scholarly journals Adverse Prognostic Impact of Intratumor HeterogeneousHER2Gene Amplification in Patients With Esophageal Adenocarcinoma

2012 ◽  
Vol 30 (32) ◽  
pp. 3932-3938 ◽  
Author(s):  
Harry H. Yoon ◽  
Qian Shi ◽  
William R. Sukov ◽  
Mark A. Lewis ◽  
Christopher A. Sattler ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Esophageal Adenocarcinoma ◽  
Gene Amplification ◽  
Prognostic Impact ◽  
Her2 Amplification ◽  
Her2 Gene ◽  
Cox Models ◽  
Node Number ◽  
Polysomy 17 ◽  
Her2 Heterogeneity

PurposeThere is increasing recognition of the existence of intratumoral heterogeneity of the human epidermal growth factor receptor (HER2), which affects interpretation of HER2 positivity in clinical practice and may have implications for patient prognosis and treatment. We determined the frequency and prognostic impact of heterogeneous HER2 gene amplification and polysomy 17 in patients with esophageal adenocarcinoma (EAC).Patients and MethodsHER2 amplification (by fluorescence in situ hybridization) was examined in surgical EAC specimens (n = 675). HER2 heterogeneity was defined according to consensus guidelines as gene amplification (HER2/CEP17 ratio ≥ 2.0) in more than 5% but less than 50% of cancer cells. No patient received neoadjuvant or HER2-targeted therapy. Cox models were used to assess disease-specific survival (DSS) and overall survival (OS).ResultsOverall, 117 EACs (17%) demonstrated HER2 amplification, of which 20 (17%) showed HER2 heterogeneity. All HER2-heterogeneous tumors were amplified. Among HER2-amplified tumors, heterogeneous tumors had significantly higher frequency of poor histologic grade and polysomy 17. In multivariable models that included number of metastatic lymph nodes, grade, tumor stage, and polysomy 17, only HER2 heterogeneity and node number were prognostic among HER2-amplified tumors, with heterogeneity showing worse DSS (hazard ratio, 2.04; 95% CI, 1.09 to 3.79; P = .025) and OS (P = .026). Among HER2-nonamplified EACs, polysomy 17 was independently associated with worse DSS (P = .012) and OS (P = .023).ConclusionAmong HER2-amplified EACs, 17% show HER2 heterogeneity, which independently predicts for worse cancer-specific death. Among HER2-nonamplified EACs, polysomy 17 is independently associated with worse survival. These novel findings demonstrate aggressive subgroups in HER2-amplified and -nonamplified EACs that have important implications for HER2 analysis and determination of benefit from HER2-targeted therapy.

Adverse prognostic impact of heterogeneous HER2 gene amplification in patients with esophageal adenocarcinoma (EAC).

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 4009-4009
Author(s):  
Harry H. Yoon ◽  
Qian Shi ◽  
William R. Sukov ◽  
Christopher A. Sattler ◽  
Anne E. Wiktor ◽  
...  
Keyword(s):  
Genetic Heterogeneity ◽  
Multivariable Analysis ◽  
Chromosome 17 ◽  
Prognostic Impact ◽  
Her2 Amplification ◽  
Her2 Gene ◽  
Digestive Cancer ◽  
Cox Models ◽  
Her2 Heterogeneity ◽  
Risk Of Cancer

4009 Background: HER2 expression in upper digestive cancer is reported to be heterogeneous, which substantially affects interpretation of HER2 positivity in the clinic. Yet the frequency and prognostic impact of HER2 genetic heterogeneity and polysomy 17 (poly17) are unknown in EAC. Methods: HER2 amplification (fluorescence in situ hybridization) and protein expression were examined in untreated surgical EAC specimens (N = 661) at Mayo Clinic. HER2 genetic heterogeneity was defined per ASCO/CAP as amplification (HER2/CEP17 ratio ≥ 2) in 5-50% of cancer cells; poly17 refers to ≥ 3 copies of chromosome 17. Most tumors were T3-4 (68%) or lymph node (LN)-positive (73%). Cox models were used to assess disease-specific (DSS) and overall survival (OS). Results: HER2 amplification was detected in 117 of 661 EACs (18%), of which 20 (17%) showed HER2 heterogeneity. HER2 heterogeneous tumors had a significantly higher frequency of poly17 and high tumor grade. HER2 heterogeneity by amplification vs expression were correlated. Since heterogeneity was limited to HER2-amplified tumors, survival analysis was stratified by amplification status. In multivariable analysis, only HER2 heterogeneity and metastatic LN number were prognostic (Table). Conclusions: Among HER2 amplified EACs, 17% show HER2 heterogeneity, which is associated with increased poly17 and independently predicts 2-fold higher risk of cancer-specific death. Among HER2-nonamplified cases, poly17 is independently associated with worse survival. These novel findings demonstrate aggressive subgroups in HER2-amplified and -nonamplified EACs that have important implications for HER2 analysis and evaluation of benefit from HER2 targeted therapy. [Table: see text]

scholarly journals Detection of HER2 Amplification in Breast Carcinomas: Comparison of Multiplex Ligation-Dependent Probe Amplification (MLPA) and Fluorescence In Situ Hybridization (FISH) combined with Automated Spot Counting

2006 ◽  
Vol 28 (4) ◽  
pp. 151-159
Author(s):  
Elna Moerland ◽  
Rens L. H. P. M. van Hezik ◽  
Toine C. J. M. van der Aa ◽  
Mike W. P. M. van Beek ◽  
Adriaan J. C. van den Brule
Keyword(s):  
In Situ Hybridization ◽  
Fluorescence In Situ Hybridization ◽  
Gene Amplification ◽  
Her2 Status ◽  
Her2 Amplification ◽  
Breast Carcinomas ◽  
Her2 Gene ◽  
Her2 Gene Amplification ◽  
Dependent Probe

In this study the detection of HER2 gene amplification was evaluated using Fluorescence In Situ Hybridization (FISH; PathVysion) in comparison with Multiplex Ligation-dependent Probe Amplification (MLPA), a PCR based technique. These two methods were evaluated on a series of 46 formalin fixed paraffin embedded breast carcinomas, previously tested for protein overexpression by HercepTest (grouped into Hercep 1+, 2+ and 3+). HER2 gene amplification (ratio ≥ 2.0) by FISH was found in 9/10, 10/30 and 0/6 in IHC 3+, 2+ and 1+/0 cases, respectively. Digitalized automated spot counting performed with recently developed CW4000 CytoFISH software was 100% concordant with manual FISH scoring. Using MLPA 18/46 samples showed a clear HER2 amplification. Comparing MLPA and IHC showed the same results as for FISH and IHC. All but one FISH positive cases (18/19) were confirmed by MLPA for the presence of the gene amplification. The overall concordance of detection of Her2 gene amplification by FISH and MLPA was 98% (45/46). Furthermore, both the level of amplification and equivocal results correlated well between both methods. In conclusion, MLPA is a reliable and reproducible technique and can be used as an either alternative or additional test to determine HER2 status in breast carcinomas.

scholarly journals HER2 Amplification Status in Feline Mammary Carcinoma: A Tissue Microarray–Fluorescence In Situ Hydridization–Based Study

2018 ◽  
Vol 56 (2) ◽  
pp. 230-238 ◽  
Author(s):  
Luisa Vera Muscatello ◽  
Enrico Di Oto ◽  
Giuseppe Sarli ◽  
Valentina Monti ◽  
Maria Pia Foschini ◽  
...  
Keyword(s):  
Protein Expression ◽  
Gene Amplification ◽  
Her2 Status ◽  
Tyrosine Kinase Receptor ◽  
Her2 Amplification ◽  
Her2 Gene ◽  
Her2 Protein ◽  
Mammary Carcinomas ◽  
Her2 Gene Amplification

Human epidermal growth factor receptor 2 (HER2) is a tyrosine kinase receptor overexpressed in a subset of breast cancer due to HER2 gene amplification. HER2 protein is expressed in feline mammary carcinomas, but little is known about its cytogenetic alterations. The aim of this study was to evaluate HER2 gene amplification status and its correlation with HER2 protein expression in feline mammary carcinomas. Feline mammary carcinomas were retrospectively selected and immunohistochemically (IHC) evaluated for HER2 protein expression. All the HER2 IHC-positive (3+) and equivocal (2+) cases and a subset of negative cases (0/1+) were selected for fluorescence in situ hybridization (FISH). Dual-core tissue microarrays were prepared for FISH. IHC and FISH were evaluated according to the 2013 American Society of Clinical Oncology/College of American Pathologists guidelines. The study included 107 feline mammary carcinomas from 88 queens. HER2 protein expression was positive (3+) in 7 cases (6.5%), equivocal (2+) in 48 cases (45%), and negative (0/1+) in 52 cases (48.5%). HER2 status was indeterminate in 8 feline mammary carcinomas (12%), amplified in 3 (4%), equivocal in 4 (6%), and nonamplified in 53 (78%). HER2 gene amplification and protein expression were significantly positively correlated ( R = 0.283; P < .0001). HER2 gene is amplified in a subset of feline mammary carcinomas despite the HER2 positive or equivocal protein expression, but it remains to be determined if the HER2 amplification is a gene alteration that drives mammary tumor carcinogenesis or only a bystander passenger mutation.

scholarly journals HER2 gene amplification in patients with breast cancer with equivocal IHC results

2011 ◽  
Vol 64 (12) ◽  
pp. 1069-1072 ◽  
Author(s):  
Sybren L Meijer ◽  
Jelle Wesseling ◽  
Vincent T Smit ◽  
Petra M Nederlof ◽  
Gerrit K J Hooijer ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Gene Amplification ◽  
In Situ Hybridisation ◽  
Gene Copy ◽  
Test Results ◽  
Her2 Gene ◽  
Gene Copies ◽  
Her2 Gene Amplification ◽  
Test Result

AimsEquivocal human epidermal growth factor receptor 2 protein (HER2) (2+) immunohistochemistry (IHC) is subject to significant interobserver variation and poses a challenge in obtaining a definitive positive or negative test result. This equivocal test result group accounts for approximately 15% of all tumours, and for optimal guidance of HER2 targeted therapy, a further analysis of quantification of gene copy number and amplification status is needed for patients with early or metastatic breast cancer.Methods553 breast-cancer specimens with equivocal HER2 IHC(2+) test results were collected and subsequently centrally retested by chromogenic in situ hybridisation (CISH), and HER2 gene copy numbers per tumour cell nucleus were determined.ResultsUsing CISH, 77 of 553 equivocal HER2 IHC(2+) test result cases (13.9% of total) showed high levels of HER2 gene amplification (≥10.0 gene copies per nucleus), and 41 of 553 (7.4% of total) showed low-level HER2 gene amplification (6.0–9.9 gene copies per nucleus). In 73.6% of cases, no amplification of the HER2 gene was shown, and in only 4.9% of cases was an equivocal test result by CISH observed (4.0–5.9 gene copies per nucleus).ConclusionsTesting by CISH of all equivocal HER2 IHC(2+) test result provides a definitive guidance in HER2 targeted therapy in 95.1% of cases. A significant proportion (21.3%) of patients with equivocal IHC(2+) test results show amplification of the HER2 gene.

Genetic Heterogeneity in HER2 Testing in Breast Cancer: Panel Summary and Guidelines

2009 ◽  
Vol 133 (4) ◽  
pp. 611-612 ◽  
Author(s):  
Gail H. Vance ◽  
Todd S. Barry ◽  
Kenneth J. Bloom ◽  
Patrick L. Fitzgibbons ◽  
David G. Hicks ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Amplification ◽  
Practice Guidelines ◽  
Genetic Heterogeneity ◽  
Her2 Amplification ◽  
Her2 Gene ◽  
Her2 Testing ◽  
Her2 Gene Amplification ◽  
Gene Status ◽  
Panel Summary

Abstract Context.—Intratumoral heterogeneity of HER2 gene amplification has been well documented and represents subclonal diversity within the tumor. The reported incidence of intratumor HER2 amplification genetic heterogeneity ranges in the literature from approximately 5% to 30%. The presence of HER2 genetic heterogeneity may increase subjectivity in HER2 interpretation by the pathologist. Objectives.—To define HER2 genetic heterogeneity and to provide practice guidelines for examining and reporting breast tumors with genetic heterogeneity for improvement of HER2 testing in breast cancer. Design.—We convened an expert panel to discuss HER2 gene amplification testing by fluorescence in situ hybridization. Components addressed included a definition of HER2 amplification heterogeneity, practice guidelines for examination of the tissue, and reporting criteria for this analysis. Results.—Genetic heterogeneity for amplification of HER2 gene status in invasive breast cancer is defined and guidelines established for assessing and reporting HER2 results in these cases. These guidelines are additive to and expand those published in 2007 by the American Society of Clinical Oncology and the College of American Pathologists. Conclusion.—Standardized methods for analysis will improve the accuracy and consistency of interpretation of HER2 gene amplification status in breast cancer.

Assessment of HER2 gene amplification in adenocarcinomas of the stomach or gastroesophageal junction in the INT-0116/SWOG9008 clinical trial.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 4010-4010 ◽  
Author(s):  
Michael Alexander Gordon ◽  
Holly Gundacker ◽  
Jacqueline Benedetti ◽  
John S. Macdonald ◽  
Joaquina Celebre Baranda ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Radiation Therapy ◽  
In Situ Hybridization ◽  
Gene Amplification ◽  
Phase Iii ◽  
Her2 Status ◽  
Her2 Amplification ◽  
Her2 Gene ◽  
Her2 Gene Amplification

4010 Background: Trastuzumab has been approved for treatment of patients with HER2-positive metastatic gastric carcinoma; however, relatively little is known about the role of HER2 in the natural history of this disease. Methods: Patients enrolled in the INT-0116/SWOG9008 phase III gastric cancer clinical trial (n=559) were retrospectively evaluated for HER2 gene amplification by fluorescence in situ hybridization (FISH)(n=258), overexpression by immunohistochemistry (IHC)(n=148) and HER2 amplification by silver-enhanced in situ hybridization (n=77) based on availability of tissue specimens. The purpose of the original clinical trial was to evaluate the benefit of post-operative 5-fluorouracil/leucovorin plus radiation therapy compared to surgery alone. Results: HER2 gene amplification rate by FISH was 10.9% in tumor tissue from 258 patients evaluated. HER2 status determined by FISH was 92% concordant with SISH. HER2 overexpression rate by IHC was 12.2% among 148 patients evaluated, with 90% agreement between FISH and IHC. There was a significant interaction between HER2 status by FISH and treatment with respect to both OS (p=0.034) and DFS (p=0.020). Among patients with HER2 non-amplified cancers, treated patients had a median OS of 44 months compared to 24 months for patients in the surgery only arm (34 and 17 months respectively for DFS, p=0.003). Among 28 patients with HER2 amplified cancers, the medians for OS were 16 months in the treated arm, and 22 months in the surgery arm (p=0.55) (13 and 11 months respectively for DFS, p=0.87). We were unable to detect a statistically significant treatment benefit in this small subset of patients with HER2 amplification. HER2 amplification status was not an independent prognostic marker of OS among patients who received no postoperative chemotherapy or radiation therapy (p=0.76). Conclusions: Patients lacking HER2 amplification responded significantly to treatment as indicated by both OS and DFS.

HER2 status in primary tumors and metastatic regional lymph nodes in patients with esophageal adenocarcinoma (EAC).

2013 ◽  
Vol 31 (15_suppl) ◽  
pp. 4071-4071
Author(s):  
Harry H. Yoon ◽  
Qian Shi ◽  
William R. Sukov ◽  
Christopher A. Sattler ◽  
Rakhee Vaidya ◽  
...  
Keyword(s):  
Targeted Therapy ◽  
Lymph Nodes ◽  
Her2 Status ◽  
Her2 Amplification ◽  
Her2 Gene ◽  
Her2 Positive ◽  
Regional Lymph Nodes ◽  
Primary Tumors ◽  
Routine Procedures

4071 Background: Selection of patients for HER2-targeted therapy is based on HER2 analysis in primary EACs. Since EACs metastasize via regional lymph nodes, concordance of HER2 gene amplification results between primary tumors and their metastatic lymph nodes (MLN) is a clinically important issue. Methods: Resected EACs (N = 103) having at least three distinct regional MLNs (total 508 MLNs; median 4 [range 3-11]) were sectioned using routine procedures and tested for HER2 amplification by fluorescence in situ hybridization (FISH). Primary tumors were also evaluated for HER2 protein expression by immunohistochemistry (IHC) and by FISH. Amplification was defined as HER2/CEP17 ≥ 2. IHC was scored as 0, 1+, 2+, or 3+. Primaries whose HER2 status was positive by both FISH and IHC (ie, amplified and IHC3+), or negative by both (ie, nonamplified and IHC0-1+), were selected. HER2 status was compared between primaries and their MLNs (kappa). Results: Concordant HER2 results between primaries and their MLNs were found in 92% (95/103) of EACs (Table; κ = .76 [95% CI .60 - .92]). However, among patients with HER2-positive primaries, 19% (4/21) had HER2-nonamplified MLNs; among these cases, either all MLNs were HER2-nonamplified (n = 2), or both HER2-nonamplified and –amplified MLNs were present (n = 2). Among HER2-negative primary EACs, 5% (4/82) of cases had MLNs that were all HER2-amplified (n = 3) or both HER2-nonamplified and -amplified (n = 1). Conclusions: A patient subset whose primary EACs were HER2-positive (by both FISH and IHC) were unexpectedly found to lack HER2 amplification in corresponding MLNs. Conversely, a subgroup with HER2-negative primaries had HER2-amplified MLNs, and would have been deemed ineligible for HER2-targeted therapy. These preliminary data suggest that evaluating MLNs in resected EACs has the potential to better identify patients who benefit from HER2-targeted therapy. [Table: see text]

HER2 gene amplification and protein overexpression in uterine clear cell carcinoma and its implications in targeted immunotherapy.

2017 ◽  
Vol 35 (7_suppl) ◽  
pp. 29-29
Author(s):  
Jain Zhou ◽  
William R. Sukov ◽  
Jodi M Carter ◽  
J. Kenneth Schoolmeester
Keyword(s):  
Gene Amplification ◽  
Clear Cell ◽  
Clear Cell Carcinoma ◽  
Her2 Overexpression ◽  
Her2 Expression ◽  
Her2 Amplification ◽  
Protein Overexpression ◽  
Her2 Gene ◽  
Her2 Gene Amplification ◽  
Uterine Clear Cell Carcinoma

29 Background: Uterine clear cell carcinoma (UCCC) is a high-grade endometrial carcinoma. The current treatment is hysterectomy with post-operative chemotherapy and/or radiation. The 5-year disease free survival remains dismal for UCCC with 65% for early-stage and 54% for advanced stage disease. In addition, UCCC may be more resistant to chemotherapy or radiation therapy than the endometrioid subtype. The aim of the current study is to investigate the HER2 gene amplification status in UCCC and its role for targeted therapy in UCCC. Methods: Twenty-nine cases of UCCC were retrieved from surgical pathology archives of Mayo Clinic at Rochester between 2011 and 2015. All cases except one case were hysterectomy specimens. The blocks contain the most characteristic morphology of UCCC were selected and corresponding paraffin sections were subjected to fluorescent in situ hybridization for amplification of HER2 gene (Hercept, Abbott Molecular) and parallel immunohistochemical (IHC) study. Results: A total of 9 (of 29; 31%) UCCCs showed HER2 amplification and 4 (of 29; 14%) were considered equivocal for HER2 amplification by FISH. A total of 3 (10%) tumors showed 3+ HER2 overexpression while 11 (38%) UCCCs showed 2+ HER2 overexpression, 9 (31%) showed 1+ expression with the remaining cases showing no expression of HER2. Importantly, we observed significant intratumoral heterogeneity with regard to HER2 expression. Comparing the results of IHC with HER2 gene status as determined by FISH, 2 (66%) of the 3 cases that showed 3+ HER2 expression also showed amplification for HER2 by FISH, while 1 (33%) was equivocal for HER2 amplification. Of the 11 tumors that showed 2+ HER2 expression, 6 (55%) were amplified by FISH and 1 (9%) was equivocal. Conclusions: This is the largest number of UCCC cases that has been studied on the HER2 amplification and corresponding protein overexpression. Our results indicate that the HER2 overexpression is common in UCCCs and is frequently associated with HER2 amplification. These results also suggest that targeted adjuvant therapy with trastuzumab-based immunotherapy should be evaluated in patients with UCCC showing HER2 protein overexpression or HER2 gene amplification.

Determining True HER2 Gene Status in Breast Cancers With Polysomy by Using Alternative Chromosome 17 Reference Genes: Implications for Anti-HER2 Targeted Therapy

2011 ◽  
Vol 29 (31) ◽  
pp. 4168-4174 ◽  
Author(s):  
Chun Hing Tse ◽  
Harry C. Hwang ◽  
Lynn C. Goldstein ◽  
Patricia L. Kandalaft ◽  
Jesse C. Wiley ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Reference Genes ◽  
Copy Number ◽  
Retinoic Acid Receptor ◽  
Chromosome 17 ◽  
Breast Cancers ◽  
Her2 Gene ◽  
Polysomy 17 ◽  
Gene Status

Purpose The ratio of human epidermal growth factor receptor 2 (HER2) to CEP17 by fluorescent in situ hybridization (FISH) with the centromeric probe CEP17 is used to determine HER2 gene status in breast cancer. Increases in CEP17 copy number have been interpreted as representing polysomy 17. However, pangenomic studies have demonstrated that polysomy 17 is rare. This study tests the hypothesis that the use of alternative chromosome 17 reference genes might more accurately assess true HER2 gene status. Patients and Methods In all, 171 patients with breast cancer who had HER2 FISH that had increased mean CEP17 copy numbers (> 2.6) were selected for additional chromosome 17 studies that used probes for Smith-Magenis syndrome (SMS), retinoic acid receptor alpha (RARA), and tumor protein p53 (TP53) genes. A eusomic copy number exhibited in one or more of these loci was used to calculate a revised HER2-to-chromosome-17 ratio by using the eusomic gene locus as the reference. Results Of 132 cases classified as nonamplified on the basis of their HER2:CEP17 ratios, 58 (43.9%) were scored as amplified by using alternative chromosome 17 reference gene probes, and 13 (92.9%) of 14 cases scored as equivocal were reclassified as amplified. Among the cases with mean HER2 copy number of 4 to 6, 41 (47.7%) of 86 had their HER2 gene status upgraded from nonamplified to amplified, and four (4.7%) of 86 were upgraded from equivocal to amplified. Conclusion Our results support the findings of recent pangenomic studies that true polysomy 17 is uncommon. Additional FISH studies that use probes to the SMS, RARA, and TP53 genes are an effective way to determine the true HER2 amplification status in patients with polysomy 17 and they have important potential implications for guiding HER2-targeted therapy in breast cancer.

PS02.092: HER2 EXPRESSION AND GENE AMPLIFICATION CORRELATES WITH BETTER SURVIVAL IN ESOPHAGEAL ADENOCARCINOMA

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 146-147
Author(s):  
Heike Loeser ◽  
Patrick Plum ◽  
Thomas Zander ◽  
Max Kraemer ◽  
Hakan Alakus ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Growth ◽  
Esophageal Adenocarcinoma ◽  
Gene Amplification ◽  
Growth Pattern ◽  
Prognostic Impact ◽  
Her2 Expression ◽  
Her2 Positive ◽  
Papillary Tumor ◽  
The Impact

Abstract Background Targeting Her2 is highly established in cancers of the upper gastrointestinal tract, since clinical studies showed a survival benefit in Her2-positive gastric cancer. To date there is conflicting data concerning the impact of Her2 expression and gene amplification in esophageal adenocarcinoma (EAC), as most studies do not differ between cancers of the esophagus, gastroesophageal junction and stomach. The aim of this study was to analyze the expression and gene amplification of Her2 in EAC in correlation to clinical and pathological data to verify the prognostic impact. Methods We analyzed 506 patients with esophageal adenocarcinomas that underwent thoraco-abdominal esophagectomy between 1997 and 2013 using a tissue micro array (TMA) for the expression of Her2 by immunohistochemistry (IHC) according to the guidelines. Fluorescence-in-situ-hybridization (FISH) was performed for IHC score 2. The Her2-status was correlated with clinical and pathological data. Results Her2-positivity was found in 11.7% (n = 59) of all EAC (IHC score 3 + or IHC score 2 + with amplification) and demonstrated a significant better overall-survival (OS) in correlation to Her2-negative tumors (median OS 55.0 vs. 22.7 months, P < 0.0001) (Figure below). Overexpression of Her2 was associated with lower tumor stages (pT1/pT2, P = 0.038), absence of lymph node metastases (pN0/pN + , P = 0.030) and was significantly associated with tubular and/or papillary tumor growth pattern (P = 0.029). Conclusion We demonstrated a positive prognostic impact of Her2 expression and gene amplification in a large cohort of EAC, contrary to other solid malignancies including gastric cancer, but according to a large study of EAC from 2012. Her2-positive tumors significantly have a tubular and/or papillary tumor growth pattern, indicating a marker of differentiation in EAC. Disclosure All authors have declared no conflicts of interest.

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