Expression of functional Y1 receptors for neuropeptide Y in human Ewing's sarcoma cell lines

1992 ◽  
Vol 118 (7) ◽  
pp. 529-536 ◽  
Author(s):  
F. van Valen ◽  
W. Winkelmann ◽  
H. Jürgens

2007 ◽  
Vol 103 (4) ◽  
pp. 1344-1354 ◽  
Author(s):  
Cristina Zanini ◽  
Giuliana Giribaldi ◽  
Giorgia Mandili ◽  
Franco Carta ◽  
Nicoletta Crescenzio ◽  
...  


Pharmaceutics ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 1553
Author(s):  
Ellie Esfandiari Nazzaro ◽  
Fahad Y. Sabei ◽  
Walter K. Vogel ◽  
Mohamad Nazari ◽  
Katelyn S. Nicholson ◽  
...  

Ewing’s sarcoma, characterized by pathognomonic t (11; 22) (q24; q12) and related chromosomal ETS family translocations, is a rare aggressive cancer of bone and soft tissue. Current protocols that include cytotoxic chemotherapeutic agents effectively treat localized disease; however, these aggressive therapies may result in treatment-related morbidities including second-site cancers in survivors. Moreover, the five-year survival rate in patients with relapsed, recurrent, or metastatic disease is less than 30%, despite intensive therapy with these cytotoxic agents. By using high-throughput phenotypic screening of small molecule libraries, we identified a previously uncharacterized compound (ML111) that inhibited in vitro proliferation of six established Ewing’s sarcoma cell lines with nanomolar potency. Proteomic studies show that ML111 treatment induced prometaphase arrest followed by rapid caspase-dependent apoptotic cell death in Ewing’s sarcoma cell lines. ML111, delivered via methoxypoly(ethylene glycol)-polycaprolactone copolymer nanoparticles, induced dose-dependent inhibition of Ewing’s sarcoma tumor growth in a murine xenograft model and invoked prometaphase arrest in vivo, consistent with in vitro data. These results suggest that ML111 represents a promising new drug lead for further preclinical studies and is a potential clinical development for the treatment of Ewing’s sarcoma.



2014 ◽  
Author(s):  
TABREZ A. MOHAMMAD ◽  
Aparna Gorthi ◽  
Andrew Robles ◽  
Xavier Bernard ◽  
Tzu-hung Hsiao ◽  
...  


1999 ◽  
Vol 91 (19) ◽  
pp. 1678-1684 ◽  
Author(s):  
N. Mitsiades ◽  
V. Poulaki ◽  
A. Leone ◽  
M. Tsokos


2015 ◽  
Vol 12 (3) ◽  
pp. 3359-3364 ◽  
Author(s):  
WEIHUA LI ◽  
YUXIA LI ◽  
JIANKUO GUO ◽  
HUAGANG PAN ◽  
YONGLE ZHANG ◽  
...  


2014 ◽  
Vol 33 (3) ◽  
pp. 136-147 ◽  
Author(s):  
Zhongzu Zhang ◽  
Lu Huang ◽  
Zhiming Yu ◽  
Xiang Chen ◽  
Dong Yang ◽  
...  


Oncogene ◽  
2001 ◽  
Vol 20 (8) ◽  
pp. 1010-1014 ◽  
Author(s):  
Arvind Kumar ◽  
Alan Jasmin ◽  
Michael T Eby ◽  
Preet M Chaudhary


1995 ◽  
Vol 63 (5) ◽  
pp. 738-743 ◽  
Author(s):  
A. Pagani ◽  
R. Fischer-Colbrie ◽  
U. Eder ◽  
A. Pellin ◽  
A. Llombart-Bosch ◽  
...  


2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Mary Depner ◽  
Daniel Namazi ◽  
Anne Kruchten


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
John P Vanden Heuvel ◽  
Ewa Maddox ◽  
Samar W Maalouf ◽  
Elizabeth Iorns ◽  
Rachel Tsui ◽  
...  

In 2016, as part of the Reproducibility Project: Cancer Biology, we published a Registered Report (Vanden Heuvel et al., 2016), that described how we intended to replicate selected experiments from the paper ‘Systematic identification of genomic markers of drug sensitivity in cancer cells’ (Garnett et al., 2012). Here we report the results. We found Ewing’s sarcoma cell lines, overall, were more sensitive to the PARP inhibitor olaparib than osteosarcoma cell lines; however, while the effect was in the same direction as the original study (Figure 4C; Garnett et al., 2012), it was not statistically significant. Further, mouse mesenchymal cells transformed with either the EWS-FLI1 or FUS-CHOP rearrangement displayed similar sensitivities to olaparib, whereas the Ewing’s sarcoma cell line SK-N-MC had increased olaparib sensitivity. In the original study, mouse mesenchymal cells transformed with the EWS-FLI1 rearrangement and SK-N-MC cells were found to have similar sensitivities to olaparib, whereas mesenchymal cells transformed with the FUS-CHOP rearrangement displayed a reduced sensitivity to olaparib (Figure 4E; Garnett et al., 2012). We also studied another Ewing’s sarcoma cell line, A673: A673 cells depleted of EWS-FLI1 or a negative control both displayed similar sensitivities to olaparib, whereas the original study reported a decreased sensitivity to olaparib when EWS-FLI1 was depleted (Figure 4F; Garnett et al., 2012). Differences between the original study and this replication attempt, such as the use of different sarcoma cell lines and level of knockdown efficiency, are factors that might have influenced the outcomes. Finally, where possible, we report meta-analyses for each result.



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