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Cancer Symposium Abstract Book Society of Surgical Oncology 69th Annual Cancer Symposium Boston, Massachusetts March 2-5, 2016 Electronic supplement to Annals of Surgical Oncology An Oncology Journal for Surgeons th 69 ANNUAL Cancer SYMPOSIUM Society of Surgical Oncology March 2-5, 2016 y Boston, Massachusetts Annals of Surgical Oncology An Oncology Journal for Surgeons The Official Journal of the Society of Surgical Oncology Abstract Book Society of Surgical Oncology 69th Annual Cancer Symposium Boston, Massachusetts March 2-5, 2016 CONTENTS Volume 20, Supplement 1, February 2016 S3: Session Titles and Abstract Contents S5: Abstracts Accepted for Plenary and Parallel Oral Presentations S41: Abstracts Accepted for Video Presentations S47: Abstracts Accepted for Poster Presentations S180: Conflict of Interest Disclosures S185: Author Index This supplement was not sponsored by outside commercial interests. Session Titles and Abstract Contents Session Title Abstract Numbers Pages Abstracts Accepted for Plenary and Parallel Oral Presentations Plenary Session I 1 – 4 S6 – S7 Plenary Session II 5 – 8 S7 – S9 Parallel Session: Hepatobiliary Cancer 9 – 18 S9 – S13 Parallel Session: Breast Cancer 1 19 – 28 S13 – S17 Parallel Session: Colorectal Cancer 29 – 38 S17 – S21 Parallel Session: Upper Gastrointestinal Cancer 39 – 48 S21 – S24 Parallel Session: Breast Cancer 2 49 – 58 S24 – S28 Parallel Session: Melanoma 59 – 68 S28 – S32 Parallel Session: Endocrine Cancer 69 – 76 S32 – S35 Parallel Session: Quality Improvement/Clinical Outcomes 77 – 84 S35 – S37 Parallel Session: Sarcoma 85 – 88 S37 – S39 Parallel Session: Thoracic/Esophageal 89 – 92 S39 – S40 Abstracts Accepted for Video Presentations Top Rated Videos V1 – V8 S42 – S43 Videos in Exhibit Hall LBV1 – LBV6 S44 – S45 Abstracts Accepted for Poster Presentations Posters: Breast Cancer P1 – P85 S48 – S74 Posters: Colorectal Cancer P86 – P155 S74 – S95 Posters: Endocrine Cancer P156 – P178 S96 – S102 Posters: Hepatobiliary Cancer P180 – P225 S102 – S118 Posters: Melanoma P226 – P266 S119 – S132 Posters: Quality Improvement/Clinical Outcomes P267 – P300 S132 – S145 Posters: Sarcoma P301 – P315 S145 – S149 Posters: Thoracic/Esophageal P316 – P330 S150 – S154 Posters: Upper Gastrointestinal Cancer P331 – P405 S154 – S178 Posters: Other: Urology/Head & Neck Cancer P406 – P409 S178 – S179 Presentations Withdrawn P3, P6, P48, P139, P140, P141, P152, P157, P160, P179, P180, P207, P224, P312, P363, P376, P392 ABSTRACTS Accepted for PLENARY and PARALLEL SESSIONS 69th Annual Cancer Symposium Society of Surgical Oncology March 2–5, 2016 Boston, Massachusetts Ann Surg Oncol (2016) 23:S6–S195 DOI 10.1245/s10434-015-5010-5 1 cytoreduction (R0) was defined as absence of macroscopic disease at the end Combination Anti-Estrogen Therapy and Anti-HER2 Dendritic of surgical procedure. Main outcome endpoints were: R0 rates, progression Cell Vaccination Improves Pathologic Complete Response in free survival (PFS) and overall survival (OS). Kaplan-Meier curves were con- ER+/HER2+ DCIS Patients L. Lowenfeld,1* S. Zaheer,1 M. Fracol,2 structed for survival analysis and univariate and multivariate analysis was J. Datta,1 S. Xu,1 E. Fitzpatrick,1 A. DeMichele,1 P. Zhang,1 E. McDon- performed. Significance was considered at p<0.05. Results. 105 patients were included: 42 in Group A and 63 in Group B. Mean patient age was 56 years old ald,1 B.J. Czerniecki.1 1. Surgery, University of Pennsylvania, Philadel- (range 32-85). There were no significant differences between groups regarding phia, PA; 2. Northwestern, Chicago, IL. demographic, clinical, surgical or pathological variables. Surgical morbidity INTRODUCTION: ER signaling has been proposed as an escape pathway was low and not different between groups and there was no surgical mortality. in the setting of HER2 inhibition, resulting in resistance to anti-HER2 ther- R0 cytoreduction was obtained in 35.5% vs. 64.5% in Groups A and B respec- apy. In our clinical trials of a neoadjuvant HER2-pulsed dendritic cell (DC) tively. Median PFS and OS for the entire cohort were 16.2 and 38 months, vaccine, we observed higher rates of pathologic complete response (pCR) in respectively. Median PFS were 17.52 and 14.71 months for Groups A and B, - hormone independent (ER ) patients. We investigated the effect of combination respectively (p=NS) and OS were 44.2 and 33.6 months for groups A and B, anti-estrogen (AE) therapy and anti-HER2 DC vaccination on clinical and respectively (p=NS). Factors associated with worse prognosis on multivari- + CD4 T-helper type 1 (Th1) immune responses. METHOD: Seventy-eight ate analysis for the entire cohort were: anemia (Hb <12 g/dl) (p=0.004) and + HER2 DCIS patients received a neoadjuvant HER2-pulsed DC1 vaccine: hypoalbuminemia (<3.5 g/dl)(p=0.007). Low performance status (Kanofski - + + ER (n=34, 43.6%), ER treated without AE therapy (ER w/o AE; n=24, < 70) was of borderline significance (p=0.05). Conclusion. In spite of nearly + + 30.8%), ER treated with concurrent AE therapy (ER w AE; n=20; 25.6%). doubling the rate of complete cytoreduction, preoperative chemotherapy does pCR was assessed at surgical resection and patients were followed clinically to not improve outcome in advanced epithelial ovarian carcinoma. detect subsequent breast events. Of available anti-HER2 CD4+ Th1 responses pre and post-vaccination (n=51; 65.4%), reactivity to an individual HER2 peptide was defined as a minimum of 20 SFC/2x105 cells after subtracting 3 unstimulated background and at least a two-fold increase over unstimulated Probing Compensatory Signaling to MEK Inhibition Uncovers background. Three metrics were used to evaluate Th1 responses: (1) respon- the Vulnerability of Pancreatic Cancer to Dual Therapy with Tra- sivity (% of patients reacting to *1 peptide), (2) response repertoire (number metinib Plus Foretinib A. Michaels,* J.M. Lindberg, T. Newhook, of reactive peptides), and (3) cumulative response (sum of SFCs across all 6 S.J. Adair, M.G. Mullen, J. Parsons, T.W. Bauer. Surgery, University of peptides). RESULTS: Eleven ER- patients (32.4%) and 5 ER+w AE patients Virginia, Charlottesville, VA. (25%) achieved pCR (p=0.76); whereas, only 4.2% of ER+w/o AE patients achieved pCR (p<0.01). Patients were followed for a minimum of 1yr, median Background: The MEK inhibitor trametinib achieves modest growth inhi- follow-up 5yrs. Subsequent breast events (DCIS or IBC) only occurred in bition in preclinical models of pancreatic ductal adenocarcinoma (PDAC). We ER+w/o AE patients (n=4; 16.7%). Each cohort mounted a significant Th1 hypothesized that in vivo evaluation of signaling pathways in PDAC tumors immune response following vaccination (pre vs post; p<0.01). However, there during trametinib treatment would reveal suitable targets for combination was no significant difference in pre or post immune responses between ER, therapy with trametinib. Methods: Mice were engrafted orthotopically with ER+w/o AE, or ER+w AE cohorts. CONCLUSION: Simultaneous neoadjuvant KRAS-mutant patient-derived xenograft (PDX) PDAC tumors and treated with AE therapy and anti-HER2 DC1 vaccination increases the rate of pCR and trametinib for 10 days, then phospho-receptor tyrosine kinase (pRTK) arrays decreases the rate of subsequent breast events in patients with ER+/HER2+ of whole tumor lysates were performed to evaluate activation of compensatory breast cancer. Combination AE and anti-HER2 therapy warrants further explo- signaling pathways. In subsequent experiments, PDAC PDXs were implanted ration with randomized controlled trials. into mice that were then treated with trametinib plus an inhibitor of compen- satory signaling pathways and serial MRI was used to monitor tumor growth. Results: Trametinib treatment of PDAC tumors led to significantly increased activation of Axl (15-fold), VEGFR2 (14-fold), and Tie2 (11-fold) (p<0.01 for all) and a trend toward increased activation of the related receptors PDGFRa (3-fold), Ron (2-fold), and Met (2-fold). Interestingly, these pRTKs were not activated in drug-naïve tumors, but only after MEK inhibition with trametinib. In subsequent experiments, PDAC PDX-bearing mice were treated with con- trol, trametinib, foretinib (inhibitor of Axl, Met, Ron, PDGFRa, VEGFR2 and Tie2), or trametinib + foretinib. Compared to control, trametinib resulted in 63% inhibition in tumor growth (p<0.01), foretinib led to 65% inhibition (p<0.01), and trametinib + foretinib led to 100% growth inhibition (p<0.01; Fig 1), confirming the importance of these compensatory signaling receptors to tumor growth. Conclusions: Combination therapy with trametinib plus an inhibitor of these compensatory signaling pathways achieved complete inhi- bition of tumor growth in vivo. The combination of trametinib plus foretinib in PDAC warrants further investigation. This in vivo paradigm for discovery of rational combination therapy in cancer is likely to be more successful than searching for targets in drug-naïve tumors. 2 Neoadjuvant Chemotherapy Increases Complete Cytoreduction Rate but Does Not Improve Final Outcome in Advanced Epithelial Ovarian Cancer H. Medina-Franco,* F. Lambreton, A. Fimbres-Mo- rales, J. Vargas-Siordia. National Institute of Medical Sciences and Nutrition, Mexico City, Mexico. Background. Most epithelial ovarian cancers present in advanced stages. Traditional management is maximum cytoreductive effort followed by plati- num-taxane based chemotherapy. We hypothesize that giving all 6 cycles of chemotherapy before surgery will increase the complete cytoreductive
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