A Multidisciplinary Approach to Pancreas Cancer in 2016: A Review

Fogel, Evan L.; Shahda, Safi; Sandrasegaran, Kumar; DeWitt, John M.; Easler, Jeffrey J.; Agarwal, David M.; Eagleson, Mackenzie A.; Zyromski, Nicholas J.; House, Michael G.; Ellsworth, Susannah G.; Hajj, Ihab El; O’Neil, Bert H.; Nakeeb, Attila; Sherman, Stuart

doi:10.1038/ajg.2016.610

Cited by 108 publications

(93 citation statements)

References 161 publications

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“…Surgical resection and chemotherapy were considered to be the main treatment options for pancreatic cancer [2]. Unfortunately, even with the advancement in medicine, pancreatic cancer is still resistant to current treatment regimens [3].…”

Section: Introductionmentioning

confidence: 99%

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Cai

Yao

et al. 2017

Oncotarget

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Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Though studies have implicated the roles of microRNAs in pancreatic cancer progression, little is known about the role of miR-613 in pancreatic cancer. In the present study, the expression of miR-613 was down-regulated in pancreatic cancer tissues and cancer cell lines. Down-regulation of miR-613 was positively correlated with tumor differentiation, advanced TNM stage, nodal metastasis and shorter overall survival in patients with pancreatic cancer. Overexpression of miR-613 suppressed cell proliferation, invasion and migration, and induced cell apoptosis and cell cycle arrest at G0/G1 phase in pancreatic cancer cells. Bioinformatics analysis, luciferase reporter assay and rescue experiments showed that notch3 was a direct target of miR-613. MiR-613 was inversely correlated with notch3 expression in pancreatic cancer tissues. The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. In vivo studies showed that stable overexpression of miR-613 or knock-down of HOTAIR suppressed tumor growth and also reduced the expression of notch3. In conclusion, these results suggest that HOTAIR functions as a competing endogenous RNA to regulate notch3 expression via sponging miR-613 in pancreatic cancer.

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Section: Introductionmentioning

confidence: 99%

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Cai

Yao

et al. 2017

Oncotarget

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“…Finally, this study included patients who are older and more often female than the general pancreatic cancer population, so the results may not be generalizable. 1 Although recent prospective studies have shown high rates of postoperative complications in patients who underwent ERCP before surgery for pancreatic cancer, ERCP still is used frequently in this situation. In this large population-based analysis, we did not find an effect of preoperative ERCP on mortality after controlling for confounding factors.…”

Section: Discussionmentioning

confidence: 99%

“…S urgical resection is the only option for cure for patients newly diagnosed with pancreatic cancer located in the head of the pancreas. 1,2 However, surgery may be delayed by the need for definitive diagnosis, symptoms of biliary obstruction, or the need for neoadjuvant treatment. [2][3][4] Endoscopic retrograde cholangiopancreatography (ERCP) may be used to relieve symptoms of jaundice as well as to normalize bilirubin levels so neoadjuvant chemotherapy can be administered before surgical resection.…”

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confidence: 99%

Preoperative Endoscopic Retrograde Cholangiopancreatography Is Not Associated With Increased Pancreatic Cancer Mortality

Rustgi¹,

Amin

Yang

et al. 2019

Clinical Gastroenterology and Hepatology

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BACKGROUND & AIMS:Endoscopic retrograde cholangiopancreatography (ERCP) before surgery for pancreatic cancer has been associated with infectious complications after surgery. Little is known about the effects of preoperative ERCP on the survival of patients with pancreatic cancer. We investigated whether ERCP before surgery affects overall survival, after controlling for confounding factors. METHODS:We used Surveillance, Epidemiology, and End Results (SEER) and linked Medicare claims data to identify patients older than 65 years with cancer localized to the head of the pancreas, from 2000 through 2011. We used inverse propensity-weighted Cox proportional hazard models to assess the effects of ERCP on the survival of patients who underwent surgery for pancreatic cancer. RESULTS:Among 16,670 patients with cancer of the head of the pancreas, 2890 (17.3%) underwent surgical resection; 1864 (64.5%) of these patients received preoperative ERCP. After we adjusted for confounders, we found that patients who received preoperative ERCP did not have an increased risk of death compared with patients who underwent resection alone (hazard ratio, 1.02; 95% CI, 0.96-1.08). CONCLUSIONS:Patients with pancreatic cancer who underwent ERCP before surgery did not have an increased risk of death compared with patients who proceeded directly to surgery. Studies are needed to identify subsets of patients who may benefit from this procedure.

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“…Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related death and tumor resection is still the only potentially curative treatment (1). However, because PDAC patients are prone to develop systemic metastasis early in the course of the disease, the risk of tumor recurrence remains extraordinarily high with a 5-year survival rate of 10% after surgery alone and up to 25% with adjuvant chemotherapy, preferably gemcitabine (2).…”

Section: Introductionmentioning

confidence: 99%

Perioperative, Spatiotemporally Coordinated Activation of T and NK Cells Prevents Recurrence of Pancreatic Cancer

et al. 2018

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Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal and disseminating cancer resistant to therapy, including checkpoint immunotherapies, and early tumor resection and (neo)adjuvant chemotherapy fails to improve a poor prognosis. In a transgenic mouse model of resectable PDAC, we investigated the coordinated activation of T and natural killier (NK) cells in addition to gemcitabine chemotherapy to prevent tumor recurrence. Only neoadjuvant, but not adjuvant treatment with a PD-1 antagonist effectively supported chemotherapy and suppressed local tumor recurrence and improved survival involving both NK and T cells. Local T-cell activation was confirmed by increased tumor infiltration with CD103CD8 T cells and neoantigen-specific CD8 T lymphocytes against the marker neoepitope LAMA4-G1254V. To achieve effective prevention of distant metastases in a complementary approach, we blocked the NK-cell checkpoint CD96, an inhibitory NK-cell receptor that binds CD155, which was abundantly expressed in primary PDAC and metastases of human patients. In gemcitabine-treated mice, neoadjuvant PD-1 blockade followed by adjuvant inhibition of CD96 significantly prevented relapse of PDAC, allowing for long-term survival. In summary, our results show in an aggressively growing transgenic mouse model of PDAC that the coordinated activation of both innate and adaptive immunity can effectively reduce the risk of tumor recurrence after surgery, facilitating long-term remission of this lethal disease. Coordinated neoadjuvant and adjuvant immunotherapies reduce the risk of disease relapse after resection of murine PDAC, suggesting this concept for future clinical trials. .

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A Multidisciplinary Approach to Pancreas Cancer in 2016: A Review

Cited by 108 publications

References 161 publications

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Preoperative Endoscopic Retrograde Cholangiopancreatography Is Not Associated With Increased Pancreatic Cancer Mortality

Perioperative, Spatiotemporally Coordinated Activation of T and NK Cells Prevents Recurrence of Pancreatic Cancer

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