scholarly journals Integrin alpha 2 (Itga2), CD49b, is differentially expressed in pancreatic ductal adenocarcinoma.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
United States ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cell Adhesion Molecule ◽  
Pancreatic Tumor ◽  
The United States ◽  
Pancreatic Tissue ◽  
Ductal Adenocarcinoma ◽  
Novel Therapies ◽  
Tissue Of Origin ◽  
Level Analysis

Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of death from cancer in the United States (1, 2). Novel therapies are required to extend survival in PDAC and systems-level analysis of the tumors transcriptome as compared to the tissue of origin can reveal the basic transcriptional nature of tumors and how they differ from the tissue in which they reside and from which they originate (3). In this study, we compared the transcriptome of PDAC tumors isolated from patients with PDAC as compared to healthy, non-affected pancreatic tissue using two separate datasets (4, 5). We found that the cell adhesion molecule integrin alpha 2 (Itga2), also known as CD49b, was among the genes whose expression was most significantly different between PDAC and the benign pancreas. Itga2 expression was significantly higher in PDAC tumors compared to non-affected pancreatic tissue. Pancreatic ductal adenocarcinomas increase the expression of Itga2 during the transition from benign pancreatic tissue to transformed pancreatic tumor.

Temporal trends of pancreatic ductal adenocarcinoma in young adults in the United States: A Population-Based Study

2020 ◽  
Vol 44 (2) ◽  
pp. 204-210
Author(s):  
Mohamed M. Gad ◽  
Anas M. Saad ◽  
Muneer J. Al-Husseini ◽  
Youssef M. Abdel-Gawad ◽  
Obai M. Alsalhani ◽  
...  
Keyword(s):  
United States ◽  
Young Adults ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Temporal Trends ◽  
The United States ◽  
Population Based ◽  
Ductal Adenocarcinoma ◽  
Population Based Study

scholarly journals Trends in the Incidence of Pancreatic Adenocarcinoma in All 50 United States Examined Through an Age-Period-Cohort Analysis

2020 ◽  
Vol 4 (4) ◽  
Author(s):  
Wilson L da Costa ◽  
Abiodun O Oluyomi ◽  
Aaron P Thrift
Keyword(s):  
United States ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Cohort Analysis ◽  
The United States ◽  
Incidence Rates ◽  
Ductal Adenocarcinoma ◽  
Birth Cohorts ◽  
Men And Women ◽  
Cancer Statistics ◽  
Incidence Trends

Abstract Background Pancreatic ductal adenocarcinoma is a major contributor to cancer-related mortality in the United States. We aimed to investigate trends in incidence rates from all 50 states from 2001 to 2016, overall and by race, sex, and state and using age-period-cohort analyses. Methods Age-adjusted incidence rates and trends in adults aged 35 years and older were calculated using data from the US Cancer Statistics registry. We used joinpoint regression to compute annual percent changes (APC) and average annual percent changes. We also analyzed incidence trends by age groups and birth cohorts through age-period-cohort modeling. Results Age-standardized incidence rates increased by 1.23% (95% confidence interval [CI] = 0.92% to 1.54%) annually between 2001 and 2008 but were stable between 2008 and 2016 (APC = 0.11%, 95% CI = -0.13% to 0.35%). APCs and inflection points were no different for men and women. Rates increased statistically significantly among non-Hispanic whites (NHW) and non-Hispanic blacks between 2001 and 2007 and between 2001 and 2008, respectively, but, in later years, rates increased slowly among NHWs (APC = 0.36%, 95% CI = 0.12% to 0.60%), and were stable among non-Hispanic blacks (APC = -0.40%, 95% CI = -0.89% to 0.10%). The number of states with age-standardized incidence rates no less than 20.4 per 100 000 increased from 16 in 2001–2003 to 40 by 2015–2016. We found a strong birth cohort effect in both men and women and increasing rates among successive birth cohorts of NHWs. Conclusions The incidence of pancreatic ductal adenocarcinoma has consistently increased in the United States, albeit at slower rates recently. We observed notable increases among NHWs and in some states in the central and southern part of the country.

scholarly journals Novel Use of Hypoxia-Inducible Polymerizable Protein to Augment Chemotherapy for Pancreatic Cancer

Pharmaceutics ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 128
Author(s):  
Andrew Gdowski ◽  
Hamed Hayatshahi ◽  
Rafal Fudala ◽  
Rohan Joshi ◽  
Jin Liu ◽  
...  
Keyword(s):  
Small Molecule ◽  
Pancreatic Tumor ◽  
Direct Injection ◽  
Locally Advanced ◽  
Tumor Stroma ◽  
The United States ◽  
Pancreatic Tissue ◽  
Tumor Xenograft ◽  
Ductal Adenocarcinoma

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies and is the fourth leading cause of cancer-related deaths in the United States. Unfortunately, 80–85% of patients are diagnosed with unresectable, advanced stage tumors. These tumors are incurable and result in a median survival less than approximately six months and an overall 5-year survival rate of less than 7%. Whilst chemotherapy is a critical treatment, cure is not possible without surgical resection. The poor clinical outcomes in PDAC can be partially attributed to its dense desmoplastic stroma, taking up roughly 80% of the tumor mass. The stroma surrounding the tumor disrupts the normal architecture of pancreatic tissue leading to poor vascularization, high intratumoral pressure along with hypoxia and an acidic tumor microenvironment. This complicated microenvironment presents a significant challenge for drug delivery. The current manuscript discusses a novel approach to overcome many of these various obstacles. A complex of gemcitabine (GEM) and hemoglobin S (HbS) was formulated, which self-polymerizes under hypoxic and acidic conditions. When polymerized, HbS has the potential to break the tumor stroma, decrease intratumoral pressure, and therefore improve the treatment efficacy of standard therapy. Intratumoral injection of HbS with a fluorescent small molecule surrogate for GEM into a pancreatic tumor xenograft resulted in improved dissemination of the small molecule throughout the pancreatic tumor. The self-polymerization of HbS + GEM was significantly more effective than either agent individually at decreasing tumor size in an in vivo PDAC mouse model. These findings would suggest a clinical benefit from delivering the complex of GEM and HbS via direct injection by endoscopic ultrasound (EUS). With such a treatment option, patients with locally advanced disease would have the potential to become surgical candidates, offering them a chance for cure.

scholarly journals Tumor-derived exosomal long noncoding RNA LINC01133, regulated by Periostin, contributes to pancreatic ductal adenocarcinoma epithelial-mesenchymal transition through the Wnt/β-catenin pathway by silencing AXIN2

Oncogene ◽  
2021 ◽  
Vol 40 (17) ◽  
pp. 3164-3179
Author(s):  
Yang Liu ◽  
Tianchi Tang ◽  
Xiaosheng Yang ◽  
Peng Qin ◽  
Pusen Wang ◽  
...  
Keyword(s):  
Pancreatic Ductal Adenocarcinoma ◽  
Noncoding Rna ◽  
Pancreatic Tumor ◽  
Epithelial Mesenchymal Transition ◽  
Noncoding Rnas ◽  
Ductal Adenocarcinoma ◽  
Overall Survival Rate ◽  
Poor Overall Survival ◽  
Mesenchymal Transition ◽  
Pancreatic Cancer Cells

AbstractPancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignancies and rapidly progressive diseases. Exosomes and long noncoding RNAs (lncRNAs) are emerging as vital mediators in tumor cells and their microenvironment. However, the detailed roles and mechanisms of exosomal lncRNAs in PDAC progression remain unknown. Here, we aimed to clarify the clinical significance and mechanisms of exosomal lncRNA 01133 (LINC01133) in PDAC. We analyzed the expression of LINC01133 in PDAC and found that exosomal LINC01133 expression was high and positively correlated with higher TNM stage and poor overall survival rate of PDAC patients. Further research demonstrated that Periostin could increase exosome secretion and then enhance LINC01133 expression. In addition, Periostin increased p-EGFR, p-Erk, and c-myc expression, and c-myc could bind to the LINC01133 promoter region. These findings suggested that LINC01133 can be regulated by Periostin via EGFR pathway activity. We also observed that LINC01133 promoted the proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of pancreatic cancer cells. We subsequently evaluated the effect of LINC01133 on the Wnt/β-catenin pathway and confirmed that LINC01133 can interact with Enhancer Of Zeste Homolog 2 (EZH2) and then promote H3K27 trimethylation. This can further silence AXIN2 and suppress GSK3 activity, ultimately activating β-catenin. Collectively, these data indicate that exosomal LINC01133 plays an important role in pancreatic tumor progression, and targeting LINC01133 may provide a potential treatment strategy for PDAC.

Biodefense and Emergency Use Authorization: Different Originations, Purposes, and Evolutionary Paths of Institutions in the United States and South Korea

2022 ◽  
Author(s):  
HyunJung Kim
Keyword(s):  
Public Health ◽  
United States ◽  
South Korea ◽  
Driving Forces ◽  
The United States ◽  
Lessons Learned ◽  
Post Exposure Prophylaxis ◽  
Meso Level ◽  
Public Health Emergencies ◽  
Level Analysis

Abstract Background: Historical institutionalism (HI) determines that institutions have been transformed by a pattern of punctuated evolution due to exogenous shocks. Although scholars frequently emphasize the role of agency - endogenous factors – when it comes to institutional changes, but the HI analytic narratives still remain in the meso-level analysis in the context of structure and agency. This article provides domestic and policy-level accounts of where biodefense institutions of the United States and South Korea come from, seeing through emergency-use-authorization (EUA) policy, and how the EUA policies have evolved by employing the policy-learning concepts through the Event-related Policy Change Model. Results: By employing the Birkland’s model, this article complements the limitation of the meso-level analysis in addressing that the 2001 Amerithrax and the 2015 Middle East Respiratory Syndrome (MERS) outbreak rooted originations and purposes of the biodefense respectively. Since the crisis, a new post-crisis agenda in society contributed to establishing new domestic coalition, which begin to act as endogenous driving forces that institutionalize new biodefense institutions and even reinforce them through path dependent way when the institutions evolved. Therefore, EUA policy cores (Post-Exposure Prophylaxis (PEP) in the United States and Non-Pharmaceutical Intervention (NPI) in South Korea keep strengthened during the policy revisions. Conclusions: The United States and South Korea have different originations and purposes of biodefense, which are institutions evolving through self-reinforce dependent way based on the lessons learned from past crises. In sum, under the homeland security biodefense institution, the US EUA focuses on the development of specialized, unlicensed PEP in response to public health emergencies; on the other hand, under the disease containment-centric biodefense institution, the Korean EUA is specialized to conduct NPI missions in response to public health emergencies.

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