scholarly journals A novel therapeutic opportunity for the most aggressive sub‐type of pancreatic cancer: Targeting keratin 17 dependency on nuclear export

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Ji Dong (Karen) Bai ◽  
Cindy V. Leiton ◽  
Chun-Hao Pan ◽  
Luisa Escobar-Hoyos ◽  
Kenneth R. Shroyer
2017 ◽  
Vol 17 (1) ◽  
pp. 183-195 ◽  
Author(s):  
Osamu Shimomura ◽  
Tatsuya Oda ◽  
Hiroaki Tateno ◽  
Yusuke Ozawa ◽  
Sota Kimura ◽  
...  

2019 ◽  
Author(s):  
Cindy V. Leiton ◽  
Chun-Hao Pan ◽  
Ji Dong Bai ◽  
Lucia Roa-Peña ◽  
Sruthi Babu ◽  
...  

2015 ◽  
Vol 15 (7) ◽  
pp. 575-592 ◽  
Author(s):  
Chuanwen Lu ◽  
Jose Figueroa ◽  
Zhongwei Liu ◽  
Venu Konala ◽  
Amardeep Aulakh ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1781
Author(s):  
Gustavo A. Arias-Pinilla ◽  
Helmout Modjtahedi

Pancreatic cancer remains as one of the most aggressive cancer types. In the absence of reliable biomarkers for its early detection and more effective therapeutic interventions, pancreatic cancer is projected to become the second leading cause of cancer death in the Western world in the next decade. Therefore, it is essential to discover novel therapeutic targets and to develop more effective and pancreatic cancer-specific therapeutic agents. To date, 45 monoclonal antibodies (mAbs) have been approved for the treatment of patients with a wide range of cancers; however, none has yet been approved for pancreatic cancer. In this comprehensive review, we discuss the FDA approved anticancer mAb-based drugs, the results of preclinical studies and clinical trials with mAbs in pancreatic cancer and the factors contributing to the poor response to antibody therapy (e.g. tumour heterogeneity, desmoplastic stroma). MAb technology is an excellent tool for studying the complex biology of pancreatic cancer, to discover novel therapeutic targets and to develop various forms of antibody-based therapeutic agents and companion diagnostic tests for the selection of patients who are more likely to benefit from such therapy. These should result in the approval and routine use of antibody-based agents for the treatment of pancreatic cancer patients in the future.


2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Ryan R Kawalerski ◽  
Lucia Roa‐Peña ◽  
Taryn Boyle ◽  
Cindy V Leiton ◽  
Natasha T Snider ◽  
...  
Keyword(s):  

2019 ◽  
Author(s):  
Anthony J. Covarrubias ◽  
Abhijit Kale ◽  
Rosalba Perrone ◽  
Jose Alberto Lopez-Dominguez ◽  
Angela Oliveira Pisco ◽  
...  

SummaryDecline in tissue NAD levels during aging is linked to aging and its associated diseases. However, the mechanism for aging-associated NAD decline remains unclear. Here we report that pro-inflammatory M1-like macrophages, but not naïve or M2 macrophages, accumulate in metabolic tissues including visceral white adipose tissue and the liver during aging. Remarkably, these M1-like macrophages highly express the NAD consuming enzyme CD38 and have enhanced CD38-dependent NADase activity. We also find that senescent cells progressively accumulate in visceral white adipose tissue during aging and that inflammatory cytokines found in the supernatant from senescent cells (Senescence associated secretory proteins, SASP) induce macrophages to proliferate and to express CD38. These results highlight a new causal link between visceral tissue senescence and tissue NAD decline during aging and represent a novel therapeutic opportunity targeting maintenance of NAD levels during aging.


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