Original contributionModification of insulin-like growth factor 1 receptor, c-Src, and Bcl-XL protein expression during the progression of barrett’s neoplasia
Section snippets
Materials and methods
We studied a total of 34 tumor specimens from patients with adenocarcinoma of the esophagus arising in Barrett’s-associated neoplasia who underwent Ivor-Lewis esophagogastrectomy at the Moffitt Cancer Center. The hematoxylin and eosin-stained slides from the resected specimens were reviewed. Two representative sections of each tumor (primary or metastatic) were selected for the study. Sometimes IM was not present adjacent to the invasive adenocarcinoma in the slides selected for this study, but
Clinical pathological characteristics
The patients in the study group had an average age of 63 years (range, 43 to 82), and 91% of the group was male. All of the patients underwent Ivor-Lewis esophagogastrectomy, including a standard lymph node dissection. The tumors, localized to the lower third of the esophagus, ranged from 0.5 to 9.0 cm in diameter (mean, 3.7 cm; standard deviation, 2.03 cm). Histologically, they were all CAs arising in a background of BE. Of the cases studied, 22 exhibited IM; 25, LGD; 28, high-grade dysplasia
Discussion
In the United States, the incidence of esophageal adenocarcinoma, arising in the background of BE, has increased since the 1970s by a factor of 6 to 8.26 It has been calculated that the incidence of adenocarcinoma in BE ranges between 30- and 125-fold greater than in the control population.3 It is well established that BE predisposes to esophageal adenocarcinoma, and that the cancer risk is limited to patients with specialized (ie, intestinalized) metaplastic epithelium.
It has been postulated
Acknowledgements
The authors are grateful to Marek Wloch (Tissue Procurement) and Sandra Livingston (Tissue Pathology Core) from the Moffitt Cancer Center for providing frozen tissues and performing the immunohistochemical stains.
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