Emily E Cannon

Publications of Emily E Cannon

• Laparoscopic and open distal pancreatectomy: a comparison of outcomes.

  Authors: Kelly R Finan, Emily E Cannon, Eugenia J Kim, Mary M Wesley, Pablo J Arnoletti, Martin J Heslin, John D Christein

  The American surgeon. 08/2009; 75(8):671-9; discussion 679-80.

  Laparoscopic (lap) pancreatic surgery has been increasingly reported since its introduction in 1992. A retrospective analysis of consecutive patients undergoing elective lap and open distalLaparoscopic (lap) pancreatic surgery has been increasingly reported since its introduction in 1992. A retrospective analysis of consecutive patients undergoing elective lap and open distal pancreatectomy from 2002 to 2007 was performed. Univariate analysis was completed to evaluate perioperative variables. Logistic regression analysis was used to model predictors of postoperative pancreatic fistula. One hundred forty-eight subjects underwent distal pancreatectomy; 98 completed open, 44 lap, and six converted to open. There was no significant difference in the incidence of postoperative morbidity or mortality between the surgical approaches. Decreased operative time (156 vs 200 minutes, P < 0.01), blood loss (157 vs 719 mL, P < 0.01), and length of stay (5.9 vs 8.6 days, P < 0.01) were seen in the lap group. There was no significant difference in the rate of all pancreatic fistula formation (50 vs 46%, P = 0.94) or clinically significant leaks (18 vs 19%, P = 0.97) between techniques. A preoperative biopsy-proven cancer, increasing body mass index, history of pancreatitis, and male gender were significant predictors of having a pancreatic fistula. Lap and open distal pancreatectomy are performed safely at high-volume pancreatic surgery centers. This report provides ongoing support of the feasibility and safety of the lap approach with improved perioperative outcomes and equivalent pancreatic fistula rate.

• ErbB3 expression and dimerization with EGFR influence pancreatic cancer cell sensitivity to erlotinib.

  Authors: Andrey Frolov, Kyle Schuller, Ching-Wei D Tzeng, Emily E Cannon, Brandon C Ku, J Harrison Howard, Selwyn M Vickers, Martin J Heslin, Donald J Buchsbaum, J Pablo Arnoletti

  Cancer biology & therapy. 05/2007; 6(4):548-54.

  Abnormal expression and signaling of ErbB receptors has been implicated in multiple epithelial malignancies, including pancreatic cancer. Erlotinib, an epidermal growth factor receptor tyrosineAbnormal expression and signaling of ErbB receptors has been implicated in multiple epithelial malignancies, including pancreatic cancer. Erlotinib, an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), has been recently approved for pancreatic cancer treatment, but there are no reliable predictors of patient response. Expression of additional ErbB receptors seems to influence tumor response to EGFR-targeted therapy. We analyzed the influence of ErbB3 expression on pancreatic cancer cell response to erlotinib treatment. Proliferation assays of five human pancreatic cancer cell lines were performed following treatment with erlotinib. Expression and phosphorylation profiles of ErbB receptors and downstream adaptor protein (Akt, ERK1/2, STAT3, mTOR) were evaluated following stimulation with EGF or neuregulin-beta. The formation of EGFR homodimers and EGFR-ErbB3 heterodimers, necessary to enable ErbB3 downstream signaling, was demonstrated by chemical cross-linking assays. The effects of RNA inhibition of ErbB3 on sensitivity to erlotinib treatment were evaluated in AsPC-1 pancreatic cancer cells. Erlotinib inhibited Akt phosphorylation and proliferation of all the ErbB3-expressing cell lines but did not affect mTOR activation. Cross-linking studies confirmed the presence of EGFR-ErbB3 heterodimers in pancreatic cancer cells. Only the ErbB3-deficient MIA PaCa-2 cells displayed persistent Akt activation and ongoing proliferation in spite of erlotinib treatment. siRNA-mediated inhibition of ErbB3 expression in AsPC-1 cells resulted in acquired resistance to erlotinib treatment. Pancreatic cancer cells which lack ErbB3 do not display activation of the ErbB3-PI3K-Akt cascade induced by EGFR/ErbB3 heterodimers and become less critically dependent on EGFR signaling and therefore resistant to erlotinib. Pancreatic cancer expression of ErbB3 may be useful for EGFR-targeted therapy patient selection.