Results 161 to 170 of about 13,696,974 (396)
Effective therapeutic targeting of CTNNB1‐mutant hepatoblastoma with WNTinib
Molecular Oncology, EarlyView.WNTinib, a Wnt/CTNNB1 inhibitor, was tested in hepatoblastoma (HB) experimental models. It delayed tumor growth and improved survival in CTNNB1‐mutant in vivo models. In organoids, WNTinib outperformed cisplatin and showed enhanced efficacy in combination therapy, supporting its potential as a targeted treatment for CTNNB1‐mutated HB.
Ugne Balaseviciute +17 more
wiley +1 more source
Strategies for Achieving Diversity through Medical School Admissions
Journal of health care for the poor and underserved, 2018 Q. Capers, Leon McDougle, D. Clinchot
semanticscholar +1 more source
Molecular Oncology, EarlyView.The cancer problem is increasing globally with projections up to the year 2050 showing unfavourable outcomes in terms of incidence and cancer‐related deaths. The main challenges are prevention, improved therapeutics resulting in increased cure rates and enhanced health‐related quality of life.
Ulrik Ringborg +43 more
wiley +1 more source
Advances in Medical Education and Practice, 2019 Uchenna Ekwochi,1 DI Chidiebere Osuorah,2 Samuel A Ohayi,1 Anthony C Nevo,1 Ikenna K Ndu,1 Stanley K Onah31College of Medicine, Enugu State University of Science and Technology, Enugu, Enugu State, Nigeria; 2Child Survival Unit, Medical Research Council,
Ekwochi U +5 more
doaj
Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition
Molecular Oncology, EarlyView.We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li +10 more
wiley +1 more source
Molecular Oncology, EarlyView.We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala +15 more
wiley +1 more source