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Contemporary Strategies for Managing Pancreatic Cancer PowerPoint Presentation

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Description : This medical presentation on cancer titled "Contemporary Strategies for Managing Pancreatic Cancer" discusses strategies for managing pancreatic cancer in the present times.

Tags : Cancer, Strategy, Management, Managing Pancreatic Cancer

Published on : May 03, 2021 | Views : 1953 | Downloads : 2

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Faculty Caio Max S. Rocha Lima, MD Professor of Medicine Co-Leader, Colorectal, Pancreatic, Liver, and Related Cancers Group Co-Director, Phase I Unit University of Miami Leonard M. Miller School of Medicine Sylvester Comprehensive Cancer Center Miami, FL
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Activity Planners Shari J. Dermer, PhD Manager, Educational Strategy and Content Med-IQ Baltimore, MD Lisa R. Rinehart, MS, ELS Director, Editorial Services Med-IQ Baltimore, MD
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Oncogenes KRAS mutations1 Very common (> 90%), usually restricted to codon 12 Early genetic event in pancreatic carcinogenesis and are considered to be a “signature” of pancreatic cancer BRAF mutations2 Observed in 30% of the pancreatic cancers with WT KRAS gene AKT1 gene, AKT2 gene, and MYB gene amplification Observed in 60%, 10% to 15%, and 10% of pancreatic cancers, respectively3-5 Almoguera C, et al. Cell. 1988;53:549-54; 2. Kanda M, et al. Gastroenterology. 2012;142:730-3; 3. Li D, et al. Lancet. 2004;363:1049-57; 4. Cheng JQ, et al. Proc Natl Acad Sci USA. 1996;93:3636-41; 5. Wallrapp C, et al. Cancer Res. 1997;57:3135-9.
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Tumor Suppressor Genes Inactivation of the p16 gene1 Observed in 80% to 95% of sporadic pancreatic cancers The combination of p16 and KRAS mutations is uncommon in other human tumors and is considered to be a molecular “signature” for pancreatic cancer Observed at a later stage in pancreatic carcinogenesis than KRAS mutations p53 gene inactivation2 Observed in 55% to 75% of cases and is a late event in tumorigenesis p21 gene inactivation Early event in the development of pancreatic carcinoma 1. Schutte M, et al. Cancer Res. 1997;57:3126-30. 2. Li D, et al. Lancet. 2004;363:1049-57.
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Tumor Suppressor Genes SMAD4 gene1 Plays a critical role in signaling through the TGF-beta pathway and occurs in about 55% BRCA2 (her-2/neu)2 Gene mutation carriers have a 10-fold increased risk of developing pancreatic cancer Prognostic and may play a role in adjuvant, neoadjuvant, and chemoXRT approaches 1. Ghaneh P, et al. Gut. 2007;56:1134-52. 2. Bachet JB et al. Ann Oncol. 2012; 23: 2327-35.
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Molecular Features and Risk of Relapse SMAD4 Poor prognosis1,2 Pattern of relapse3,4 CXCR45 Notch/hedgehog6 Stromal SPARC7-9 Cancer stem cells6 1. Kojima K, et al. Cancer Res. 2007;67:8121-30; 2. Blackford A, et al. Clin Cancer Res. 2009:15:4674-79; 3. Iacobuzio-Donahue CA, et al. J Clin Oncol. 2009;27:1806-13; 4. Crane CH, et al. J Clin Oncol. 2011;29:3037-43; 5. Bachet JB, et al. Ann Oncol. 2012;23:2327-35; 6. Hezel AF, et al. Genes Devel. 2006;20:1216-49; 7. Infante JR, et al. J Clin Oncol. 2007;20:319-25; 8. Neuzillet C, et al. Cancer Metastasis Rev. 2013;32:585-602; 9. Sinn M, et al. J Surg Oncol. 2013;108:398-402.
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NCCN Definitions: Locally Advanced and Borderline Resectable Locally advanced SMA encasement > 180 degrees Unreconstructable SMV/portal vein occlusion Any celiac abutment (head) or celiac encasement > 180 degrees (body/tail) Aortic invasion or encasement Lymph node metastases beyond field of resection Borderline resectable SMA encasement < 180 degrees SMV/portal impingement Short-segment SMV occlusion Celiac encasement < 180 degrees (tail) Abutment/encasement of hepatic artery NCCN Guidelines. Pancreatic Adenocarcinoma V1.2013; Varadhachary GR. J Gastrointest Oncol 2011;2:136-42.
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Chemo Alone vs. Chemo-RT 1. Klaassen DJ, et al. J Clin Oncol. 1985;3:373-8; 2. GITSG. J Natl Cancer Inst. 1988;80:751-5; 3. Chauffert B, et al. Ann Oncol. 2008;19:1592-9; 4. Loehrer PJ, et al. J Clin Oncol. 2011;29:4105-12. *Investigational
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FOLFIRINOX* Experience in LAPC Hosein P, et al. BMC Cancer. 2012;12:199. *Investigational use.
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FOLFIRINOX* Outcomes in LAPC 4 still unresectable 3 resectable by imaging 3 R0 resections 3 post-op combined chemoradiation 14 patients FOLFIRINOX (3-12 cycles) 9 unresectable at maximum response or tolerability Combined chemoradiation (2 ongoing) 1 progressed after 3 cycles 4 resectable by imaging 2 R0 resections 1 R1 resection 1 unresectable at E-lap 1 still unresectable 4 patients FOLFIRINOX (6-17 cycles) 1 unresectable at maximum response or tolerability Combined chemoradiation 3 post-op combined chemoradiation 3 resectable by imaging 3 R0 resections Patient flowchart for patients assessed as having unresectable disease (panel A, n = 14), and for those assessed as having borderline resectable disease (panel B). Hosein P, et al. BMC Cancer. 2012;12:199. A B *Investigational use.
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LAPC: Conclusions XRT + chemotherapy better then XRT alone Gemcitabine + XRT is potentially superior to gemcitabine alone The ECOG study had poor accrual and closed early Retrospective data: chemo followed by chemoXRT superior to chemoXRT upfront The role of XRT in LAPC is questioned due to the results of the LAP 07 study Gemcitabine may be a superior radiosensitizer to 5-FU The role of FOLFIRINOX in the neoadjuvant setting is emerging
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International Phase 3 Trial Pancreatic cancer (metastatic) Gemcitabine 1,000 mg/m2 IV weekly x 7 of 8 Gemcitabine 1,000 mg/m2 + Nab-paclitaxel 125 mg/m2 weekly x 3 of 4 Von Hoff DD, et al. N Engl J Med.2013;369:1691-703.
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Phase 3 Trial: Gemcitabine and Nab-Paclitaxel Von Hoff DD, et al. GI Cancers Symposium 2013[Abstract LBA148].
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PRODIGE 4—ACCORD 11 Trial Design Stratification: Center PS: 0 vs. 1 Location of the tumor: head vs. other location of the primary tumor Conroy T, et al. N Engl J Med. 2011;364:1817-25. *Investigational use.
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PFS Median PFS FOLFIRINOX: 6.4 mos Median PFS gemcitabine: 3.3 mos 0.00 0.25 0.50 0.75 1.00 Probability 171 121 85 42 17 7 4 1 1 0 0 0 0 FOLFIRINOX 171 88 26 8 5 2 0 0 0 0 0 0 0 Gemcitabine Number at risk 0 3 6 9 12 15 18 21 24 27 30 33 36 Months Reprinted with permission from Conroy T, Desseigne F, Ychou M, et al. FOLFIRINOX versus gemcitabine for metastatic pancreatic cancer. N Engl J Med. 2011;364(19):1817-1825.
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Acknowledgement of Commercial Support This activity is supported by educational grants from Bayer HealthCare Pharmaceuticals, Onyx Pharmaceuticals, Celgene Corporation, Daiichi Sankyo, Inc., and Lilly. For further information concerning Lilly grant funding visit www.lillygrantoffice.com Copyright © 2014 Med-IQ®. All rights reserved.