A research article authored by our customers in Southern Medical University in China has been recently published in Clinical Cancer Research. The paper titled “Etk Interaction with PFKFB4 Modulates Chemoresistance of Small-cell Lung Cancer by Regulating Autophagy” demonstrated for the first time the molecular mechanisms underlying endothelial tyrosine kinase (Etk) role in modulating the chemoresistance of small-cell lung cancer (SCLC). By interacting with PFKFB4, a member of the bi-functional PFKFB enzyme family, Etk can regulate autophagy and promote chemoresistance. Therefore, Etk and PFKFB4 are promising biomarkers for the chemotherapy response in SCLC patients. Moreover, these novel modulators are potential candidates to develop clinical strategies to treat SCLC patients. Please see http://clincancerres.aacrjournals.org/content/24/4/950 to read the abstract.
In this paper, a patient-derived xenograft (PDX) model developed with SCLC patient tissue was used to test the synergistic effect of chemotherapy coupled to Ibrutinib, an Etk inhibitor. The results suggested that Ibrutinib suppresses chemoresistance in SCLC and further confirmed Etk's role in promoting chemoresistance. The immune-deficient B-NDG mouse model (previously named “B-NSG”, B-NDG has been used to replace “B-NSG”) was used for the PDX experiments. The B-NDG mouse model (NOD-Prkdcscid IL2rgtm1/Bcgen) was independently designed and generated by Biocytogen. This model has the highest degree of immunodeficiency and longer life span than other immune-deficient models and thus is ideal for PDX experiments. For more information, please see http://www.biocytogen.com/read/23126.html. Please feel free to contact us (email@example.com) if you are interested in this mouse model.
*B-NDG has been used to replace “B-NSG”