Robert D Odze

Harvard Medical School, Boston, Massachusetts, United States

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Publications (142)874.11 Total impact

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    ABSTRACT: Enhanced imaging technologies such as narrow band imaging, flexible spectral imaging color enhancement, i-Scan, confocal laser endomicroscopy, and optical coherence tomography are readily available for use by endoscopists in routine clinical practice. In November 2014, the American Gastroenterological Association's Center for GI Innovation and Technology conducted a 2-day workshop to discuss endoscopic image enhancement technologies, focusing on their role in 2 specific clinical conditions (colon polyps and Barrett's esophagus) and on issues relating to training and implementation of these technologies (white papers). Although the majority of the studies that use enhanced imaging technologies have been positive, these techniques ideally need to be validated in larger cohorts and in community centers. As it stands today, detailed endoscopic examination with high-definition white-light endoscopy and random 4-quadrant biopsy remains the standard of care. However, the workshop panelists agreed that in the hands of endoscopists who have met the preservation and incorporation of valuable endoscopic innovation thresholds (diagnostic accuracy) with enhanced imaging techniques (specific technologies), use of the technique in Barrett's esophagus patients is appropriate.
    No preview · Article · Oct 2015 · Clinical Gastroenterology and Hepatology
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    ABSTRACT: Barrett's esophagus is thought to progress to esophageal adenocarcinoma (EAC) through a stepwise progression with loss of CDKN2A followed by TP53 inactivation and aneuploidy. Here we present whole-exome sequencing from 25 pairs of EAC and Barrett's esophagus and from 5 patients whose Barrett's esophagus and tumor were extensively sampled. Our analysis showed that oncogene amplification typically occurred as a late event and that TP53 mutations often occurred early in Barrett's esophagus progression, including in non-dysplastic epithelium. Reanalysis of additional EAC exome data showed that the majority (62.5%) of EACs emerged following genome doubling and that tumors with genomic doubling had different patterns of genomic alterations, with more frequent oncogenic amplification and less frequent inactivation of tumor suppressors, including CDKN2A. These data suggest that many EACs emerge not through the gradual accumulation of tumor-suppressor alterations but rather through a more direct path whereby a TP53-mutant cell undergoes genome doubling, followed by the acquisition of oncogenic amplifications.
    No preview · Article · Jul 2015 · Nature Genetics
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    ABSTRACT: Diminutive colon polyps, defined as less than or equal to 5mm, are increasingly encountered at colonoscopy. The risk of serious pathology in such polyps is low. There is a risk and cost of resecting all such polyps and sending tissue for pathologic evaluation. Enhancement of endoluminal imaging may enable discrimination of neoplastic versus non-neoplastic polyps. If this discrimination can be performed accurately with high confidence, it may be possible to either resect and discard diminutive adenomas, or inspect and do-not-resect diminutive hyperplastic polyps. In 2011, an expert group recommended thresholds of 90% negative predictive value for adenoma, and 90% accuracy in predicting appropriate surveillance interval. Since 2011, criteria for polyp discrimination have been published and validated by experts and non-expects. In-vivo studies have been performed to compare endoscopic impression and pathologic diagnosis. An expert panel was convened in late 2014 to review the literature to determine if proposed thresholds for discrimination can be attained and recommend the next steps for introducing changes in clinical practice. The review concludes that threshold levels can be achieved with several endoscopic image enhancements. Next steps to implementation of practice change include acquiring data on training and competence, determining best practices for auditing performance, understanding patient education needs, and the potential cost-benefit of such changes. Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved.
    No preview · Article · Jul 2015 · Clinical gastroenterology and hepatology: the official clinical practice journal of the American Gastroenterological Association
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    ABSTRACT: Our study reveals a non-canonical role for CCL2 in modulating non-macrophage, myeloid-derived suppressor cells (MDSCs) and shaping a tumor-permissive microenvironment during colon cancer development. We found that intratumoral CCL2 levels increased in patients with colitis-associated colorectal cancer (CRC), adenocarcinomas, and adenomas. Deletion of CCL2 blocked progression from dysplasia to adenocarcinoma and reduced the number of colonic MDSCs in a spontaneous mouse model of colitis-associated CRC. In a transplantable mouse model of adenocarcinoma and an APC-driven adenoma model, CCL2 fostered MDSC accumulation in evolving colonic tumors and enhanced polymorphonuclear (PMN)-MDSC immunosuppressive features. Mechanistically, CCL2 regulated T cell suppression of PMN-MDSCs in a STAT3-mediated manner. Furthermore, CCL2 neutralization decreased tumor numbers and MDSC accumulation and function. Collectively, our experiments support that perturbing CCL2 and targeting MDSCs may afford therapeutic opportunities for colon cancer interception and prevention. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.
    Preview · Article · Jul 2015 · Cell Reports
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    ABSTRACT: The American Journal of Gastroenterology is published by Nature Publishing Group (NPG) on behalf of the American College of Gastroenterology (ACG). Ranked the #1 clinical journal covering gastroenterology and hepatology*, The American Journal of Gastroenterology (AJG) provides practical and professional support for clinicians dealing with the gastroenterological disorders seen most often in patients. Published with practicing clinicians in mind, the journal aims to be easily accessible, organizing its content by topic, both online and in print. www.amjgastro.com, *2007 Journal Citation Report (Thomson Reuters, 2008)
    No preview · Article · Jun 2015 · The American Journal of Gastroenterology
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    ABSTRACT: Identifying specific genes that are differentially expressed during inflammatory bowel disease flares may help stratify disease activity. The aim of this study was to identify panels of genes to be able to distinguish disease activity in Crohn's disease (CD) and ulcerative colitis (UC). Patients were grouped into categories based on disease and severity determined by histological grading. Whole blood was collected by PAXgene Blood RNA collection tubes, (PreAnalytiX) and gene expression analysis using messenger RNA was conducted. Logistic regression was performed on multiple combinations of common probe sets, and data were evaluated in terms of discrimination by computing the area under the receiving operator characteristic curve (ROC-AUC). Nine inactive CD, 8 mild CD, 10 moderate-to-severe CD, 9 inactive UC, 8 mild UC, 10 moderate-to-severe UC, and 120 controls were hybridized to Affymetrix U133 Plus 2 microarrays. Panels of 6 individual genes discriminated the stages of disease activity: CD with mild severity {ROC-AUC, 0.89 (95% confidence interval [CI], 0.84%-0.95%)}, CD with moderate-to-severe severity (ROC-AUC 0.98 [95% CI, 0.97-1.0]), UC with mild severity (ROC-AUC 0.92 [95% CI, 0.87-0.96]), and UC with moderate-to-severe severity (ROC-AUC 0.99 [95% CI, 0.97-1.0]). Validation by real-time reverse transcription-PCR confirmed the Affymetrix microarray data. The specific whole blood gene panels reliably distinguished CD and UC and determined the activity of disease, with high sensitivity and specificity in our cohorts of patients. This simple serological test has the potential to become a biomarker to determine the activity of disease.
    Full-text · Article · May 2015 · Inflammatory Bowel Diseases
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    ABSTRACT: doi: 10.1038/ajg.2015.55 http://www.nature.com/ajg/journal/vaop/ncurrent/abs/ajg201555a.html OBJECTIVES: Barrett’s esophagus (BE) is a common premalignant lesion for which surveillance is recommended. This strategy is limited by considerable variations in clinical practice. We conducted an international, multidisciplinary, systematic search and evidence-based review of BE and provided consensus recommendations for clinical use in patients with nondysplastic, indefinite, and low-grade dysplasia (LGD). METHODS: We defined the scope, proposed statements, and searched electronic databases, yielding 20,558 publications that were screened, selected online, and formed the evidence base. We used a Delphi consensus process, with an 80% agreement threshold, using GRADE (Grading of Recommendations Assessment, Development and Evaluation) to categorize the quality of evidence and strength of recommendations. RESULTS: In total, 80% of respondents agreed with 55 of 127 statements in the final voting rounds. Population endoscopic screening is not recommended and screening should target only very high-risk cases of males aged over 60 years with chronic uncontrolled reflux. A new international definition of BE was agreed upon. For any degree of dysplasia, at least two specialist gastrointestinal (GI) pathologists are required. Risk factors for cancer include male gender, length of BE, and central obesity. Endoscopic resection should be used for visible, nodular areas. Surveillance is not recommended for <5 years of life expectancy. Management strategies for indefinite dysplasia (IND) and LGD were identified, including a de-escalation strategy for lower-risk patients and escalation to intervention with follow-up for higher-risk patients. CONCLUSIONS: In this uniquely large consensus process in gastroenterology, we made key clinical recommendations for the escalation/de-escalation of BE in clinical practice. We made strong recommendations for the prioritization of future research.
    Full-text · Article · Apr 2015 · The American Journal of Gastroenterology
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    ABSTRACT: Objectives: Barrett's esophagus (BE) is a common premalignant lesion for which surveillance is recommended. This strategy is limited by considerable variations in clinical practice. We conducted an international, multidisciplinary, systematic search and evidence-based review of BE and provided consensus recommendations for clinical use in patients with nondysplastic, indefinite, and low-grade dysplasia (LGD). Methods: We defined the scope, proposed statements, and searched electronic databases, yielding 20,558 publications that were screened, selected online, and formed the evidence base. We used a Delphi consensus process, with an 80% agreement threshold, using GRADE (Grading of Recommendations Assessment, Development and Evaluation) to categorize the quality of evidence and strength of recommendations. Results: In total, 80% of respondents agreed with 55 of 127 statements in the final voting rounds. Population endoscopic screening is not recommended and screening should target only very high-risk cases of males aged over 60 years with chronic uncontrolled reflux. A new international definition of BE was agreed upon. For any degree of dysplasia, at least two specialist gastrointestinal (GI) pathologists are required. Risk factors for cancer include male gender, length of BE, and central obesity. Endoscopic resection should be used for visible, nodular areas. Surveillance is not recommended for <5 years of life expectancy. Management strategies for indefinite dysplasia (IND) and LGD were identified, including a de-escalation strategy for lower-risk patients and escalation to intervention with follow-up for higher-risk patients. Conclusions: In this uniquely large consensus process in gastroenterology, we made key clinical recommendations for the escalation/de-escalation of BE in clinical practice. We made strong recommendations for the prioritization of future research.
    Full-text · Article · Apr 2015 · The American Journal of Gastroenterology
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    ABSTRACT: Routine tumor genotyping enables identification of concurrent mutations in tumors and reveals low-frequency mutations that may be associated with a particular tumor phenotype. We genotyped 311 colorectal carcinomas (CRCs) for 471 mutation hot spots in 41 cancer-associated genes. At least 1 mutation was present in 239 (77%) of 311 tumors. Two concurrent mutations were identified in 89 (29%) tumors, 3 mutations in 24 (8%), 4 mutations in 6 (2%), and 5 mutations in 1 tumor. KRAS mutations were most frequent and identified in 132 (42%) tumors, followed by APC in 79 (25%) and TP53 in 64 (21%) tumors. Mutations in PIK3CA, BRAF, CTNNB1, and NRAS were identified in 41, 27, 11, and 9 cases, respectively. Rare mutations not typically associated with CRC included AKT1 (4), AKT2 (1), IDH1 (1), KIT (1), MAP2K1 (1), PTEN (2), and GNAS (6). GNAS mutations in CRC correlated with a mucinous phenotype and were present in 20% of all mucinous adenocarcinomas evaluated in this study. Among CRCs with a PIK3CA mutation, 77% showed concurrent mutations in other cancer-associated genes, and 4% of CRC did not neatly fit into either the chromosomal instability pathway or CpG island methylator phenotype/microsatellite instability pathway, suggesting overlapping mutational profile in some tumors. Our findings indicate that routine tumor genotyping is helpful in identifying low-frequency mutations, such as GNAS, that may correlate with a specific morphological phenotype and also reveal multiplicity of concurrent mutations in a significant proportion of CRC that may have significant implications for clinical trial design and personalized therapy. Copyright © 2015 Elsevier Inc. All rights reserved.
    No preview · Article · Jan 2015 · Human pathology
  • Robert D Odze
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    ABSTRACT: Distinguishing ulcerative colitis (UC) from Crohn's disease (CD) is normally based on evaluation of a variety of clinical, radiologic, serologic and pathologic findings, the latter in biopsy and/or resection specimens. Unfortunately, some patients with IBD show overlapping pathologic features of UC and CD, which makes definite distinction between these two disorders difficult or even impossible. In most instances of uncertainty, the patient shows clinical and pathologic features of UC, but in addition, the patient's colon resection specimen reveals one or more CD-like features. In this setting, a diagnosis of indeterminate colitis (IC) is often rendered. IC is not a distinct disease entity, and, thus, it has no diagnostic criteria. The most common causes of uncertainty in IBD pathology that may lead to a diagnosis of IC in a colon resection specimen includes the presence of fulminant (severe and toxic) colitis, insufficient radiologic, endoscopic, or pathologic information (including analysis of prior biopsies) on the patient, failure to utilize major diagnostic criteria as hard evidence in favor of CD, failure to recognize unusual variants of UC and CD that may mimic each other, failure to recognize non-IBD mimics and other superimposed diseases that cause unusual pathologic features in a resection specimen, an attempt to distinguish UC from CD in mucosal biopsies of the colon and ileum, or an attempt to change the patients diagnosis (of UC or CD) based on pouch or diversion-related complications. Details of each of these causes of uncertainty are discussed, in detail, in this review article. A diagnosis of IC should never be made clinically or by pathologists based on evaluation of pre-resection colonic mucosal biopsies. Ultimately, the majority of indeterminate cases represent UC, and, thus, most of these patient can be treated safely with a colectomy combined with an ileal pouch anal anastomosis procedure.
    No preview · Article · Jan 2015 · Modern Pathology
  • Kyle Viani · Robert D. Odze
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    ABSTRACT: Polypoid lesions are frequently encountered during IBD surveillance colonoscopy. Accurate endoscopic and pathologic classification of these lesions is essential for appropriate management. Of particular importance are polypoid dysplastic lesions, which have historically been referred to by the term DALM (dysplasia-associated-lesion or mass). This chapter provides a review of the endoscopic features, pathology, natural history, and management of DALMs. Based on endoscopic features, DALMs can be subclassified as adenoma-like (endoscopically resectable) and non-adenoma-like (non-endoscopically resectable). The presence of a non-adenoma-like DALM is an indication for colectomy. In contrast, adenoma-like DALMs can be treated conservatively by polypectomy and endoscopic surveillance provided the lesion is completely removed and no flat dysplasia is identified in the colon.
    No preview · Article · Jan 2015
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    ABSTRACT: Background Mipomersen is an antisense oligonucleotide that inhibits apolipoprotein (apo) B synthesis and lowers plasma low density lipoprotein (LDL) cholesterol even in the absence of LDL receptor function, presumably due to the inhibition of hepatic production of triglyceride-rich very low density lipoprotein (VLDL) particles. By virtue of this mechanism, mipomersen therapy commonly results in the development of hepatic steatosis. Because this is frequently accompanied by alanine aminotransferase (ALT) elevations, concern has arisen that mipomersen could promote the development of steatohepatitis, which could in turn lead to fibrosis and cirrhosis over time. Objective The objective of this study was to assess the liver biopsy findings in patients treated with mipomersen. Methods We describe 7 patients who underwent liver biopsy during the mipomersen clinical development programs. Liver biopsies were reviewed by a single, blinded pathologist. Results The histopathological features were characterized by simple steatosis, without significant inflammation or fibrosis. Conclusion These findings suggest that hepatic steatosis due to mipomersen is distinct from non-alcoholic steatohepatitis.
    Full-text · Article · Aug 2014 · Journal of Clinical Lipidology
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    ABSTRACT: To investigate whether drugs others than mycophenolic acid and ipilimumab might cause graft-versus-host-like apoptotic enteropathy, the clinicopathological findings in four patients were examined who had developed watery diarrhoea and apoptotic enteropathy (three cases from colon and one case from ileal pouch) after intake of antimetabolites (methotrexate and capecitabine) and/or tumour necrosis factor-α inhibitors (etanercept and infliximab). The clinical charts, endoscopy reports and intestinal biopsies from all endoscopies were reviewed for all patients. Biopsies were evaluated semiquantitatively for apoptosis of basal crypts, dilated damaged crypts, defined as cystically dilated crypts with flattened degenerated epithelium containing apoptotic debris and few neutrophils, and mucosal architecture. Further, the presence of intraepithelial lymphocytes, chronic inflammatory cells in the lamina propria and mucosal ulcerations was recorded and immunohistochemical analysis for human cytomegalovirus and herpes simplex virus was performed. Endoscopic examination revealed normal mucosa in two patients, whereas the other two showed focal ulcerations. Histological changes included increased apoptosis of basal crypts, the presence of dilated damaged crypts and architecture distortion. In all cases, a temporal association between drug intake and/or dose increase, and onset of diarrhoea, was observed, and no convincing evidence of other potentially underlying causes of colitis/enteritis was found, including infections. Pathologists should be aware of the expanding spectrum of drugs that can cause apoptotic enteropathy, including antimetabolites and tumour necrosis factor-α inhibitors.
    Full-text · Article · Apr 2014 · Journal of clinical pathology
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    Preview · Article · Apr 2014 · Journal of the American College of Cardiology
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    ABSTRACT: Endoscopic ampullectomy is increasingly performed in patients with familial adenomatous polyposis (FAP)-associated ampullary adenomas. We sought to define the procedure-associated morbidities and long-term outcomes. We performed a retrospective chart review of patients with FAP who underwent endoscopic ampullectomy at two tertiary institutions between 1999 and 2010. The severity of duodenal polyposis was classified according to Spigelman's classification. Of 26 FAP patients who underwent endoscopic ampullectomy, 21 arose in the setting of Spigelman's stage II duodenal polyposis. Adverse events associated with endoscopic ampullectomy included acute pancreatitis (19.2 %), abdominal pain (7.6 %), and bleeding (3.8 %). The mean resected adenoma size was 0.99 ± 0.34 cm. Three adenomas (12.0 %) contained foci of high-grade dysplasia. Follow-up data were available for 24 patients. The mean follow-up duration was 84.5 ± 36.2 months. Adenoma recurrence was observed in 14 patients (58.3 %; 14/24) at a mean of 38.3 months after initial ampullectomy. Adenomas ≥10 mm recurred more frequently than smaller adenomas (76.9 vs. 36.4 %; p = 0.002). Positive margins were not associated with higher recurrence rates. No cancers were observed during long-term follow-up. Three patients underwent a Whipple procedure, but none was performed for a recurrent ampullary adenoma. Endoscopic ampullectomy in FAP can be performed safely. Because ampullary adenomas frequently recur after endoscopic ampullectomy, close surveillance is essential. Smaller tumors are less likely to recur, suggesting a benefit for early recognition of these lesions.
    No preview · Article · Feb 2014 · Surgical Endoscopy
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    ABSTRACT: Most patients with familial adenomatous polyposis (FAP) develop gastric fundic gland polyps, with many displaying low grade dysplasia. This study evaluates the natural history and morphologic phenotype of dysplasia in FAP associated fundic gland polyps. Patients with FAP and dysplastic fundic gland polyps (n=24) were identified. 22 of 24 FAP associated dysplastic fundic gland polyps showed a gastric phenotype and two had mixed phenotype. Over a mean 6.1 year follow up (range 0.8-12.6 years) and 5.7 endoscopies (range 2-22), one patient (4%) was diagnosed with a fundic gland polyp with high grade dysplasia, while 23 patients (96%) in this cohort had either no dysplasia or persistent low grade dysplasia. Contemporary patients with sporadic fundic gland polyps with low grade dyplasia had similar morphology and outcomes to the FAP associated fundic gland polyp cohort. Dysplasia in fundic gland polyps (FAP associated and sporadic) was less frequently associated with intestinal phenotype, high grade dysplasia, and the finding of concurrent or subsequent carcinoma compared to contemporary patients with sporadic gastric dysplasia not occurring in fundic gland polyps. This cohort of patients with FAP associated dysplastic fundic gland polyps rarely developed high grade dysplasia and gastric adenocarcinoma was absent. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2014 · Histopathology
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    ABSTRACT: The purpose of this survey was to ascertain reporting habits of pathologists towards sessile serrated adenomas/polyps (SSA/P). A questionnaire designed to highlight diagnostic criteria, approach and clinical implications of SSA/P was circulated electronically to 45 pathologists in the UK and North America. Forty-three of 45 pathologists agreed to participate. The vast majority (88%) had a special interest in gastrointestinal (GI) pathology, had great exposure to GI polyps in general with 40% diagnosing SSA/P at least once a week if not more, abnormal architecture was thought by all participants to be histologically diagnostic, and 11% would make the diagnosis if a single diagnostic histological feature was present in one crypt only, while a further 19% would diagnose SSA/P in one crypt if more than one diagnostic feature was present. The vast majority agreed that deeper sections were useful and 88% did not feel proliferation markers were useful. More than one-third did not know whether, or did not feel that, their clinicians were aware of the implications of SSA/P. 98% of pathologists surveyed are aware that SSA/P is a precursor lesion to colorectal cancer, the majority agree on diagnostic criteria, and a significant number feel that there needs to be greater communication and awareness among pathologists and gastroenterologists about SSA/P.
    Full-text · Article · Jan 2014 · Journal of clinical pathology
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    ABSTRACT: Cancers arising in mucosal tissues account for a disproportionately large fraction of malignancies. Immunoglobulin G (IgG) and the neonatal Fc receptor for IgG (FcRn) have an important function in the mucosal immune system that we have now shown extends to the induction of CD8(+) T cell-mediated antitumor immunity. We demonstrate that FcRn within dendritic cells (DCs) was critical for homeostatic activation of mucosal CD8(+) T cells that drove protection against the development of colorectal cancers and lung metastases. FcRn-mediated tumor protection was driven by DCs activation of endogenous tumor-reactive CD8(+) T cells via the cross-presentation of IgG complexed antigens (IgG IC), as well as the induction of cytotoxicity-promoting cytokine secretion, particularly interleukin-12, both of which were independently triggered by the FcRn-IgG IC interaction in murine and human DCs. FcRn thus has a primary role within mucosal tissues in activating local immune responses that are critical for priming efficient anti-tumor immunosurveillance.
    Full-text · Article · Nov 2013 · Immunity
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    ABSTRACT: All cancers are believed to arise by dynamic, stochastic somatic genomic evolution with genome instability, generation of diversity and selection of genomic alterations that underlie multi-stage progression to cancer. Advanced esophageal adenocarcinomas (EAs) have high levels of somatic copy number alterations. Barrett's esophagus (BE) is a risk factor for developing EA, and somatic chromosomal alterations (SCAs) are known to occur in BE. The vast majority (~95%) of individuals with BE do not progress to EA during their lifetimes, but a small subset develop EA, many of which arise rapidly even in carefully monitored patients without visible endoscopic abnormalities at the index endoscopy. Using a well-designed, longitudinal case-cohort study, we characterized SCA as assessed by SNP arrays over space and time in 79 "progressors" with BE as they approach the diagnosis of cancer and 169 "nonprogressors" with BE who did not progress to EA over 20,425 person-months of follow-up. The genomes of nonprogressors typically had small localized deletions involving fragile sites and 9p loss/copy neutral LOH that generate little genetic diversity and remained relatively stable over prolonged follow-up. As progressors approach the diagnosis of cancer, their genomes developed chromosome instability with initial gains and losses, genomic diversity, and selection of SCAs followed by catastrophic genome doublings. Our results support a model of differential disease dynamics in which nonprogressor genomes largely remain stable over prolonged periods whereas progressor genomes evolve significantly increased SCA and diversity within four years of EA diagnosis, suggesting a window of opportunity for early detection.
    Full-text · Article · Nov 2013 · Cancer Prevention Research
  • Robert D Odze
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    ABSTRACT: Much understanding of IBD pathology is based on personal experience, anecdotal observations and small case studies. A paper on the histopathology of IBD provides an exhaustive literature review, and attempts to delineate guidelines for pathologists to use by providing evidence for consensus statements developed by a European contingent of gastrointestinal pathologists and clinicians.
    No preview · Article · Oct 2013 · Nature Reviews Gastroenterology &#38 Hepatology

Publication Stats

5k Citations
874.11 Total Impact Points

Institutions

  • 1997-2015
    • Harvard Medical School
      • Department of Pathology
      Boston, Massachusetts, United States
    • Beth Israel Medical Center
      New York, New York, United States
  • 1995-2015
    • Brigham and Women's Hospital
      • Department of Pathology
      Boston, Massachusetts, United States
    • Harvard University
      • Department of Molecular and Cell Biology
      Cambridge, Massachusetts, United States
  • 2010
    • University of Southern California
      • Department of Surgery
      Los Ángeles, California, United States
  • 2004
    • University of Pennsylvania
      • Department of Pathology
      Filadelfia, Pennsylvania, United States
  • 1998
    • Beth Israel Deaconess Medical Center
      • Department of Pathology
      Boston, MA, United States
  • 1993-1995
    • Mount Sinai Hospital, Toronto
      • Department of Surgery
      Toronto, Ontario, Canada
    • Samuel Lunenfeld Research Institute
      Toronto, Ontario, Canada
  • 1993-1994
    • Mount Sinai Hospital
      New York City, New York, United States