scholarly journals The Role of Intracellular Signaling Pathways in the Pathogenesis of Multiple Myeloma and Novel Therapeutic Approaches

2016 ◽  
Vol 56 (1) ◽  
pp. 20-27 ◽  
Author(s):  
Masahiro Kizaki ◽  
Takayuki Tabayashi
2017 ◽  
Vol 59 (4) ◽  
pp. R141-R154 ◽  
Author(s):  
Marika H Tesselaar ◽  
Johannes W Smit ◽  
James Nagarajah ◽  
Romana T Netea-Maier ◽  
Theo S Plantinga

While in most patients with non-medullary thyroid cancer (TC), disease remission is achieved by thyroidectomy and ablation of tumor remnants by radioactive iodide (RAI), a substantial subgroup of patients with metastatic disease present tumor lesions that have acquired RAI resistance as a result of dedifferentiation. Although oncogenic mutations inBRAF,TERTpromoter andTP53are associated with an increased propensity for induction of dedifferentiation, the role of genetic and epigenetic aberrations and their effects on important intracellular signaling pathways is not yet fully elucidated. Also immune, metabolic, stemness and microRNA pathways have emerged as important determinants of TC dedifferentiation and RAI resistance. These signaling pathways have major clinical implications since their targeting could inhibit TC progression and could enable redifferentiation to restore RAI sensitivity. In this review, we discuss the current insights into the pathological processes conferring dedifferentiation and RAI resistance in TC and elaborate on novel advances in diagnostics and therapy to improve the clinical outcome of RAI-refractory TC patients.


2012 ◽  
Vol 7 (2) ◽  
pp. 104-110 ◽  
Author(s):  
Fabrizio Montecucco ◽  
Vincent Braunersreuther ◽  
Giorgio Luciano Viviani ◽  
Sébastien Lenglet ◽  
François Mach

2011 ◽  
Vol 300 (3) ◽  
pp. E500-E507 ◽  
Author(s):  
Tao Hong ◽  
Jie Ning ◽  
Xuefeng Yang ◽  
Hui-Yu Liu ◽  
Jianmin Han ◽  
...  

It has previously been known that transcription of the PGC-1α gene can be either inhibited or stimulated by p38 MAP kinase (p38 MAPK). To determine whether p38 MAPK plays an inhibitory or stimulatory role in PGC-1α gene transcription, we further investigated the role of p38 MAPK in this study. Our results showed that the basal level of p38 MAPK phosphorylation was increased in gastrocnemius of mice under HFD and that p38 MAPK stimulated PGC-1α gene transcription in C2C12 myotubes. Our results also provided new mechanisms in myotubes that the p38 MAPK-induced PGC-1α gene transcription was mediated by CREB. In exploring the role of the Akt-dependent insulin signaling on PGC-1α gene transcription, we found that the basal Akt-dependent signaling was increased in gastrocnemius of mice under HFD. The p38 MAPK-induced PGC-1α gene transcription was prevented by insulin. Insulin suppression of PGC-1α gene transcription was neutralized by overexpression of the constitutively nuclear form of FoxO1. Finally, we located three insulin response elements (IREs) in the PGC-1α promoter, and mutations of these IREs abolish or blunt activity of the PGC-1α promoter. Together, our results show that transcription of the PGC-1α gene is balanced by different intracellular signaling pathways.


Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 818 ◽  
Author(s):  
Tateiwa ◽  
Yoshikawa ◽  
Kaito

Arthritis is inflammation of the joints accompanied by osteochondral destruction. It can take many forms, including osteoarthritis, rheumatoid arthritis, and psoriatic arthritis. These diseases share one commonality—osteochondral destruction based on inflammation. The background includes a close interaction between osseous tissues and immune cells through various inflammatory cytokines. However, the tissues and cytokines that play major roles are different in each disease, and as a result, the mechanism of osteochondral destruction also differs. In recent years, there have been many findings regarding not only extracellular signaling pathways but also intracellular signaling pathways. In particular, we anticipate that the intracellular signals of osteoclasts, which play a central role in bone destruction, will become novel therapeutic targets. In this review, we have summarized the pathology of arthritis and the latest findings on the mechanism of osteochondral destruction, as well as present and future therapeutic strategies for these targets.


2015 ◽  
Vol 3 ◽  
pp. 373-379 ◽  
Author(s):  
Robert Zdanowski ◽  
Małgorzata Krzyżowska ◽  
Dominika Ujazdowska ◽  
Aneta Lewicka ◽  
Sławomir Lewicki

1999 ◽  
Vol 120 (1) ◽  
pp. 51-53 ◽  
Author(s):  
Masahiko Kato ◽  
Hirokazu Kimura ◽  
Atsushi Tachibana ◽  
Youichi Motegi ◽  
Kenichi Tokuyama ◽  
...  

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