| First Author | Mondragón L | Year | 2019 |
| Journal | Cancer Cell | Volume | 36 |
| Issue | 3 | Pages | 268-287.e10 |
| PubMed ID | 31447347 | Mgi Jnum | J:279380 |
| Mgi Id | MGI:6360835 | Doi | 10.1016/j.ccell.2019.07.008 |
| Citation | Mondragon L, et al. (2019) GAPDH Overexpression in the T Cell Lineage Promotes Angioimmunoblastic T Cell Lymphoma through an NF-kappaB-Dependent Mechanism. Cancer Cell 36(3):268-287.e10 |
| abstractText | GAPDH is emerging as a key player in T cell development and function. To investigate the role of GAPDH in T cells, we generated a transgenic mouse model overexpressing GAPDH in the T cell lineage. Aged mice developed a peripheral Tfh-like lymphoma that recapitulated key molecular, pathological, and immunophenotypic features of human angioimmunoblastic T cell lymphoma (AITL). GAPDH induced non-canonical NF-kappaB pathway activation in mouse T cells, which was strongly activated in human AITL. We developed a NIK inhibitor to reveal that targeting the NF-kappaB pathway prolonged AITL-bearing mouse survival alone and in combination with anti-PD-1. These findings suggest the therapeutic potential of targeting NF-kappaB signaling in AITL and provide a model for future AITL therapeutic investigations. |
