IDH1 overexpression

GATM acts as a tumour suppressor in CCA by regulating the phosphorylation of the JNK/c-Jun pathway. IDH1 interacted with GATM to regulate CCA progression.

Furthermore, we found that RNA binding motif protein 47 (RBM47) was the downstream target of miR-518c-5p, that upregulation of RBM47 inhibited EOC cell proliferation, and that RBM47 overexpressing plasmid counteracted the proliferation-promoting effect caused by the IDH1-AS1 knockdown. Taken together, IDH1-AS1 may suppress EOC cell proliferation and tumor growth via the miR-518c-5p/RBM47 axis.

WHO grade 4 IDH-mutant astrocytoma is more radiosensitive than IDH-wildtype GBM patients. Our 4-gene radiotherapy-related signature can predict the radiation efficacy of WHO grade 4 glioma patients, and it may provide some reference for clinical treatment options.

RT + PARPi reshapes the IDH1 tumor immune suppression microenvironment, thereby potentiating the antitumor effect and efficiency of immune checkpoint inhibitor.

RT + PARPi reshapes the IDH1 mut tumor immune suppression microenvironment, thereby potentiating the antitumor effect and efficiency of immune checkpoint inhibitor.

The effect of LBH (panobinostat) on gene expression and chromatin structure was tested on patient-derived IDH1 mutant lines...The gene dysregulation induced by the IDH1 mutation is wide-spread and only partially reversible by direct IDH1 inhibition. This study identifies HDAC1 and HDAC6 as important and drug-targetable enzymes that are necessary for growth and invasiveness in IDH1 mutant gliomas.

Surgical operation is the main treatment. We suggest that patients with ovarian juvenile granulosa cell tumors and Ollier's disease should undergo regular investigation.

Adoptive cell therapy through T cells with Chimeric Antigen Receptor (CAR) including Tisagenlecleucel and Axicabtagene Ciloleucel introduced a breakthrough in cancer immunotherapy against CLL and have risen as game changers in the cancer care scenario but still remain several challenges including durable remission and lack of expansion after infusion. This study therefore suggests that the functional disruption of TET2 via the overexpression of the IDH1 neomorph results in augmented memory function of CAR T cells with preservation of effector function. Our discovery introduced an alternative approach for functional TET2 disruption for CAR T cell improvement.

Our results highlighted IDH1 mutation upregulate mTOR signaling pathway and promote cell proliferation, invasion and migration.

Genes with mechanistic links to IDH1 were involved in brain neuronal development, cell proliferation, cytokinesis, and O-mannosylation as well as tumor suppression and anaplerosis. Results highlight metabolic vulnerabilities and therapeutic targets for use in future clinical trials.

In addition, silencing IDH1 sensitized melanoma cells to temozolomide (TMZ), a DNA-alkylating agent, as indicated by a decrease in relative cell survival compared with controls. IDH1 plays a critical role in tumorigenesis and chemoresistance in melanoma. IDH1 plays a critical role in tumorigenesis and chemoresistance in melanoma. Our data show that IDH1 inhibition sensitizes melanoma cells to TMZ therapy. Our study suggests that IDH1 is a potential target in melanoma as a monotherapy or in combination with existing chemotherapies.

wt-IDH1i-13 is brain-penetrant, and similar to genetic ablation, reduces progression and extends the survival of wt-IDH1 high HGG bearing mice, alone and in combination with RT. These studies credential to wt-IDH1i-13 as a novel therapeutic modality for the treatment of wt-IDH1 gliomas.