Pancreatic Cancer Chemoprevention Translational Workshop

Miller, Mark Steven; Allen, Peter J.; Brentnall, Teresa A.; Goggins, Michael; Hruban, Ralph H.; Petersen, Gloria M.; Rao, Chinthalapally V.; Whitcomb, David C.; Brand, Randall E.; Chari, Suresh T.; Klein, Alison P.; Lubman, David M.; Rhim, Andrew D.; Simeone, Diane M.; Wolpin, Brian M.; Umar, Asad; Srivastava, Sudhir; Steele, Vernon E.; Rinaudo, Jo Ann

doi:10.1097/mpa.0000000000000705

Cited by 23 publications

(16 citation statements)

References 108 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Despite the development of guidelines for the management of BD-IPMNs, it is still challenging to determine which BD-IPMNs harbor PDAC and even more difficult to determine which BD-IPMNs will undergo malignant transformation within the patient's lifetime. 91,125 In addition, the quality of evidence on which these recommendations are based is admittedly poor. The aforementioned management algorithms do not address every possible clinical scenario, and consequently, it is imperative to tailor surveillance and treatment to the individual patient.…”

Section: Current Guidelines For Surveillance and Management Of Patienmentioning

confidence: 99%

Early Detection of Pancreatic Cancer: Opportunities and Challenges

et al. 2019

Self Cite

View full text Add to dashboard Cite

Most patients with pancreatic ductal adenocarcinoma (PDAC) present with symptomatic, surgically unresectable disease. Although the goal of early detection of PDAC is laudable and likely to result in significant improvement in overall survival, the relatively low prevalence of PDAC renders general population screening infeasible. The challenges of early detection include identification of atrisk individuals in the general population who would benefit from longitudinal surveillance programs and appropriate biomarker and imaging-based modalities used for PDAC surveillance in such cohorts. In recent years, various subgroups at higher-than-average risk for PDAC have been identified, including those with familial risk due to germline mutations, a history of pancreatitis, patients with mucinous pancreatic cysts, and elderly patients with new-onset diabetes. The last 2 categories are discussed at length in terms of the opportunities and challenges they present for PDAC early detection. We also discuss current and emerging imaging modalities that are critical to identifying early, potentially curable PDAC in high-risk cohorts on surveillance.

show abstract

Section: Current Guidelines For Surveillance and Management Of Patienmentioning

confidence: 99%

Early Detection of Pancreatic Cancer: Opportunities and Challenges

et al. 2019

Self Cite

View full text Add to dashboard Cite

show abstract

“…In fact, total deaths due to PDAC are projected to rise to become the second leading cause of cancer-related deaths before 2030 [3]. Consequently, research efforts are increasingly focusing on prevention and interception, a novel concept, which encompasses halting transformed cells from becoming malignant [4][5][6][7][8]. The identification of modifiable risk factors and a better understanding of the molecular mechanisms of PDAC promotion will clearly guide the discovery of novel targets and agents for prevention.…”

Section: Importance Of Kras Mutations In Pancreatic Cancermentioning

confidence: 99%

KRAS, YAP, and obesity in pancreatic cancer: A signaling network with multiple loops

Eibl

Rozengurt

2019

Seminars in Cancer Biology

View full text Add to dashboard Cite

Pancreatic ductal adenocarcinoma (PDAC) continues to be a lethal disease with no efficacious treatment modalities. The incidence of PDAC is expected to increase, at least partially because of the obesity epidemic. Increased efforts to prevent or intercept this disease are clearly needed. Mutations in KRAS are initiating events in pancreatic carcinogenesis supported by genetically engineered mouse models of the disease. However, oncogenic KRAS is not entirely sufficient for the development of fully invasive PDAC. Additional genetic mutations and/or environmental, nutritional, and metabolic stressors, e.g. inflammation and obesity, are required for efficient PDAC formation with activation of KRAS downstream effectors. Multiple factors "upstream" of KRAS associated with obesity, including insulin resistance, inflammation, changes in gut microbiota and GI peptides, can enhance/modulate downstream signals. Multiple signaling networks and feedback loops "downstream" of KRAS have been described that respond to obesogenic diets. We propose that KRAS mutations potentiate a signaling network that is promoted by environmental factors. Specifically, we envisage that KRAS mutations increase the intensity and duration of the growth-promoting signaling network. As the transcriptional activator YAP plays a critical role in the network, we conclude that the rationale for targeting the network (at different points), e.g. with FDA approved drugs such as statins and metformin, is therefore compelling.

show abstract

“…The incidence of pancreatic cancer (PC) has been increasing rapidly in recent years, and it is currently the fourth leading cause of cancer deaths for both men and women [ 1 , 2 ]. Most of PCs are pancreatic ductal adenocarcinomas (PDAC), which is characterized by a late presentation.…”

Section: Introductionmentioning

confidence: 99%

ENO1 Overexpression in Pancreatic Cancer Patients and Its Clinical and Diagnostic Significance

Yin

Wang

Liu

2018

Gastroenterology Research and Practice

View full text Add to dashboard Cite

We investigated in this study the expression of ENO1 in tissues and plasma of PDAC patients to evaluate its clinicopathological and diagnostic significance. ENO1 protein expression was detected in tissue microarray of human PDAC and adjacent noncancer tissues. Electrochemiluminescence immunoassay and amplified luminescent proximity homogeneous assay (AlphaLISA) were performed to measure CA19-9 and ENO1 concentration in plasma from PDAC patients and healthy controls. We demonstrated that ENO1 overexpression is positively correlated with clinical stage, lymph node metastasis, and poor prognosis of PDAC; ENO1 may function as a hopeful candidate diagnostic marker in combination with CA19-9 in PDAC diagnosis.

show abstract

Pancreatic Cancer Chemoprevention Translational Workshop

Cited by 23 publications

References 108 publications

Early Detection of Pancreatic Cancer: Opportunities and Challenges

Early Detection of Pancreatic Cancer: Opportunities and Challenges

KRAS, YAP, and obesity in pancreatic cancer: A signaling network with multiple loops

ENO1 Overexpression in Pancreatic Cancer Patients and Its Clinical and Diagnostic Significance

Contact Info

Product

Resources

About