Histologic Changes in Non-Neoplastic Pancreas after Neoadjuvant Therapy for Pancreatic Ductal Adenocarcinoma
Deyali Chatterjee, Matthew H Katz, Asif Rashid, Hua Wang, Gauri R Varadhachary, Robert A Wolff, Jeffrey E Lee, Peter W Pisters, James L Abbruzzese, Jason B Fleming, Huamin Wang. University of Texas MD Anderson Cancer Center, Houston, TX
Background: Neoadjuvant chemoradiation therapy (NCRT) has been increasingly used to treat patients with pancreatic ductal adenocarcinoma (PDAC). However, the histologic changes in non-neoplastic pancreatic parenchyma after NCRT have not been examined in detail.
Design: We retrospectively reviewed the archival H & E slides from 218 patients with PDAC who completed NCRT and underwent pancreatectomy at our institution. Seventy-five patients who underwent pancreatectomy for PDAC without NCRT were used as the control group. All the cases were reviewed by two pathologists for the presence of pancreatic intraepithelial neoplasia (PanIN) of different histologic grades; “neuroma-like” nerve proliferation; islet cell hyperplasia; pancreatic fibrosis (none, mild, moderate or severe) and inflammation (none, mild or moderate to severe). The neuroma-like nerve proliferation was defined as haphazardly dispersed, hypertrophic nerve bundles within fibrous stroma in the peripancreatic tissue, unrelated to perineural invasion. The islet cell hyperplasia was defined as increase in the number and size of the existing islets, as well as linear and anastomosing cords segueing into ductal formations. Data analyses were performed using Chi-square analysis or Fisher's exact tests with two-sided significance level of 0.05.
Results: Among the 218 patients who received NCRT, none, mild, moderate and severe fibrosis were present in none, 4.6%, 68.4% and 27.0% patients respectively compared to 18.7%, 40.0%, 32.0% and 9.3% patients in the control group (p=0.01). Neuroma-like nerve proliferation and islet cell hyperplasia were present in 34 (15.6%) and 79 (36.2%) patients respectively in the NCRT group, compared to 5.3% and 12.0% respectively in the control group (P=0.02 and P<0.01, respectively). Moderate to severe inflammation were present in 15 (20%) patients in control group compared to 12 (5.5%) patients in the NCRT group (p=0.01). However, we did not observe significant difference in the frequencies of PanIN lesions of any histologic grade (grades I, II and III in 84%, 72.5% and 37% respectively in the NCRT group, and 85%, 76% and 39% respectively in the control group; p>0.05).
Conclusions: This study demonstrates that patients who received NCRT have more pancreatic fibrosis, higher frequencies of neuroma-like nerve proliferation and islet cell hyperplasia, but less frequent moderate to severe inflammatory infiltrates than those who did not received NCRT. However there is no significant difference in the incidence of PanIN lesions between these two groups.
Tuesday, March 5, 2013 9:30 AM
Poster Session III # 210, Tuesday Morning