das (New Brunswick)
4 How does abnormal methylation contribute to neoplastic progression in Barrett's esophagus? S.J. Meltzer (Baltimore)
5 How useful is flow cytometry for the evaluation of neoplastic progression in BE? P. Rabinovitch (Seattle)      

6 What are the genetic alterations to occur early in the stromal cells in the metaplasia-dysplasia-cancer sequence?
7 What specific genetic genomic changes can be shown in the epithelial cells in neoplastic progression? M. Younes (Houston)
   

.Is there an order to change in genes in neoplastic progression? 

8 What is the role of telomerase inhibitors on neoplastic progression in cell lines? P. Rabinovitch (Seattle)

9 What is the role of IGF (insulin-like growth factor) in progression to adenocarcinoma?
   

. What is the role of microRNA? L.J. Hardie (Leeds)

10 Can expression and localization of epithelial mesenchymal regulators in the progression of squamous mucosa to adenocarcinoma be demonstrated?
C. Tselepis (Birmingham)
11 Is confocal laser endomicroscopy , allowing subsurface analysis of the mucosa, a reliable tool for detection of BE associated neoplasia? W.M. Weinstein (Los Angeles)
12 Is combination of AFI (Auto-Fluorescence Imaging) with NBI (Narrow Band Imaging) and HRE (High Resolution Endoscopy) likely to reduce the rate of false positive findings of High Grade intra-epithelial neoplasia?
13 What can be expected from Statins, inducing apoptosis in BE adenocarcinoma cells, as adjuvant chemotherapeutic agent? I.L.P. Beales (Norwich)

14 How can proteins involved in EMT (epithelial mesenchymal transition) be considered for a therapeutic strategy in patients with adenocarcinoma? A.C. Chang (Ann Arbor)

    Markers
15 What is the value of macroscopic markers (esophagitis-ulcer-nodularity-stricture) in defining a subset of Barrett's patients at high risk of HGD and adenocarcinoma? W. Nilton Felix (Sao Paulo)
16 Can a panel of molecular pathways that may allow for prediction of cancer be defined? B.McKenna (Ann Arbor)
17 What is the value of Cyclin D overexpression in the armentarium of biomarkers for cancer? K.E. Bani-Hani (Irbid)
18 What should be the current interpretation of p53 mutations (17p loss of heterozygosity-overexpression) for identification of Barrett's patients at high risk of cancer? P. Schneider (Zurich)
19 Should inhibition of the pro-inflammatory cytokine pathway be considered in chemoprevention strategy against the dysplasia-adenocarcinoma sequence?  J.V. Reynolds (Dublin)
20 Can the sequence of molecular events interacting in malignant progression in Barrett's mucosa be more precisely defined in 2010? A.M. Bellizzi (Boston)

     


Tuesday, August 31, 4:25 - 6:45 p.m. - Amphitheater

Prevalence - Incidence of adenocarcinoma

Chairs: R.K. Goyal (Boston) - P.D. Siersema (Utrecht)
Discussants: L. Murray (Belfast) - Y. Romero (Rochester, MN)

1

What is the effect of PPI therapy on the risk of neoplastic progression in patients with Barrett's esophagus? H.M. Shields (Boston)
2 Is there a potential dose-response associated with PPIs and reduced adenocarcinoma risk?  I.J.S. Cook (Sydney)
3 What are the mechanisms by which PPIs may exert a protective effect on progression of BE to HGD and carcinoma?
4 Are there dietary compounds with increased expression in the Barrett's tissue, that may be likely to induce changes in the rates of cell proliferation?
5 Is there any evidence of geographical variation in adenocarcinoma incidence? G. Eslick (Boston) - J. Zhang (Xian)
6 What are the possible confounding factors that may influence the cancer incidence rates? Y. Romero (Rochester, MN)
7 Is there a clear relationship between length of BE and cancer development? H.M. Shields (Boston)
8 What is the efficacy of Celocoxib (Cox2 inhibition) in decreasing cancer incidence in Barrett's patients with dysplasia? A. Maitra (Baltimore)
   

. The data from the CEBET trial

9 May the effects of PPIs by increasing cell differentiation and apoptosis as well as reduction of Cox-2 expression be an indication for their role in the diminution of cancer risk? K. Dvorak (Tucson)
10 Can the current cancer incidence in HGD patients undergoing surveillance endoscopy be specified? A. Rastogi (Kansas City)
11 In terms of submucosal invasion, what information can be drawn from esophagectomy findings in patients with HGD and adenocarcinoma? K. Takubo (Tokyo)
12 Is the presence of foci of occult neoplasia with submucosal invasion in surgical specimens of esophagectomy for HGD overestimated?  C.A. Pellegrini (Seattle)
13 What is the true prevalence of unsuspected invasive cancer (submucosal invasion) in the esophageal specimens resected for HGD? J. Lee (Chicago)
14 In spite of the current dramatic increase in the incidence of adenocarcinomas, has lower prevalence of concomitant adenocarcinoma in HGD led to a shift in treatment favoring endoscopic therapy? D. Peura (Charlottesville)
   

. Is the compared rate of long-term cancer development with PPI therapy alone or associated to endoscopic treatments currently available?
15 What information can be drawn from the comparative incidence rates of progression to adenocarcinoma in Barrett's patients treated with medical therapy or having undergone anti-reflux surgery?
   

. Are the two cohorts of patients comparable? B.A. Jobe (Pittsburgh)
16 May the inappropriate consideration of inflammation as LGD be a reason for overestimation of regression rates in surgical series? R.P. Tatum (Seattle)
17 What is the proof that a diagnosis of LGD puts a patient at greater risk for progression to carcinoma than a diagnosis of negative for dysplasia?
G.Y. Lauwers (Boston)

18 May minimally invasive anti-reflux surgery have an impact on the evaluation of incidence rates?
19 What is the potential for errors in the evaluation of incidence of adenocarcinoma in patients with BE? K.E. Bani-Hani (Aman)
20 What are the reasons for the drastic variations of cancer incidence per patient follow-up year in the literature?

     


Tuesday, August 31, 1:15 - 3:35 p.m. - Waterfront I-II

Treatments of adenocarcinomas (1)

Chairs: B. Gayet (Paris) - K.K. Wang (Rochester, MN)
Discussants: H. Inoue (Yokohama)- J.M. Collard (Brussels) - B. P.L. Wijnhoven (Rotterdam)

    Endoscopic treatments
    EMR
1

Is EMR to be considered as a valuable tool for the endoscopic removal of HGD or early cancer in BE?       
   

. In 2010, what is the best indication for EMR? M. Conio (San Remo)
2 Following EMR, is accurate tumor staging possible by pathologic examination of margins with neoplastic involvement? G.Y. Lauwers (Boston)
   

. What must a pathologist know in order to interpret an EMR specimen from Barrett's mucosa?
3

What are the current results of EMR in lesions confined to the mucosa? S. Komanduri  (Chicago)
   

. What is the rate of recurrence in the mucosa remaining after endoscopic resection?

4 What are the criteria for logical choice between EMR and other ablative therapies?
(Suck & cut technique - Lift & cut resection - Cao-assisted aspiration - Band ligation mucosectomy - endoscopic submucosal dissection) P. Deprez (Brussels)
    SRER
(Stepwise Radical Endoscopic mucosal Resection)
5 What are the advantages of the circumferential resection?
6 The CBE-EMR (Complete Barrett's Eradication-Endoscopic Mucosal resection) I. Waxman (Chicago)
7 Can it be assumed that, following SRER of BE, the neosquamous epithelium is free of genetic abnormalities? S. Komanduri (Chicago)
8 How can genetic alterations be best evaluated? K.K. Krisnadath (Amsterdam)  
   

. The advantages of DNA-FISH technique (Fluorescent In Situ Hybridization)

9 What are the limitations of FISH in determining chromosomal changes?  
   

.How can the results of genomic hybridization, FISH, cytogenetics and high fidelity DNA histograms be compared?
10 Can it be assumed that the neo-squamous mucosa may not arise from Barrett's epithelium, but from submucosal glands? R.C. Orlando (Chapel Hill)
11 In 2010, can long-term recurrence rate after SRER be evaluated?
12 What are the cost-benefit advantages of the Photonic Tumor Therapy System (Fotelo-Fotesi-PDT) in endoscopic treatment of adenocarcinoma?  G. Hofmann (Vienna)
13 What is the role of CT in the evaluation of TNM classification of early stages in Barrett's carcinoma? F.I. Habib (Rome)
14 Is lymphadenectomy justified for intra-mucosal disease? J.M. Collard (Brussels)
15 What is the lymph node yield with transthoracic vs transhiatal dissection? B. P.L. Wijnhoven (Rotterdam)
16 What are the indications and limits of video-assisted lymphadenectomy? R.J.J. Verhage (Utrecht)
17 Is it justified to enlarge the extent of the mediastinal lymphadenectomy? B. Brücher (Tubingen)
18 In terms of long-term survival, what is the difference between endoscopic therapy and esophagectomy for patients with mucosal adenocarcinoma? G.A. Prasad (Rochester, MN)
19 Following R0 resection for Siewert types I, II, III, what is the influence of proximal esophageal resection on survival of patients?  C. Schuhmacher (Munich)
   

. In patients with adenocarcinoma at the GEJ having undergone R0 resection, what is the length of ex vivo proximal esophagus that is associated with better outcome?

20 In 2010, what are the indications of the sentinel node dissection? M. Feith (Munich)                   

     


Tuesday, August 31, 4:25 - 6:45 p.m. - Waterfront I-II

Treatments of adenocarcinomas (2)

Chairs: P.M. Schneider (Zurich) - J.D. Luketich (Pittsburgh)
Discussants: D.H. Ilson (New York)

1

Should immuno-histochemistry be systematically indicated for the elimination of false negative aspects and identification of micro-metastases? E. Wiley (Chicago)
2 What is the accuracy of intra-operative frozen sections?W. Twaddel (Baltimore)
3

What is the best way for mediastinal SN dissection (Thoracoscopy? Special probes through trans-hiatal dissection? New PET probes?) P.C. WU (Seattle)
4 What is the role of robotic surgery? R. Van Hillegersberg (Utrecht)
5 Can the SN concept be still considered following CRT? M. Feith (Munich)
   

. What are the characteristics of the best candidate for SN dissection?

6 In 2010, is it futuristic to foresee a "translymphatic delivery system" of anticancer agents for the control of minimal disease? H.S. Garewal (Tucson)
7 Does Siewert's classification allow for distinction of patients with different life expectancy? C. Schuhmacher (Munich)
8 Is video-endoscopic approach to be discussed for high-risk patients? J.D. Luketich (Pittsburgh)
9 What are the indications of two-step esophagectomy? B. Brücher (Tubingen)
10

What are the limits of radicallymph node dissection performed by thorascopy? H. Inoue (Yokohama)
11 What are the advantages of the prone position? C. Palanivelu  (Coimbatore)
12 Is it conceivable to identify clinical variables or biomarkers predictive of pathologic complete response? D. Vallböhmer (Cologne)
13

What role does PET scan play in response assessment and restaging in esophageal adenocarcinoma? W. Hofstetter (Houston)
14 Would it be possible to define two different groups of patients, those who would not undergo surgery (complete response to CRT expected) and those who would not be exposed to the risks of combined treatments (less aggressive tumor)? M.J. Krasna (Towson)

15 Can P53 mutations be of help for such patients?
16 Are there indications for exclusive RCT for loco-regionally advanced disease in patients responding to induction CT? R. Schmid (Vienna)
   

. Is there a relationship between therapeutic resistance and active oxygen scavengers produced by the tumor?
17 In 2010, what are the indications of Non CDDP and Non 5FU regimens? D.H. Ilson (New York)
18 Are there new advances for the use of specific monoclonal antibodies? P.M. Schneider (Zurich)        
   

. What can be expected from novel monoclonal antibodies that may control cell proliferation (EGFR) using micro-array technology?
19 In 2010, can a valid stage-specific therapy for esophageal adenocarcinoma be defined? M.J. Krasna (Towson)               
20 Are there promising targets for selective therapy? B.P.L. Wijnhoven (Rotterdam)

     


Tuesday, August 31, 4:25 - 6:45 p.m. - Cityview I

Natural history

Chairs: R.C. Orlando (Chapel Hill) - S.J. Spechler (Dallas)
Discussants: R.W. McCallum (El Paso) - B.K. Oelschlager (Seattle)

1

What is the proof that Barrett's mucosa develops in areas of damaged, previously normal squamous mucosa? H.D. Appelman (Ann Arbor)
2 In GERD patients, can the risks factors for development of Barrett's mucosa be determined?
   

 . Is it possible to envisage a clinical risk classification tool?
3 Can temporal evaluation of reflux events in Barrett's patients allow for the understanding of mucosal damage?
4 Can it be stated that BE follows a phenotypic presentation model in the natural history of GERD? R. Orlando (Chapel Hill)
5 What should be the screening criteria for the general population? N.J. Shaheen (Chapel Hill)
6 Is differentiation between LSBE and SSBE still valid? Aren't these findings the result of the same process? S.J. Spechler (Dallas)
7 What is the current (2010) knowledge of the natural history of dysplasia for the wise management of patients with HGD? S.J. Sontag (Chicago)
8 Can correlation between the degree of dysplasia and the expectable subsequent biologic behavior of the lesion be evaluated? B.P.L. Wijnhoven (Rotterdam)
9 Is it possible to predict which patients with HGD will progress to adenocarcinoma? S.J. Sontag (Chicago)
10 Which biopsy protocol should be most likely to detect dysplasia in Barrett's mucosa? S. Nandurkar (Melbourne)                                            

11 According to the results of antibody testing (Cag A protein) can it be anticipated that H. pylori colonization protects against BE? P. Malfertheiner (Magdeburg)
12 Can gastric atrophy be an explanation of the inverse association of adenocarcinoma with H. pylori infection? H. El Zimaity (Hamilton)
13 What are the arguments against the decrease of the risk of BE by H. Pylori infection? A. Lanas (Zaragoza)

14 Is there an effect of PPIs in the natural history of the disease? S.J. Spechler (Dallas)
15

Should decrease of PPI efficacy following eradication of H. Pylori be considered in the treatment of Barrett's patients? A. Lanas (Zaragoza)

16 May PDT alter the natural history of dysplasia in BE? J.L. Hornick (Boston)
17 Is surgical treatment likely to modify the progression the natural history Barrett's esophagus? P. Parise (Pisa)
18 Is trimodal esophageal imaging (HRE-AFI-NBI) the best tool for enhancement of detection of early neoplasia in Barrett's patients? R. Lambert (Lyons)
19 How accurate is endoscopy to assess progression or regression of BE? R. Tutuian (Bern)
20 The essential importance of natural history for the wise management of high grade dysplasia. H.M. Shields (Boston)