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Livia Garavelli Viviana Cordeddu Stefania Errico Patrizia Bertolini Maria Elisabeth Street Simonetta Rosato Marzia Pollazzon Anita Wischmeijer Ivan Ivanovski Paola Daniele Ermanno Bacchini Alfonsa Anna Lombardi Giancarlo Izzi Giacomo Biasucci Carmine Del Rossi Domenico Corradi Giovanni Cazzaniga Carlo Dominici Cesare Rossi Alessandro De Luca Sergio Bernasconi Riccardo Riccardi Eric Legius Marco Tartaglia 《American journal of medical genetics. Part A》2015,167(8):1902-1907
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Valentina E. Schneeberger Yuan Ren Noreen Luetteke Qingling Huang Liwei Chen Harshani R. Lawrence Nicholas J. Lawrence Eric B. Haura John M. Koomen Domenico Coppola Jie Wu 《Oncotarget》2015,6(8):6191-6202
Epidermal growth factor receptor (EGFR) mutants drive lung tumorigenesis and are targeted for therapy. However, resistance to EGFR inhibitors has been observed, in which the mutant EGFR remains active. Thus, it is important to uncover mediators of EGFR mutant-driven lung tumors to develop new treatment strategies. The protein tyrosine phosphatase (PTP) Shp2 mediates EGF signaling. Nevertheless, it is unclear if Shp2 is activated by oncogenic EGFR mutants in lung carcinoma or if inhibiting the Shp2 PTP activity can suppress EGFR mutant-induced lung adenocarcinoma. Here, we generated transgenic mice containing a doxycycline (Dox)-inducible PTP-defective Shp2 mutant (tetO-Shp2CSDA). Using the rat Clara cell secretory protein (CCSP)-rtTA-directed transgene expression in the type II lung pneumocytes of transgenic mice, we found that the Gab1-Shp2 pathway was activated by EGFRL858R in the lungs of transgenic mice. Consistently, the Gab1-Shp2 pathway was activated in human lung adenocarcinoma cells containing mutant EGFR. Importantly, Shp2CSDA inhibited EGFRL858R-induced lung adenocarcinoma in transgenic animals. Analysis of lung tissues showed that Shp2CSDA suppressed Gab1 tyrosine phosphorylation and Gab1-Shp2 association, suggesting that Shp2 modulates a positive feedback loop to regulate its own activity. These results show that inhibition of the Shp2 PTP activity impairs mutant EGFR signaling and suppresses EGFRL858R-driven lung adenocarcinoma. 相似文献
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F Liotta V Querci G Mannelli V Santarlasci L Maggi M Capone M C Rossi A Mazzoni L Cosmi S Romagnani E Maggi O Gallo F Annunziato 《British journal of cancer》2015,112(4):745-754
Background:
Cancer is a multifactorial disease not only restricted to transformed epithelium, but also involving cells of the immune system and cells of mesenchymal origin, particularly mesenchymal stem cells (MSCs). Mesenchymal stem cells contribute to blood- and lymph- neoangiogenesis, generate myofibroblasts, with pro-invasive activity and may suppress anti-tumour immunity.Methods:
In this paper, we evaluated the presence and features of MSCs isolated from human head neck squamous cell carcinoma (HNSCC).Results:
Fresh specimens of HNSCC showed higher proportions of CD90+ cells compared with normal tissue; these cells co-expressed CD29, CD105, and CD73, but not CD31, CD45, CD133, and human epithelial antigen similarly to bone marrow-derived MSCs (BM-MSCs). Adherent stromal cells isolated from tumour shared also differentiation potential with BM-MSCs, thus we named them as tumour-MSCs. Interestingly, tumour-MSCs showed a clear immunosuppressive activity on in vitro stimulated T lymphocytes, mainly mediated by indoelamine 2,3 dioxygenase activity, like BM-MSCs. To evaluate their possible role in tumour growth in vivo, we correlated tumour-MSC proportions with neoplasm size. Tumour-MSCs frequency directly correlated with tumour volume and inversely with the frequency of tumour-infiltrating leukocytes.Conclusions:
These data support the concept that tumour-MSCs may favour tumour growth not only through their effect on stromal development, but also by inhibiting the anti-tumour immune response. 相似文献88.
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Off‐label use of nicardipine as tocolytic and acute pulmonary oedema: a post‐marketing analysis of adverse drug reaction reports in EudraVigilance 下载免费PDF全文