AB079. P051. Blockage of CTR1-dependent copper absorption increases autophagy to resist apoptosis of pancreatic ductal carcinoma cells

2018 ◽  
Vol 1 (1) ◽  
pp. AB079-AB079
Author(s):  
Sheng Tai ◽  
Chun-Bo Teng
2003 ◽  
Vol 24 (24) ◽  
pp. 4291-4303 ◽  
Author(s):  
Daniela Cecconi ◽  
Hubert Astner ◽  
Massimo Donadelli ◽  
Marta Palmieri ◽  
Edoardo Missiaglia ◽  
...  

2019 ◽  
Vol 17 (9) ◽  
pp. 1815-1827 ◽  
Author(s):  
Erika Parasido ◽  
George S. Avetian ◽  
Aisha Naeem ◽  
Garrett Graham ◽  
Michael Pishvaian ◽  
...  

2005 ◽  
Vol 4 (6) ◽  
pp. 1909-1916 ◽  
Author(s):  
Daniela Cecconi ◽  
Massimo Donadelli ◽  
Aldo Scarpa ◽  
Alberto Milli ◽  
Marta Palmieri ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 3085
Author(s):  
Louay Bettaieb ◽  
Maxime Brulé ◽  
Axel Chomy ◽  
Mel Diedro ◽  
Malory Fruit ◽  
...  

Pancreatic cancer (PC) is a major cause of cancer-associated mortality in Western countries (and estimated to be the second cause of cancer deaths by 2030). The main form of PC is pancreatic adenocarcinoma, which is the fourth most common cause of cancer-related death, and this situation has remained virtually unchanged for several decades. Pancreatic ductal adenocarcinoma (PDAC) is inherently linked to the unique physiology and microenvironment of the exocrine pancreas, such as pH, mechanical stress, and hypoxia. Of them, calcium (Ca2+) signals, being pivotal molecular devices in sensing and integrating signals from the microenvironment, are emerging to be particularly relevant in cancer. Mutations or aberrant expression of key proteins that control Ca2+ levels can cause deregulation of Ca2+-dependent effectors that control signaling pathways determining the cells’ behavior in a way that promotes pathophysiological cancer hallmarks, such as enhanced proliferation, survival and invasion. So far, it is essentially unknown how the cancer-associated Ca2+ signaling is regulated within the characteristic landscape of PDAC. This work provides a complete overview of the Ca2+ signaling and its main players in PDAC. Special consideration is given to the Ca2+ signaling as a potential target in PDAC treatment and its role in drug resistance.


Oncotarget ◽  
2017 ◽  
Vol 8 (22) ◽  
pp. 35835-35847 ◽  
Author(s):  
Rekha Khandia ◽  
Bramhadev Pattnaik ◽  
Katherukamem Rajukumar ◽  
Atul Pateriya ◽  
Sandeep Bhatia ◽  
...  

2016 ◽  
Vol 22 (3) ◽  
pp. 198 ◽  
Author(s):  
Toshiyuki Uekitani ◽  
Seiji Kaino ◽  
Hirofumi Harima ◽  
Shigeyuki Suenaga ◽  
Manabu Sen-yo ◽  
...  

Author(s):  
Gia-Buu Tran

Breast cancer is the neoplastic disease which is characterized by unregulated ductal and lobular hyperplasia. Some herbal remedies have been researched and proved the inhibitory effect on breast cancer such as, Crilin-extracted from Cirnum latifolum and curcumin-isolated from Cucuma longa. However, the synergistic effect of crilin and nanocurcumin have not been studied yet. In this study, we established the mouse model of breast cancer induced by DMBA and evaluated the effectiveness of combination of crilin and nanocurcumin on treatment of breast cancer. After 12 weeks, co-administration of crilin and nanocurcumin inversed alteration of body weight, the number of erythrocytes and leukocytes induced by DMBA. Furthermore, the synergistic effect of crilin and nanocucumin on reduction of tumor volume was proven. Histological analysis revealed that co-administration of crilin and nanocurcumin inhibited invasion of mammary ductal carcinoma cells into surrounding tissue, recovered lobular cells structure, and diminished leukocyte composition. Thereby, the combination of crilin and nanocurcumin recovers immune system and prevent the development of breast cancer.


Author(s):  
Shree Harsha Vijaya Chandra ◽  
Ramasamy Srinivas ◽  
Thomas L. Dawson ◽  
John E. Common

The skin microbial community is a multifunctional ecosystem aiding prevention of infections from transient pathogens, maintenance of host immune homeostasis, and skin health. A better understanding of the complex milieu of microbe-microbe and host-microbe interactions will be required to define the ecosystem’s optimal function and enable rational design of microbiome targeted interventions. Malassezia, a fungal genus currently comprising 18 species and numerous functionally distinct strains, are lipid-dependent basidiomycetous yeasts and integral components of the skin microbiome. The high proportion of Malassezia in the skin microbiome makes understanding their role in healthy and diseased skin crucial to development of functional skin health knowledge and understanding of normal, healthy skin homeostasis. Over the last decade, new tools for Malassezia culture, detection, and genetic manipulation have revealed not only the ubiquity of Malassezia on skin but new pathogenic roles in seborrheic dermatitis, psoriasis, Crohn’s disease, and pancreatic ductal carcinoma. Application of these tools continues to peel back the layers of Malassezia/skin interactions, including clear examples of pathogenicity, commensalism, and potential protective or beneficial activities creating mutualism. Our increased understanding of host- and microbe-specific interactions should lead to identification of key factors that maintain skin in a state of healthy mutualism or, in turn, initiate pathogenic changes. These approaches are leading toward development of new therapeutic targets and treatment options. This review discusses recent developments that have expanded our understanding of Malassezia’s role in the skin microbiome, with a focus on its multiple roles in health and disease as commensal, pathogen, and protector.


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