Research
Targeting leukemia metabolism to improve CAR-T responses
50% of relapsed/refractory B-ALL patients will fail CAR-T therapy - however, not all failures can be explained by CAR antigen loss or T cell exhaustion. We have found that leukemic cells alter their fatty acid metabolism to survive CAR-T attacks.
Project Goals:
- Determine the precise leukemia-intrinsic mechanisms of CAR-T resistance, specifically fatty acid metabolism adaptations.
- Establish therapeutic approaches to improve B-ALL CAR sensitivity.
Funding: NIH/NCI 1R37CA295527-01
![Lele_V2[72504].JPG](https://static.wixstatic.com/media/bbb6d9_3cc7eb0c9a27469f85d483855b0c8db0~mv2.jpg/v1/fill/w_373,h_373,al_c,q_80,usm_0.66_1.00_0.01,enc_avif,quality_auto/Lele_V2%5B72504%5D_JPG.jpg)
Understanding genetic predispositions to B-ALL
Genome-wide association studies have established a link between B-ALL incidence and genetic variants found within specific transcription factors. One such transcription factor, ARID5B, often harbors variants leading to reduced activity and higher ALL incidence.
Project Goals:
- Identify epigenetic basis of ARID5B variants in ALL incidence.
- Understand how these variants act in a tumor suppressive manner to promote B-ALL.
Funding: ASH HIP Award, CU Cancer Center Innovation Pilot Grant