These findings indicated that DMC functions as an effective chemosensitizer, elevating TMZ efficacy. Combining DMC with DNA repair inhibitors may represent a promising therapeutic strategy to overcome resistance and improve IDH-wildtype grade diffuse glioma treatment outcomes.

The patient underwent chemoradiotherapy consisting of 60 Gy in 30 fractions combined with gemcitabine+nab-paclitaxel...Histopathological evaluation revealed no viable cancer cells, showing only post-treatment changes, consistent with a pathological complete response(Grade 4). The postoperative course was uneventful, and at 6 months post-adrenalectomy, the patient remains recurrence-free without further adjuvant therapy.

P3, N=70, Recruiting, UroGen Pharma Ltd. | N=50 --> 70 | Trial completion date: Mar 2027 --> Oct 2027 | Trial primary completion date: Mar 2026 --> Oct 2026

P=N/A, N=200, Recruiting, British Columbia Cancer Agency | Not yet recruiting --> Recruiting

The authors apologize to the Editor of Oncology Reports and to the readership for any inconvenience caused. [Oncology Reports 45: 69, 2021; DOI: 10.3892/or.2021.8020].

circ72309 affected multiple steps in the gemcitabine metabolic pathway and its overexpression resulted in markedly increased gemcitabine sensitivity. Therefore, circ72309 expression in the pre‑treatment serum samples may serve as a predictor of gemcitabine sensitivity in patients with PC..

In the first-line setting, targeted therapy and SSAs were associated with longer PFS than chemotherapy, with surufatinib and lanreotide showing favorable disease control. SDHx pathogenic variant status did not show a clear association with response to TKIs or temozolomide, underscoring the need for validation in larger cohorts.

Mechanistically, MMP-14 translocates to the nucleus and binds to chromatin following DNA damage induced by ionizing radiation or cisplatin...These findings reveal a novel nuclear function for MMP-14 in DNA repair and identify MMP-14 as a promising therapeutic target in ACC. Targeting MMP-14 may sensitize ACC tumors to DNA-damaging chemotherapy by impairing the repair of therapy-induced lesions.

Crucially, these effects were reversed by N-acetylcysteine (NAC), and lipid peroxidation was abrogated by the iron chelator deferoxamine (DFX), unequivocally confirming iron-dependent ferroptosis. Critically, cyst(e)inase synergized with temozolomide (TMZ), markedly enhancing its anti-tumor efficacy and prolonging survival, even in TMZ-resistant xenografts. These findings establish cysteine metabolism as a promising therapeutic target and position cyst(e)inase, especially with TMZ, as a potent strategy to overcome GBM resistance.

AHVAC-I decreases proliferation and invasion of MKN-28/DDP cells by downregulating RAI14 expression.