Su1854 Association of TP53 Arg72pro Variants With Gastric Cancer Risk in Helicobacter pylori...
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data of cases were collected, characteristics of the carcinomas were described, and available FFPE tissue slides were immunostained for β-catenin, P53 and phospho-S6 (a downstream target of mTOR). Furthermore, we performed DNA mutation analyses for BRAF, KRAS, and P53, and LOH analyses for LKB1 and P53. Results: Twenty-eight of the 144 patients (19%, 64% males) from 20 families developed 30 GI malignancies at a median age of 44 years (IQR 35-57) at diagnosis of first cancer (Table). Two patients were diagnosed with two primary GI carcinomas. Three (10%) malignancies were discovered during surveillance; all carcinomas in situ (one colorectal and two gastric lesions). Twenty-three patients (82%) deceased at a median age of 54 years (IQR 36-61); 19 (68%) of whom had died as a direct cause of GI cancer. Of these 23 patients, median survival after GI cancer diagnosis was 6 months (IQR 1-18). Of 16 carcinomas FFPE tissue was available for molecular analysis. Nuclear β-catenin was detected in 3/5 (60%) primary intestinal carcinomas. Overexpression of P53 was observed in 7/16 (44%) carcinomas, and a total absence of P53 was observed in one (6%) sample. All available samples showed heterogeneous expression of pS6, in which epithelial expression was more pronounced compared to the stromal component in 9/14 (64%) cases. Mutation and LOH analyses are currently being performed. Conclusion: Gastrointestinal cancer often affects PJS patients already at a young age. Alterations in Wnt/ β-catenin signaling and in P53 are observed in a subset of PJS carcinomas, while activation of mTOR signaling seems to be altered in the majority of these carcinomas, predominantly in the epithelial compartment. These results suggest that treatment with mTOR inhibitors may be beneficial in the anti-cancer treatment of PJS patients. Location of gastrointestinal carcinomas in Peutz-Jeghers syndrome patients Su1851 Family History and Pathology Features in Early-Onset Colorectal Cancer Cases With a BRAF P.V600e Mutation Daniel D. Buchanan, Aung Ko Win, Rhiannon J. Walters, Michael D. Walsh, Mark Clendenning, Belinda N. Nagler, Erika Pavluk, Sally- Ann Pearson, Christophe Rosty, Susan Parry, John Hopper, Mark A. Jenkins, Joanne P. Young Background: The BRAF p.V600E somatic mutation is present in approximately 10-20% of unselected colorectal cancer (CRC) and 30% -75% of CRCs demonstrating high levels of microsatellite instability (MSI-H). Recent evidence suggests that the BRAF p.V600E somatic mutation is associated with an increased risk of CRC and possibly extra-colonic cancers in relatives. The aim of this study was to determine 1) if early-onset CRC with the BRAF p.V600E mutation is associated with a family history of CRC, and 2) if pathological features of BRAF positive CRCs associate with CRC development in relatives. Methods: Population- based recruitment of probands into the Australasian Colon Cancer Family Study between 1997 and 2006 was undertaken for newly diagnosed CRC irrespective of any family history of cancer but limited to a first primary adenocarcinoma of the colon or rectum between the ages of 18-60yrs. Patients with Lynch syndrome and MutYH associated polyposis were excluded from the analysis. The BRAF p.V600E mutation was determined using a previously described allele-specific PCR assay on DNA from formalin-fixed paraffin embedded colorectal cancer tissue. Results: The average age of onset for the 709 probands (49.5% female) was 46.3yrs ± 7.9yrs (SD) with a range of 18yrs to 60yrs. A history of CRC in at least one first degree relative (FDR) or second degree relative (SDR) was reported in 39.5% (280/709) of the probands. The BRAF p.V600E mutation was present in 54/709 (7.6%) CRCs. Overall, probands with a BRAF p.V600E positive CRC were less likely to have a FDR with CRC than probands with a BRAF wildtype CRC (OR=0.42, 95%CI=0.16-1.09; P=0.07) regardless of MSI status. Among the probands with a BRAF p.V600E mutated CRC, the mean age at diagnosis was significantly older for probands with a CRC-affected FDR or SDR (50.4 years, 95%CI=47.1-53.7) when compared to probands without a family history (44.0 years, 95%CI= 40.7-42.3; P = 0.02). The odds (risk) of having a family history of CRC significantly increased 11% per year of age (OR 1.11; 95% CI 1.01 - 1.21; P = 0.02) in probands with a BRAF p.V600E mutation positive CRC. When considering only BRAF p.V600E positive CRC, a mucinous histology was increased 4.4 fold in probands with a FDR or SDR with CRC (n= 17) when compared to probands without a family history of CRC (n=37), although this was not significantly different (OR=4.40; 95%CI = 0.59 - 32.62; P=0.15). Conclusions: In this study of early-onset CRC, we describe evidence for a relationship between the BRAF p.V600E mutation and a family history of CRC that is related to an increasing age of CRC onset. These findings, in conjunction with observations suggesting certain pathological features are associated with a family history of CRC in BRAF p.V600E mutated CRC warrant further investigation. Su1852 Synchronous Cancerization Increases Metastatic Potential in MSS Colorectal Cancers (CRCs) Luigi Laghi, Lucia Fini, Gianluca Basso, Paolo Bianchi, Gabriele Delconte, Massimo Roncalli, Alessandro Repici, Alberto Malesci Background: Presence of Synchronous Colorectal Cancer (S-CRCs) is included in the Bethesda Criteria panel addressing the assessment of microsatellite instability (MSI), a CRC phenotype with better prognosis. In contrast with such association, data suggest that S-CRCs have a poorer outcome compared to single counterparts. Although DNA hypermethylation has been S-519 AGA Abstracts claimed as a major contributor to S-CRCs development, the majority remains ascribable to CIN phenotype. AIMS & METHODS: In a large consecutive and mono-institutional series of 1000 CRC, we aimed to assess the frequency and clinical and molecular features of S- CRCs. Retrospective analysis included clinico-pathological characteristics, MS- and BRAF- status, and disease specific survival (DSS). Prognostic impact of synchronous adenomas was assessed in 515 pts undergone colonoscopy at our institution. Mutations at the hypermutable hot-spots 1309 and 1450 of APC were assessed in S-CRCs pairs and 267 controls. RESULTS: We identify 47 (4.7%) pts with S-CRCs. Upon multivariate analysis, stage IV (p=0.01) and HNPCC (p<0.001) were independently associated with S-CRCs. Stage IV rate was lower in MSI (8/102; 7.8%) than in MSS (243/898; 27.1%; p < 0.001) tumors and was similar in pts with MSI single (7/92; 7.6%) and S-CRCs (1/10; 10%); MSS S-CRCs had a higher stage IV rate (15/33, 45.5%) than MSS single (230/865, 26.6%; p= 0.01), or MSI (9/102; 8.8%; p=<0.001) CRCs. MSS S-CRC pts had a worse prognosis than their MSI counterparts (p= 0.004), and than pts with MSS single CRC (p=0.04). BRAFV600E was not associated with S-CRCs and did not impact MSI pt prognosis. The survival of pts with single MSS BRAFV600E CRC was worse than that of pts with MSS BRAFwt (p<0.001), and similar to the survival pts with MSS S-CRCs. At Cox multivariate analysis, S-CRCs (HR=1.92, 95% CI 1.24, 2.98; p=0.003) and of BRAFV600E MSS CRC (HR=2.01, 95% CI 1.24, 3.28; p=0.005) were independent predictors of CRC-related death. MSI phenotype was associated with a reduced CRC-related death, irrespective of BRAF-status, and pts with HNPCC had the greatest reduction (HR=0.12, 95% CI 0.03-0.49; p=0.003). MSS CRCs with high grade dysplasia (S-HGDs) adenomas had an intermediate mortality rate between MSS single (p =0.04) and S-CRCs (p=0.15). Mutation at APC hot-spots were mutually exclusive with BRAFV600E and significantly associated with MSS S-CRCs and MSS S-HGD (p=0.01). CONCLUSION: Based on the MS-status, S-CRCs display opposite behaviours. High metastatic potential and decreased survival is confined to MSS CRC pts. MSI CRCs are almost always HNPCC, a signature reverting the negative impact of synchronicity. S-CRC and their suspect precursor S-HGD may be considered a paradigm of accelerated MSS carcinogenesis, which could be in part mediated by highly selected APC mutations and, only for a minor quote, by BRAFV600E associated hypermethylation. Su1854 Association of TP53 Arg72pro Variants With Gastric Cancer Risk in Helicobacter pylori Infected Subjects: A Nation-Wide Case-Control Study in Spain Maria Asuncion Garcia-Gonzalez, Enrique Quintero, Luis Bujanda, David Nicolás-Pérez, Rafael Benito, Mark Strunk, Santos Santolaria, Federico Sopena, Maria Badia, Elizabeth Hijona, Concepción Thomson, Angeles Perez Aisa, Isabel María Méndez-Sánchez, Elena Piazuelo, Pilar Jimenez, Manuel Zaballa, Jesus Espinel, Fernando Geijo, Maria Pellise, Rafael Campo, Marisa Manzano, Ferrán González-Huix, Jorge C. Espinos, LLúcia Titó, Roberto A. Pazo Cid, Luis Barranco, Angel Lanas Background & aim: The TP53 tumor suppressor gene encodes a 53-kDa protein (p53) which regulates target genes with important functions in cell cycle arrest, apoptosis, DNA repair, and DNA transcription. A polymorphism at codon 72 (Arg/Pro) in exon 4 of the TP53 gene (rs1042522) has been shown to affect the ability to induce target gene transcription and apoptosis. Since alterations in p53 tumor suppressor capacity may increase the probability of mutations leading to cancer development, we aimed to assess the role of TP53 Arg72Pro gene variants on gastric cancer (GC) risk and phenotype in a large case-control study in Spain, and to assess the potential interaction with other environmental and lifestyle factors such as Helicobacter pylori (H. pylori) infection and smoking habits. Methods: Six hundred and three unrelated Spanish Caucasian patients with primary GC and 603 sex- and aged- (± 5 years) matched cancer-free healthy controls were included in the study. Genomic DNA from patients and controls was typed for the TP53 Arg72Pro gene polymorphism (rs1042522) by PCR-TaqMan assays. H. pylori infection and CagA/VacA antibody status were determined by western blot in patients and controls. Results: H. pylori infection with CagA strains (OR:2.24; 95% CI:1.76-2.85; p<0.0001), smoking habit (OR:2.03; 95% CI:1.33-2.54; p<0.0001) and positive family history of GC (OR:3.25; 95% CI:1.95-4.91; p<0.0001) were identified as independent risk factors for GC. Moreover, homozygosity for the TP53 Arg72- Pro*G allele (Arg/Arg) was significantly higher in patients with GC than in controls (61.5% vs. 52.7%, OR:1.43; 95% CI:1.41-1.81; p=0.002). When subgroup analysis for tumor location was performed, we observed that smoking habit was strongly associated with cardia GC (OR:4.34; 95% CI:1.78-8.64; p=0.001) whereas H. pylori infection with CagA strains (OR:2.55; 95% CI:1.94-3.34; p<0.0001), positive family history of GC (OR:3.19; 95% CI:1.98-5.13; P<0.0001), and the TP53 Arg72Pro GG genotype (OR:1.57; 95% CI:1.2-2.02; p=0.0006) were specifically associated with a higher risk of non-cardia GC. Interestingly, the association between the TP53 Arg72Pro GG genotype and distal GC risk was restricted to H. pylori infected individuals (OR:1.65; 95% CI:1.17-2.33; p=0.004). Finally, no differ- ences in genotype distribution were found when GC patients were categorized according to smoking habit, gender, age, histological subtype of the tumor, past ulcer history, and family history of GC. Conclusion: Our data show that, in our population, the TP53 Arg72Pro gene polymorphism (rs1042522) is involved in the susceptibility to GC in H. pylori-positive individuals, and provide further evidence that host genetic factors are relevant in determining the final outcome of H. pylori infection. Su1855 18F-FDG PET - Detected Synchronous Primary Neoplasms in Oesophageal Cancer: Incidence, Cost and Impact on Management Vinod Malik, Ciaran Johnston, Claire L. Donohoe, Ravi Narayanasamy, John V. Reynolds Purpose: 18F-Fluorodeoxyglucose positron emission tomography (18F-FDG PET) imaging is increasingly the standard of care in esophageal cancer. Synchronous neoplasms, benign and malignant, may also be identified, and this study evaluated the prevalence of synchronous neoplasms, and impact on management. Methods: From January 2003 to December 2009, 591 (73.6%) of 803 patients with biopsy proven esophageal cancer underwent staging 18F- FDG PET or PET/CT scans. 18F-FDG avid lesions were considered synchronous primary neoplasms if occurring at locations atypical for metastases from the known primary, a marked AGA Abstracts
Transcript of Su1854 Association of TP53 Arg72pro Variants With Gastric Cancer Risk in Helicobacter pylori...
data of cases were collected, characteristics of the carcinomas were described, and availableFFPE tissue slides were immunostained for β-catenin, P53 and phospho-S6 (a downstreamtarget of mTOR). Furthermore, we performed DNA mutation analyses for BRAF, KRAS, andP53, and LOH analyses for LKB1 and P53. Results: Twenty-eight of the 144 patients (19%,64% males) from 20 families developed 30 GI malignancies at a median age of 44 years(IQR 35-57) at diagnosis of first cancer (Table). Two patients were diagnosed with twoprimary GI carcinomas. Three (10%) malignancies were discovered during surveillance; allcarcinomas in situ (one colorectal and two gastric lesions). Twenty-three patients (82%)deceased at a median age of 54 years (IQR 36-61); 19 (68%) of whom had died as a directcause of GI cancer. Of these 23 patients, median survival after GI cancer diagnosis was 6months (IQR 1-18). Of 16 carcinomas FFPE tissue was available for molecular analysis.Nuclear β-catenin was detected in 3/5 (60%) primary intestinal carcinomas. Overexpressionof P53 was observed in 7/16 (44%) carcinomas, and a total absence of P53 was observedin one (6%) sample. All available samples showed heterogeneous expression of pS6, inwhich epithelial expression was more pronounced compared to the stromal component in9/14 (64%) cases. Mutation and LOH analyses are currently being performed. Conclusion:Gastrointestinal cancer often affects PJS patients already at a young age. Alterations in Wnt/β-catenin signaling and in P53 are observed in a subset of PJS carcinomas, while activationof mTOR signaling seems to be altered in the majority of these carcinomas, predominantlyin the epithelial compartment. These results suggest that treatment with mTOR inhibitorsmay be beneficial in the anti-cancer treatment of PJS patients.Location of gastrointestinal carcinomas in Peutz-Jeghers syndrome patients
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Family History and Pathology Features in Early-Onset Colorectal CancerCases With a BRAF P.V600e MutationDaniel D. Buchanan, Aung Ko Win, Rhiannon J. Walters, Michael D. Walsh, MarkClendenning, Belinda N. Nagler, Erika Pavluk, Sally- Ann Pearson, Christophe Rosty,Susan Parry, John Hopper, Mark A. Jenkins, Joanne P. Young
Background: The BRAF p.V600E somatic mutation is present in approximately 10-20% ofunselected colorectal cancer (CRC) and 30% -75% of CRCs demonstrating high levels ofmicrosatellite instability (MSI-H). Recent evidence suggests that the BRAF p.V600E somaticmutation is associated with an increased risk of CRC and possibly extra-colonic cancers inrelatives. The aim of this study was to determine 1) if early-onset CRC with the BRAFp.V600E mutation is associated with a family history of CRC, and 2) if pathological featuresof BRAF positive CRCs associate with CRC development in relatives. Methods: Population-based recruitment of probands into the Australasian Colon Cancer Family Study between1997 and 2006 was undertaken for newly diagnosed CRC irrespective of any family historyof cancer but limited to a first primary adenocarcinoma of the colon or rectum between theages of 18-60yrs. Patients with Lynch syndrome and MutYH associated polyposis wereexcluded from the analysis. The BRAF p.V600E mutation was determined using a previouslydescribed allele-specific PCR assay on DNA from formalin-fixed paraffin embedded colorectalcancer tissue. Results: The average age of onset for the 709 probands (49.5% female) was46.3yrs ± 7.9yrs (SD) with a range of 18yrs to 60yrs. A history of CRC in at least one firstdegree relative (FDR) or second degree relative (SDR) was reported in 39.5% (280/709) ofthe probands. The BRAF p.V600E mutation was present in 54/709 (7.6%) CRCs. Overall,probands with a BRAF p.V600E positive CRC were less likely to have a FDR with CRC thanprobands with a BRAF wildtype CRC (OR=0.42, 95%CI=0.16-1.09; P=0.07) regardless ofMSI status. Among the probands with a BRAF p.V600E mutated CRC, the mean age atdiagnosis was significantly older for probands with a CRC-affected FDR or SDR (50.4 years,95%CI=47.1-53.7) when compared to probands without a family history (44.0 years, 95%CI=40.7-42.3; P = 0.02). The odds (risk) of having a family history of CRC significantly increased11% per year of age (OR 1.11; 95% CI 1.01 - 1.21; P = 0.02) in probands with a BRAFp.V600E mutation positive CRC. When considering only BRAF p.V600E positive CRC, amucinous histology was increased 4.4 fold in probands with a FDR or SDR with CRC (n=17) when compared to probands without a family history of CRC (n=37), although thiswas not significantly different (OR=4.40; 95%CI = 0.59 - 32.62; P=0.15). Conclusions: Inthis study of early-onset CRC, we describe evidence for a relationship between the BRAFp.V600E mutation and a family history of CRC that is related to an increasing age of CRConset. These findings, in conjunction with observations suggesting certain pathologicalfeatures are associated with a family history of CRC in BRAF p.V600E mutated CRC warrantfurther investigation.
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Synchronous Cancerization Increases Metastatic Potential in MSS ColorectalCancers (CRCs)Luigi Laghi, Lucia Fini, Gianluca Basso, Paolo Bianchi, Gabriele Delconte, MassimoRoncalli, Alessandro Repici, Alberto Malesci
Background: Presence of Synchronous Colorectal Cancer (S-CRCs) is included in the BethesdaCriteria panel addressing the assessment of microsatellite instability (MSI), a CRC phenotypewith better prognosis. In contrast with such association, data suggest that S-CRCs have apoorer outcome compared to single counterparts. Although DNA hypermethylation has been
S-519 AGA Abstracts
claimed as a major contributor to S-CRCs development, the majority remains ascribable toCIN phenotype. AIMS & METHODS: In a large consecutive and mono-institutional seriesof 1000 CRC, we aimed to assess the frequency and clinical and molecular features of S-CRCs. Retrospective analysis included clinico-pathological characteristics, MS- and BRAF-status, and disease specific survival (DSS). Prognostic impact of synchronous adenomas wasassessed in 515 pts undergone colonoscopy at our institution. Mutations at the hypermutablehot-spots 1309 and 1450 of APC were assessed in S-CRCs pairs and 267 controls. RESULTS:We identify 47 (4.7%) pts with S-CRCs. Upon multivariate analysis, stage IV (p=0.01) andHNPCC (p<0.001) were independently associated with S-CRCs. Stage IV rate was lower inMSI (8/102; 7.8%) than in MSS (243/898; 27.1%; p < 0.001) tumors and was similar inpts with MSI single (7/92; 7.6%) and S-CRCs (1/10; 10%); MSS S-CRCs had a higher stageIV rate (15/33, 45.5%) than MSS single (230/865, 26.6%; p= 0.01), or MSI (9/102; 8.8%;p=<0.001) CRCs. MSS S-CRC pts had a worse prognosis than their MSI counterparts (p=0.004), and than pts with MSS single CRC (p=0.04). BRAFV600E was not associated withS-CRCs and did not impact MSI pt prognosis. The survival of pts with single MSS BRAFV600ECRC was worse than that of pts with MSS BRAFwt (p<0.001), and similar to the survivalpts with MSS S-CRCs. At Cox multivariate analysis, S-CRCs (HR=1.92, 95% CI 1.24, 2.98;p=0.003) and of BRAFV600E MSS CRC (HR=2.01, 95% CI 1.24, 3.28; p=0.005) wereindependent predictors of CRC-related death. MSI phenotype was associated with a reducedCRC-related death, irrespective of BRAF-status, and pts with HNPCC had the greatestreduction (HR=0.12, 95% CI 0.03-0.49; p=0.003). MSS CRCs with high grade dysplasia(S-HGDs) adenomas had an intermediate mortality rate between MSS single (p =0.04) andS-CRCs (p=0.15). Mutation at APC hot-spots were mutually exclusive with BRAFV600E andsignificantly associated with MSS S-CRCs and MSS S-HGD (p=0.01). CONCLUSION: Basedon the MS-status, S-CRCs display opposite behaviours. High metastatic potential anddecreased survival is confined to MSS CRC pts. MSI CRCs are almost always HNPCC, asignature reverting the negative impact of synchronicity. S-CRC and their suspect precursorS-HGD may be considered a paradigm of accelerated MSS carcinogenesis, which could be inpart mediated by highly selected APC mutations and, only for a minor quote, by BRAFV600Eassociated hypermethylation.
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Association of TP53 Arg72pro Variants With Gastric Cancer Risk inHelicobacter pylori Infected Subjects: A Nation-Wide Case-Control Study inSpainMaria Asuncion Garcia-Gonzalez, Enrique Quintero, Luis Bujanda, David Nicolás-Pérez,Rafael Benito, Mark Strunk, Santos Santolaria, Federico Sopena, Maria Badia, ElizabethHijona, Concepción Thomson, Angeles Perez Aisa, Isabel María Méndez-Sánchez, ElenaPiazuelo, Pilar Jimenez, Manuel Zaballa, Jesus Espinel, Fernando Geijo, Maria Pellise,Rafael Campo, Marisa Manzano, Ferrán González-Huix, Jorge C. Espinos, LLúcia Titó,Roberto A. Pazo Cid, Luis Barranco, Angel Lanas
Background & aim: The TP53 tumor suppressor gene encodes a 53-kDa protein (p53)which regulates target genes with important functions in cell cycle arrest, apoptosis, DNArepair, and DNA transcription. A polymorphism at codon 72 (Arg/Pro) in exon 4 of theTP53 gene (rs1042522) has been shown to affect the ability to induce target gene transcriptionand apoptosis. Since alterations in p53 tumor suppressor capacitymay increase the probabilityof mutations leading to cancer development, we aimed to assess the role of TP53 Arg72Progene variants on gastric cancer (GC) risk and phenotype in a large case-control study inSpain, and to assess the potential interaction with other environmental and lifestyle factorssuch as Helicobacter pylori (H. pylori) infection and smoking habits. Methods: Six hundredand three unrelated Spanish Caucasian patients with primary GC and 603 sex- and aged-(± 5 years) matched cancer-free healthy controls were included in the study. Genomic DNAfrom patients and controls was typed for the TP53 Arg72Pro gene polymorphism (rs1042522)by PCR-TaqMan assays. H. pylori infection and CagA/VacA antibody status were determinedby western blot in patients and controls. Results: H. pylori infection with CagA strains(OR:2.24; 95% CI:1.76-2.85; p<0.0001), smoking habit (OR:2.03; 95% CI:1.33-2.54;p<0.0001) and positive family history of GC (OR:3.25; 95% CI:1.95-4.91; p<0.0001) wereidentified as independent risk factors for GC. Moreover, homozygosity for the TP53 Arg72-Pro*G allele (Arg/Arg) was significantly higher in patients with GC than in controls (61.5%vs. 52.7%, OR:1.43; 95% CI:1.41-1.81; p=0.002). When subgroup analysis for tumorlocation was performed, we observed that smoking habit was strongly associated with cardiaGC (OR:4.34; 95% CI:1.78-8.64; p=0.001) whereas H. pylori infection with CagA strains(OR:2.55; 95% CI:1.94-3.34; p<0.0001), positive family history of GC (OR:3.19; 95%CI:1.98-5.13; P<0.0001), and the TP53 Arg72Pro GG genotype (OR:1.57; 95% CI:1.2-2.02;p=0.0006) were specifically associated with a higher risk of non-cardia GC. Interestingly,the association between the TP53 Arg72Pro GG genotype and distal GC risk was restrictedto H. pylori infected individuals (OR:1.65; 95% CI:1.17-2.33; p=0.004). Finally, no differ-ences in genotype distribution were found when GC patients were categorized accordingto smoking habit, gender, age, histological subtype of the tumor, past ulcer history, andfamily history of GC. Conclusion: Our data show that, in our population, the TP53 Arg72Progene polymorphism (rs1042522) is involved in the susceptibility to GC in H. pylori-positiveindividuals, and provide further evidence that host genetic factors are relevant in determiningthe final outcome of H. pylori infection.
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18F-FDG PET - Detected Synchronous Primary Neoplasms in OesophagealCancer: Incidence, Cost and Impact on ManagementVinod Malik, Ciaran Johnston, Claire L. Donohoe, Ravi Narayanasamy, John V. Reynolds
Purpose: 18F-Fluorodeoxyglucose positron emission tomography (18F-FDG PET) imagingis increasingly the standard of care in esophageal cancer. Synchronous neoplasms, benignand malignant, may also be identified, and this study evaluated the prevalence of synchronousneoplasms, and impact on management. Methods: From January 2003 to December 2009,591 (73.6%) of 803 patients with biopsy proven esophageal cancer underwent staging 18F-FDG PET or PET/CT scans. 18F-FDG avid lesions were considered synchronous primaryneoplasms if occurring at locations atypical for metastases from the known primary, a marked
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