IDH1 R132

P2, N=14, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Feb 2026 --> Mar 2027

P1, N=25, Recruiting, Servier Bio-Innovation LLC

The review is structured in two sections, the first introducing the IBDs and the homeostatic mechanisms that preserve integrity and prevent colorectal neoplasia. The second section compares failure modes in sporadic and colitic settings and describes the differences in the resulting neoplasms.

P1, N=60, Active, not recruiting, Institut de Recherches Internationales Servier | Recruiting --> Active, not recruiting

P2, N=60, Not yet recruiting, French Innovative Leukemia Organisation

Nevertheless, the comprehensive analysis of the simulated trajectory of ICT_NADPH-bound R132H_IDH1 reveals a non-canonical interaction region that is dynamically accessible to ICT/NADPH, which is probably responsible for the gain in the neomorphic activity that has not been previously detected or reported. Hence, we strongly believe that these findings may lead to therapeutic advances in the treatment of glioma.

P3, N=398, Not yet recruiting, NRG Oncology

P2/3, N=159, Completed, National Cancer Institute (NCI) | Trial completion date: Sep 2026 --> Dec 2025 | Active, not recruiting --> Completed

P1, N=62, Active, not recruiting, Dana-Farber Cancer Institute | Recruiting --> Active, not recruiting | Trial completion date: Jan 2027 --> Jan 2028 | Trial primary completion date: Jan 2026 --> Jan 2027

Using stable isotope tracing to track the synthesis of S-adenosylmethionine (SAM) and acetyl-Coenzyme A (acetyl-CoA), our method reveals new insights into metabolism linked to epigenetic modifications, including glycolysis, the pentose phosphate pathway, de novo glycine synthesis, and the folate and methionine cycle. Demonstrating practical utility in case-control studies, this approach supports integrative multi-omics strategies to explore the interplay between metabolism and epigenetics across various biological systems and diseases.

Importantly, enforced nuclear actin polymerization in D-2-HG-treated cells restored lamin A expression, rescued diminished TERT levels, and decreased γH2AX; thereby suggesting a functional link between actin dynamics and nuclear state. Collectively, our findings uncover a previously unrecognized role for oncometabolite D-2-HG in modulating actin dynamics, and bridges the mechanistic gap between the structural-metabolic coupling mechanism in glioma.