primary bone
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2022 ◽  
Vol 42 (2) ◽  
pp. 282-285
Author(s):  
Hongkyung Kim ◽  
Hye Min Kim ◽  
Jin Ju Kim ◽  
Saeam Shin ◽  
Doh Yu Hwang ◽  
...  

Cureus ◽  
2022 ◽  
Author(s):  
Guilherme Cunha ◽  
Martim Alçada ◽  
Ana Mestre ◽  
Marta B Duarte ◽  
Filomena Roque

Cancers ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 330
Author(s):  
Ioannis Gkouveris ◽  
Akrivoula Soundia ◽  
Panagiotis Gouveris ◽  
Dionysia Zouki ◽  
Danny Hadaya ◽  
...  

Antiresorptive agents such as bisphosphonates (BP) and denosumab are commonly prescribed for the management of primary bone malignancy, bone metastasis, osteoporosis, Paget disease, or other bone disorders. Medication-related osteonecrosis of the Jaws (MRONJ) is a rare but significant complication of antiresorptive medications. Duration, dose, and antiresorptive potency as well as concomitant diseases, additional medications, and local factors affect MRONJ incidence and severity. MRONJ pathophysiology is still poorly understood. Nevertheless, decreased bone resorption due to osteoclastic inhibition along with trauma, infection/inflammation, or blood supply inhibition are considered synergistic factors for disease development. In addition, previous data research examined the effects of antiresorptive medication on immune system components and introduced potential alterations on immune response as novel elements in MRONJ pathogenesis. Considering that macrophages are the first cells in the nonspecific immune response, it is not surprising that these multifaceted players attracted increased attention in MRONJ research recently. This current review attempted to elucidate the effects of antiresorptive medications on several aspects of macrophage activity in relation to the complex inflammatory microenvironment of MRONJ. Collectively, unravelling the mode of action and extent of macrophages’ potential contribution in MRONJ occurrence will provide novel insight in disease pathogenesis and potentially identify intrinsic therapeutic targets.


2022 ◽  
Vol 21 (1) ◽  
Author(s):  
Yun Ma ◽  
Guijie Guo ◽  
Tingting Li ◽  
Faxin Wen ◽  
Jianling Yang ◽  
...  

Abstract Background Dysregulation of long noncoding RNAs (lncRNAs) has been linked to various human cancers. Bcr-Abl oncogene that results from a reciprocal translocation between human chromosome 9 and 22, is associated with several hematological malignancies. However, the role of lncRNAs in Bcr-Abl-induced leukemia remains largely unexplored. Methods LncRNA cDNA microarray was employed to identify key lncRNAs involved in Bcr-Abl-mediated cellular transformation. Abl-transformed cell survival and xenografted tumor growth in mice were evaluated to dissect the role of imatinib-upregulated lncRNA 1 (IUR1) in Abl-induced tumorigenesis. Primary bone marrow transformation and in vivo leukemia transplant using lncRNA-IUR1 knockout (KO) mice were further conducted to address the functional relevance of lncRNA-IUR1 in Abl-mediated leukemia. Transcriptome RNA-seq and Western blotting were performed to determine the mechanisms by which lncRNA-IUR1 regulates Bcr-Abl-induced tumorigenesis. Results We identified lncRNA-IUR1 as a critical negative regulator of Bcr-Abl-induced tumorigenesis. LncRNA-IUR1 expressed in a very low level in Bcr-Abl-positive cells from chronic myeloid leukemia patients. Interestingly, it was significantly induced in Abl-positive leukemic cells treated by imatinib. Depletion of lncRNA-IUR1 promoted survival of Abl-transformed human leukemic cells in experiments in vitro and xenografted tumor growth in mice, whereas ectopic expression of lncRNA-IUR1 sensitized the cells to apoptosis and suppressed tumor growth. In concert, silencing murine lncRNA-IUR1 in Abl-transformed cells accelerated cell survival and the development of leukemia in mice. Furthermore, lncRNA-IUR1 deficient mice were generated, and we observed that knockout of murine lncRNA-IUR1 facilitated Bcr-Abl-mediated primary bone marrow transformation. Moreover, animal leukemia model revealed that lncRNA-IUR1 deficiency promoted Abl-transformed cell survival and development of leukemia in mice. Mechanistically, we demonstrated that lncRNA-IUR1 suppressed Bcr-Abl-induced tumorigenesis through negatively regulating STAT5-mediated GATA3 expression. Conclusions These findings unveil an inhibitory role of lncRNA-IUR1 in Abl-mediated cellular transformation, and provide new insights into molecular mechanisms underlying Abl-induced leukemogenesis.


2022 ◽  
pp. 431-445
Author(s):  
Peter Peneder ◽  
Eleni M. Tomazou ◽  
Marcus Tötzl
Keyword(s):  

2022 ◽  
pp. 531-542
Author(s):  
Camila M. Melo ◽  
Jeremy A. Squire

2022 ◽  
pp. 727-753
Author(s):  
Ollivier Luc ◽  
Stéphane Supiot ◽  
Martin Valentine ◽  
Jouglar Emmanuel

2022 ◽  
pp. 285-293
Author(s):  
Julie Talbot ◽  
Maryne Dupuy ◽  
Sarah Morice ◽  
Franck Verrecchia

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