ERBB2 Amplifications in Esophageal Adenocarcinoma

Dahlberg, Peter S.; Jacobson, Blake A.; Dahal, G.; Fink, Jürgen; Kratzke, Robert A.; Maddaus, Michael A.; Ferrin, Lance J.

doi:10.1016/j.athoracsur.2004.05.037

Cited by 62 publications

(56 citation statements)

References 22 publications

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“…19,20 But more recently, studies have examined the frequency of HER2 gene amplification in esophageal adenocarcinoma at the DNA level using either polymerase chain reaction (PCR) or some form of in-situ hybridization (ISH). 7,10,[26][27][28][29] Our results correspond to these latter studies (except one 26 with a small sample size of 25) in which frequencies of HER2 amplification are consistently lower and range from 12-24%.…”

Section: -25supporting

confidence: 77%

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HER-2/neu Gene Amplification in Esophageal Adenocarcinoma and Its Influence on Survival

et al. 2011

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Section: -25supporting

confidence: 77%

“…2,3 However, its role in other solid tumors is controversial. [4][5][6][7][8][9] The published frequency of HER2 overexpression in esophageal cancer ranges from 11 to 73%. 10 Reports evaluating its significance are also varied in their conclusions.…”

Section: Introductionmentioning

confidence: 99%

HER-2/neu Gene Amplification in Esophageal Adenocarcinoma and Its Influence on Survival

et al. 2011

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“…Studies on esophageal cell lines have suggested cytotoxic as well as growth inhibitory effects of trastuzumab in both adenocarcinoma and squamous cell carcinoma cell lines [60,74,75]. Furthermore, in a phase I trial on esophageal adenocarcinomas, Safran et al [61] studied trastuzumab given in combination with cisplatin, paclitaxel, and radiation.…”

Section: The Role Of Her-2 In Esophageal Cancermentioning

confidence: 99%

Activation of Growth Factor Receptors in Esophageal Cancer—Implications for Therapy

et al. 2007

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Esophageal cancer is a highly aggressive disease and is the seventh most common cause of cancer-related death in the western world. Worldwide, it ranks as the sixth most frequent cause of cancer death. Despite advances in surgical techniques and treatment, the prognosis of esophageal cancer remains poor, with very few longterm survivors. The need for novel strategies to detect esophageal cancer earlier and to improve current therapy is urgent.It is well established that growth factors and growth factor receptor-mediated signaling pathways are important components of the transformation process in many forms of cancer, including esophageal cancer. With the recent advances in drug development, there are emerging possibilities to use growth factor signal transduction pathways in targeted therapy. This review provides a summary of the role of growth factors and their receptors in esophageal cancer and discusses their potential roles as biomarkers and as targets in therapy.

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“…In addition, the HER2-overexpressing esophageal adenocarcinoma cell line OE19 (27) was used for xenograft experiments. Both tumor models had comparable tumor growth kinetics in vivo, which allowed the evaluation of both before-and during-treatment scans at a comparable tumor size.…”

Section: Animals and Tumor Inoculationmentioning

confidence: 99%

Bevacizumab-Induced Normalization of Blood Vessels in Tumors Hampers Antibody Uptake

et al. 2013

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In solid tumors, angiogenesis occurs in the setting of a defective vasculature and impaired lymphatic drainage that is associated with increased vascular permeability and enhanced tumor permeability. These universal aspects of the tumor microenvironment can have a marked influence on intratumoral drug delivery that may often be underappreciated. In this study, we investigated the effect of blood vessel normalization in tumors by the antiangiogenic drug bevacizumab on antibody uptake by tumors. In mouse xenograft models of human ovarian and esophageal cancer (SKOV-3 and OE19), we evaluated antibody uptake in tumors by positron emission tomographic imaging 24 and 144 hours after injection of Zr-IgG (SKOV-3) before or after treatment with bevacizumab. Intratumor distribution was assessed by fluorescence microscopy along with mean vessel density (MVD) and vessel normalization. Notably, bevacizumab treatment decreased tumor uptake and intratumoral accumulation compared with baseline in the tumor models relative to controls. Bevacizumab treatment also reduced MVD in tumors and increased vessel pericyte coverage. These findings are clinically important, suggesting caution in designing combinatorial trials with therapeutic antibodies due to a possible reduction in tumoral accumulation that may be caused by bevacizumab cotreatment. Cancer Res; 73(11); 3347-55. Ó2013 AACR.

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ERBB2 Amplifications in Esophageal Adenocarcinoma

Cited by 62 publications

References 22 publications

HER-2/neu Gene Amplification in Esophageal Adenocarcinoma and Its Influence on Survival

HER-2/neu Gene Amplification in Esophageal Adenocarcinoma and Its Influence on Survival

Activation of Growth Factor Receptors in Esophageal Cancer—Implications for Therapy

Bevacizumab-Induced Normalization of Blood Vessels in Tumors Hampers Antibody Uptake

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