add some PMCIDs

@article{gongExpressionClinicalValue2021,

title = {Expression and {{Clinical Value}} of {{Eukaryotic Translation Elongation Factor 1A1}} ({{EEF1A1}}) in {{Diffuse Large B Cell Lymphoma}}},

author = {Gong, Tiejun and Shuang, Yuerong},

journaltitle = {International Journal of General Medicine},

shortjournal = {Int J Gen Med},

volume = {14},

@article{gongSequentialInverseDysregulation2021,

title = {Sequential Inverse Dysregulation of the {{RNA}} Helicases {{DDX3X}} and {{DDX3Y}} Facilitates {{MYC-driven}} Lymphomagenesis},

author = {Gong, Chun and Krupka, Joanna A. and Gao, Jie and Grigoropoulos, Nicholas F. and Giotopoulos, George and Asby, Ryan and Screen, Michael and Usheva, Zelvera and Cucco, Francesco and Barrans, Sharon and Painter, Daniel and Zaini, Nurmahirah Binte Mohammed and Haupl, Björn and Bornelöv, Susanne and Ruiz De Los Mozos, Igor and Meng, Wei and Zhou, Peixun and Blain, Alex E. and Forde, Sorcha and Matthews, Jamie and Khim Tan, Michelle Guet and Burke, G. A. Amos and Sze, Siu Kwan and Beer, Philip and Burton, Cathy and Campbell, Peter and Rand, Vikki and Turner, Suzanne D. and Ule, Jernej and Roman, Eve and Tooze, Reuben and Oellerich, Thomas and Huntly, Brian J. and Turner, Martin and Du, Ming-Qing and Samarajiwa, Shamith A. and Hodson, Daniel J.},

journaltitle = {Molecular Cell},

shortjournal = {Molecular Cell},

issn = {1097-2765},

doi = {10.1016/j.molcel.2021.07.041},

abstract = {DDX3X is a ubiquitously expressed RNA helicase involved in multiple stages of RNA biogenesis. DDX3X is frequently mutated in Burkitt lymphoma, but the functional basis for this is unknown. Here, we show that loss-of-function DDX3X mutations are also enriched in MYC-translocated diffuse large B cell lymphoma and reveal functional cooperation between mutant DDX3X and MYC. DDX3X promotes the translation of mRNA encoding components of the core translational machinery, thereby driving global protein synthesis. Loss-of-function DDX3X mutations moderate MYC-driven global protein synthesis, thereby buffering MYC-induced proteotoxic stress during early lymphomagenesis. Established lymphoma cells restore full protein synthetic capacity by aberrant expression of DDX3Y, a Y chromosome homolog, the expression of which is normally restricted to the testis. These findings show that DDX3X loss of function can buffer MYC-driven proteotoxic stress and highlight the capacity of male B cell lymphomas to then compensate for this loss by ectopic DDX3Y expression.},

langid = {english},

keywords = {Burkitt lymphoma,DDX3X,germinal center,MYC,proteotoxic stress,RNA helicase,translation}