Person: Odze, Robert
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Odze
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Odze, Robert
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Publication Long-term regeneration and remodeling of the pig esophagus after circumferential resection using a retrievable synthetic scaffold carrying autologous cells(Nature Publishing Group UK, 2018) La Francesca, Saverio; Aho, Johnathon M.; Barron, Matthew R.; Blanco, Ellen W.; Soliman, Sherif; Kalenjian, Lena; Hanson, Ariel D.; Todorova, Elisaveta; Marsh, Matthew; Burnette, KaLia; DerSimonian, Harout; Odze, Robert; Wigle, Dennis A.Treatment of esophageal disease can necessitate resection and reconstruction of the esophagus. Current reconstruction approaches are limited to utilization of an autologous conduit such as stomach, small bowel, or colon. A tissue engineered construct providing an alternative for esophageal replacement in circumferential, full thickness resection would have significant clinical applications. In the current study, we demonstrate that regeneration of esophageal tissue is feasible and reproducible in a large animal model using synthetic polyurethane electro-spun grafts seeded with autologous adipose-derived mesenchymal stem cells (aMSCs) and a disposable bioreactor. The scaffolds were not incorporated into the regrown esophageal tissue and were retrieved endoscopically. Animals underwent adipose tissue biopsy to harvest and expand autologous aMSCs for seeding on electro-spun polyurethane conduits in a bioreactor. Anesthetized pigs underwent full thickness circumferential resection of the mid-lower thoracic esophagus followed by implantation of the cell seeded scaffold. Results from these animals showed gradual structural regrowth of endogenous esophageal tissue, including squamous esophageal mucosa, submucosa, and smooth muscle layers with blood vessel formation. Scaffolds carrying autologous adipose-derived mesenchymal stem cells may provide an alternative to the use of a gastro-intestinal conduit for some patients following resection of the esophagus.Publication Comparison of gastro-oesophageal junction carcinomas in Chinese versus American patients(Wiley-Blackwell, 2011) Huang, Qin; Fan, Xiangshan; Agoston, Agoston; Feng, Anning; Yu, Huiping; Lauwers, Gregory Y.; Zhang, Lihua; Odze, RobertAims: To compare the clinical and pathological features of gastro-oesophageal junction (GEJ) carcinomas in Chinese and American patients. Methods and results: Eighty consecutive patients with a GEJ carcinoma (43 from mainland China, and 37 from the USA) were evaluated for association with Barrett oesophagus (BO), chronic Helicobacter pylori gastritis, intestinal metaplasia, and outcome. GEJ carcinomas were defined as tumours that were located within 20 mm of, and crossed, the GEJ. Overall, GEJ carcinomas from Chinese patients revealed significantly more frequent location in the proximal stomach, higher pathological stage, larger size, younger patient age, and association with chronic H. pylori gastritis. In contrast, GEJ cancers from American patients showed a strong association with distal oesophageal location, BO, and associated intestinal metaplasia and dysplasia. Pathologically, GEJ carcinomas from American patients were predominantly adenocarcinomas, whereas Chinese patients showed a higher proportion of mucinous, adenosquamous, acinar or neuroendocrine tumours. Overall, 3- and 5-year survival rates were statistically similar between both patient groups, but upon multivariate analysis, Chinese patients showed statistically better survival rates for stage III tumours. Conclusions: Most GEJ carcinomas in patients from China represent proximal gastric cancers associated with chronic H. pylori gastritis, and BO-associated carcinomas are rare among this patient population.Publication Neonatal Fc Receptor Expression in Dendritic Cells Mediates Protective Immunity against Colorectal Cancer(Elsevier BV, 2013) Baker, Kristi; Rath, Timo; Flak, Magdalena B.; Arthur, Janelle C.; Chen, Zhangguo; Glickman, Jonathan; Zlobec, Inti; Karamitopoulou, Eva; Stachler, Matthew; Odze, Robert; Lencer, Wayne; Jobin, Christian; Blumberg, RichardCancers 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.Publication NSAIDs Modulate Clonal Evolution in Barrett's Esophagus(Public Library of Science, 2013) Kostadinov, Rumen L.; Kuhner, Mary K.; Li, Xiaohong; Sanchez, Carissa A.; Galipeau, Patricia C.; Paulson, Thomas G.; Sather, Cassandra L.; Srivastava, Amitabh; Odze, Robert; Blount, Patricia L.; Vaughan, Thomas L.; Reid, Brian J.; Maley, Carlo C.Cancer is considered an outcome of decades-long clonal evolution fueled by acquisition of somatic genomic abnormalities (SGAs). Non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce cancer risk, including risk of progression from Barrett's esophagus (BE) to esophageal adenocarcinoma (EA). However, the cancer chemopreventive mechanisms of NSAIDs are not fully understood. We hypothesized that NSAIDs modulate clonal evolution by reducing SGA acquisition rate. We evaluated thirteen individuals with BE. Eleven had not used NSAIDs for 6.2±3.5 (mean±standard deviation) years and then began using NSAIDs for 5.6±2.7 years, whereas two had used NSAIDs for 3.3±1.4 years and then discontinued use for 7.9±0.7 years. 161 BE biopsies, collected at 5–8 time points over 6.4–19 years, were analyzed using 1Million-SNP arrays to detect SGAs. Even in the earliest biopsies there were many SGAs (284±246 in 10/13 and 1442±560 in 3/13 individuals) and in most individuals the number of SGAs changed little over time, with both increases and decreases in SGAs detected. The estimated SGA rate was 7.8 per genome per year (95% support interval [SI], 7.1–8.6) off-NSAIDs and 0.6 (95% SI 0.3–1.5) on-NSAIDs. Twelve individuals did not progress to EA. In ten we detected 279±86 SGAs affecting 53±30 Mb of the genome per biopsy per time point and in two we detected 1,463±375 SGAs affecting 180±100 Mb. In one individual who progressed to EA we detected a clone having 2,291±78 SGAs affecting 588±18 Mb of the genome at three time points in the last three of 11.4 years of follow-up. NSAIDs were associated with reduced rate of acquisition of SGAs in eleven of thirteen individuals. Barrett's cells maintained relative equilibrium level of SGAs over time with occasional punctuations by expansion of clones having massive amount of SGAs.Publication Gastritis Cystica Profunda Versus Invasive Adenocarcinoma(Ovid Technologies (Wolters Kluwer Health), 2012) Odze, Robert; Greenson, Joel; Lauwers, Gregory Y.; Goldblum, JohnPublication Pathologic Features of Ulcerative Colitis in Patients With Primary Sclerosing Cholangitis(Ovid Technologies (Wolters Kluwer Health), 2009) Joo, Mee; Abreu-e-Lima, Paula; Farraye, Francis; Smith, Timothy; Swaroop, Prabhakar; Gardner, Laura; Lauwers, Gregory Y.; Odze, RobertBACKGROUND: The pathologic features of ulcerative colitis (UC) in patients with primary sclerosing cholangitis (PSC) are, essentially, unknown. One previous clinical study suggested that UC-PSC patients reveal a high rate of rectal sparing and backwash ileitis. The purpose of this study was to systematically evaluate the pathologic characteristics and distribution of colonic disease in UC-PSC patients and to compare the results with a matched control group of UC patients without PSC. METHODS: Forty UC-PSC patients and 40 matched UC patients without PSC (controls) were identified from the files of 3 hospitals between the years 1989 and 2005. Clinical, endoscopic, and follow-up data (including incidence of pouchitis) were evaluated, and a detailed pathologic evaluation of biopsy and resection specimens (when available) was performed in a blinded fashion. The degree of activity and chronicity in mucosal biopsies and/or tissue from resection specimens was graded on a 5-point grading system (0 to 4), and each portion of the colon (cecum, ascending colon, transverse colon, descending colon, rectum) was assessed separately. Rectal sparing and patchiness of disease were evaluated, and scored as either absolute or relative depending on the complete absence of inflammatory disease in the former, or less inflammatory disease in the rectum compared with other parts of the colon in the latter. RESULTS: In this matched case-control study, UC-PSC patients presented at a significantly earlier age (24.5 y), had a higher prevalence rate of pancolitis (85%), and an overall significantly lower grade of inflammation in the colon (mean grade: 2.09+/-0.085) compared with UC controls (mean age: 33.8 y, pancolitis: 45%, inflammation grade: 2.59+/-0.92, P<0.05 for all comparisons). The incidence rate of absolute and relative rectal sparing (27.5%) and of patchy inflammatory disease proximal to the rectum (5.7%) was not significantly different between the UC-PSC cases and the UC controls (25% and 7.9%, respectively). UC-PSC patients had a higher prevalence rate of ileitis (35.7%) and pouchitis (42.8%), but the values were not significantly different from controls (26.9% and 26.6%, respectively). The incidence rate of dysplasia was similar between the 2 patient groups. CONCLUSIONS: UC patients with PSC show a propensity for more extensive, but less active, disease but are otherwise characterized by similar pathologic findings compared with UC patients without PSC. Rectal sparing and patchy disease activity is not characteristic of UC patients with PSC.Publication Clinical and pathological analysis of colonic Crohn's disease, including a subgroup with ulcerative colitis-like features(Springer Nature, 2011) Soucy, Genevieve; Wang, Helen; Farraye, Francis A; Schmidt, Jason F; Farris, Alton B; Lauwers, Gregory Y.; Cerda, Sandra R; Dendrinos, Kleanthis G; Odze, RobertLittle is known regarding the clinical and, in particular, pathological manifestations of patients with isolated colonic Crohn's disease. The purpose of this study was to evaluate the clinical and pathological features of patients with Crohn's disease limited to the colon at initial presentation, and to determine whether there are any histological features that are predictive of outcome after surgery. The clinical features, outcome after surgery, and pathological features of colonic resection specimens of 73 patients who presented initially with isolated colonic Crohn's disease were evaluated and compared with 45 Crohn's disease patients who presented initially with both ileal and colonic involvement. Clinically, patients with isolated colonic Crohn's disease presented at a significantly older age at the time of diagnosis, and had a significantly shorter duration of colitis before surgical resection, than did patients with ileocolonic Crohn's disease at disease onset. Pathologically, patients with isolated colonic Crohn's disease showed a significantly higher proportion of cases with subtotal, total, or left-sided colitis, and significantly fewer strictures/stenosis, pericolonic adhesions, pyloric metaplasia, and cases with proximal worse than distal colonic disease. Overall, patients with isolated colonic Crohn's disease showed a trend toward a lower number of major microscopic Crohn's disease features. A small proportion of patients from both Crohn's disease groups (14% and 13%, respectively) showed inflammatory disease limited to the mucosa, without mural involvement, reminiscent of ulcerative colitis, and these were termed ‘ulcerative colitis-like Crohn's disease’. These patients were significantly younger than those with mural involvement. Overall, 44% of patients from both Crohn's disease groups developed at least one adverse outcome, and neither the number nor the type of major Crohn's disease features correlated with adverse outcome. Patients with isolated colonic involvement have distinctive clinical and pathological features. A small subgroup of Crohn's patients shows only mucosal involvement reminiscent of ulcerative colitis.Publication Comprehensive molecular characterization of gastric adenocarcinoma(2014) Bass, Adam J.; Thorsson, Vesteinn; Shmulevich, Ilya; Reynolds, Sheila M.; Miller, Michael; Bernard, Brady; Hinoue, Toshinori; Laird, Peter W.; Curtis, Christina; Shen, Hui; Weisenberger, Daniel J.; Schultz, Nikolaus; Shen, Ronglai; Weinhold, Nils; Kelsen, David P.; Bowlby, Reanne; Chu, Andy; Kasaian, Katayoon; Mungall, Andrew J.; Robertson, A. Gordon; Sipahimalani, Payal; Cherniack, Andrew; Getz, Gad; Liu, Yingchun; Noble, Michael S.; Pedamallu, Chandra; Sougnez, Carrie; Taylor-Weiner, Amaro; Akbani, Rehan; Lee, Ju-Seog; Liu, Wenbin; Mills, Gordon B.; Yang, Da; Zhang, Wei; Pantazi, Angeliki; Parfenov, Michael; Gulley, Margaret; Piazuelo, M. Blanca; Schneider, Barbara G.; Kim, Jihun; Boussioutas, Alex; Sheth, Margi; Demchok, John A.; Rabkin, Charles S.; Willis, Joseph E.; Ng, Sam; Garman, Katherine; Beer, David G.; Pennathur, Arjun; Raphael, Benjamin J.; Wu, Hsin-Ta; Odze, Robert; Kim, Hark K.; Bowen, Jay; Leraas, Kristen M.; Lichtenberg, Tara M.; Weaver, Stephanie; McLellan, Michael; Wiznerowicz, Maciej; Sakai, Ryo; Lawrence, Michael S.; Cibulskis, Kristian; Lichtenstein, Lee; Fisher, Sheila; Gabriel, Stacey B.; Lander, Eric S.; Ding, Li; Niu, Beifang; Ally, Adrian; Balasundaram, Miruna; Birol, Inanc; Brooks, Denise; Butterfield, Yaron S. N.; Carlsen, Rebecca; Chu, Justin; Chuah, Eric; Chun, Hye-Jung E.; Clarke, Amanda; Dhalla, Noreen; Guin, Ranabir; Holt, Robert A.; Jones, Steven J.M.; Lee, Darlene; Li, Haiyan A.; Lim, Emilia; Ma, Yussanne; Marra, Marco A.; Mayo, Michael; Moore, Richard A.; Mungall, Karen L.; Nip, Ka Ming; Schein, Jacqueline E.; Tam, Angela; Thiessen, Nina; Beroukhim, Rameen; Carter, Scott L.; Cherniack, Andrew D.; Cho, Juok; DiCara, Daniel; Frazer, Scott; Gehlenborg, Nils; Heiman, David I.; Jung, Joonil; Kim, Jaegil; Lin, Pei; Meyerson, Matthew; Ojesina, Akinyemi I.; Pedamallu, Chandra Sekhar; Saksena, Gordon; Schumacher, Steven E.; Stojanov, Petar; Tabak, Barbara; Voet, Doug; Rosenberg, Mara; Zack, Travis I.; Zhang, Hailei; Zou, Lihua; Protopopov, Alexei; Santoso, Netty; Lee, Semin; Zhang, Jianhua; Mahadeshwar, Harshad S.; Tang, Jiabin; Ren, Xiaojia; Seth, Sahil; Yang, Lixing; Xu, Andrew W.; Song, Xingzhi; Xi, Ruibin; Bristow, Christopher A.; Hadjipanayis, Angela; Seidman, Jonathan; Chin, Lynda; Park, Peter; Kucherlapati, Raju; Ling, Shiyun; Rao, Arvind; Weinstein, John N.; Kim, Sang-Bae; Lu, Yiling; Mills, Gordon; Bootwalla, Moiz S.; Lai, Phillip H.; Triche, Timothy; Van Den Berg, David J.; Baylin, Stephen B.; Herman, James G.; Murray, Bradley A.; Askoy, B. Arman; Ciriello, Giovanni; Dresdner, Gideon; Gao, Jianjiong; Gross, Benjamin; Jacobsen, Anders; Lee, William; Ramirez, Ricardo; Sander, Chris; Senbabaoglu, Yasin; Sinha, Rileen; Sumer, S. Onur; Sun, Yichao; Thorsson, Vésteinn; Iype, Lisa; Kramer, Roger W.; Kreisberg, Richard; Rovira, Hector; Tasman, Natalie; Ng, Santa Cruz Sam; Haussler, David; Stuart, Josh M.; Verhaak, Roeland G.W.; Leiserson, Mark D. M.; Taylor, Barry S.; Black, Aaron D.; Carney, Julie Ann; Gastier-Foster, Julie M.; Helsel, Carmen; McAllister, Cynthia; Ramirez, Nilsa C.; Tabler, Teresa R.; Wise, Lisa; Zmuda, Erik; Penny, Robert; Crain, Daniel; Gardner, Johanna; Lau, Kevin; Curely, Erin; Mallery, David; Morris, Scott; Paulauskis, Joseph; Shelton, Troy; Shelton, Candace; Sherman, Mark; Benz, Christopher; Lee, Jae-Hyuk; Fedosenko, Konstantin; Manikhas, Georgy; Potapova, Olga; Voronina, Olga; Belyaev, Smitry; Dolzhansky, Oleg; Rathmell, W. Kimryn; Brzezinski, Jakub; Ibbs, Matthew; Korski, Konstanty; Kycler, Witold; ŁaŸniak, Radoslaw; Leporowska, Ewa; Mackiewicz, Andrzej; Murawa, Dawid; Murawa, Pawel; Spychała, Arkadiusz; Suchorska, Wiktoria M.; Tatka, Honorata; Teresiak, Marek; Abdel-Misih, Raafat; Bennett, Joseph; Brown, Jennifer; Iacocca, Mary; Rabeno, Brenda; Kwon, Sun-Young; Kemkes, Ariane; Curley, Erin; Alexopoulou, Iakovina; Engel, Jay; Bartlett, John; Albert, Monique; Park, Do-Youn; Dhir, Rajiv; Luketich, James; Landreneau, Rodney; Janjigian, Yelena Y.; Cho, Eunjung; Ladanyi, Marc; Tang, Laura; McCall, Shannon J.; Park, Young S.; Cheong, Jae-Ho; Ajani, Jaffer; Camargo, M. Constanza; Alonso, Shelley; Ayala, Brenda; Jensen, Mark A.; Pihl, Todd; Raman, Rohini; Walton, Jessica; Wan, Yunhu; Eley, Greg; Mills Shaw, Kenna R.; Tarnuzzer, Roy; Wang, Zhining; Yang, Liming; Zenklusen, Jean Claude; Davidsen, Tanja; Hutter, Carolyn M.; Sofia, Heidi J.; Burton, Robert; Chudamani, Sudha; Liu, JiaGastric cancer is a leading cause of cancer deaths, but analysis of its molecular and clinical characteristics has been complicated by histological and aetiological heterogeneity. Here we describe a comprehensive molecular evaluation of 295 primary gastric adenocarcinomas as part of The Cancer Genome Atlas (TCGA) project. We propose a molecular classification dividing gastric cancer into four subtypes: tumours positive for Epstein–Barr virus, which display recurrent PIK3CA mutations, extreme DNA hypermethylation, and amplification of JAK2, CD274 (also known as PD-L1) and PDCD1LG2 (also knownasPD-L2); microsatellite unstable tumours, which show elevated mutation rates, including mutations of genes encoding targetable oncogenic signalling proteins; genomically stable tumours, which are enriched for the diffuse histological variant and mutations of RHOA or fusions involving RHO-family GTPase-activating proteins; and tumours with chromosomal instability, which show marked aneuploidy and focal amplification of receptor tyrosine kinases. Identification of these subtypes provides a roadmap for patient stratification and trials of targeted therapies.Publication Paired Exome Analysis of Barrett’s Esophagus and Adenocarcinoma(2015) Stachler, Matthew; Taylor-Weiner, Amaro; Peng, Shouyong; McKenna, Aaron; Agoston, Agoston; Odze, Robert; Davison, Jon M.; Nason, Katie S.; Loda, Massimo; Leshchiner, Ignaty; Stewart, Chip; Stojanov, Petar; Seepo, Sara; Lawrence, Michael S.; Ferrer-Torres, Daysha; Lin, Jules; Chang, Andrew C.; Gabriel, Stacey B.; Lander, Eric S.; Beer, David G.; Getz, Gad; Carter, Scott; Bass, Adam J.Barrett’s esophagus, is thought to progress to esophageal adenocarcinoma (EAC) through a step-wise progression with loss of CDKN2A followed by p53 inactivation and aneuploidy. Here, we present whole exome sequencing from 25 pairs of EAC and Barrett’s and five patients whose Barrett’s and tumor were extensively sampled. Our analysis revealed that oncogene amplification typically occurred as a late event and that TP53 mutations often occur early in Barrett’s progression, including in non-dysplastic epithelium. Reanalysis of additional EAC exome data revealed 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 amplifications and less frequent inactivation of tumor suppressors, including CDKN2A. These data suggest that many EACs emerge not through gradual accumulation of tumor suppressor alterations but rather through a more direct path whereby a TP53-mutant cell undergoes genome doubling, followed by acquisition of oncogenic amplifications.Publication CCL2 Promotes Colorectal Carcinogenesis by Enhancing Polymorphonuclear Myeloid-Derived Suppressor Cell Population and Function(2015) Chun, Eunyoung; Lavoie, Sydney; Michaud, Monia; Gallini, Carey; Kim, Jason; Soucy, Genevieve; Odze, Robert; Glickman, Jonathan; Garrett, WendySummary 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.