temozolomide

These coordinated pathways drive an "angiogenic switch," facilitate "metabolic migration," and induce significant resistance to chemotherapies, including gemcitabine and temozolomide. The hypoxamir-TAM axis is a fundamental driver of immune evasion and therapeutic failure. Targeting this dual-axis framework offers a viable strategy for restoring anti-tumor immunity, while circulating hypoxamirs represent high-value liquid biopsy biomarkers for real-time TME monitoring.

ECM stiffening is linked to stemness maintenance and temozolomide resistance in recurrent GBM through H3K18la-associated epigenetic regulation, while ITGA4/YAP-related mechanosensing provides a membrane-proximal axis that can be attenuated by multivalent VCAM1-Fc. Multivalent VCAM1-Fc may therefore reduce stiffness-associated malignant phenotypes by limiting ITGA4-dependent mechanotransduction.

P2, N=78, Recruiting, University of Zurich | Not yet recruiting --> Recruiting | Initiation date: Dec 2025 --> Jun 2026

P3, N=18, Completed, University of Texas Southwestern Medical Center | Active, not recruiting --> Completed | Trial completion date: Jun 2027 --> Oct 2025

P1, N=29, Active, not recruiting, M.D. Anderson Cancer Center | Recruiting --> Active, not recruiting

This study highlights the essential role of mtDNA content in modulating GBM cell sensitivity to chemotherapy, as variations in mtDNA levels can influence cellular responses to treatment. These findings suggest that mtDNA content could act as a potential biomarker and that its modulation may offer a promising strategy to overcome drug resistance in GBM. Cite this article as: Radzak SMA, Patar A, Lee H, Yusoff AAM. Mitochondrial DNA content modulates chemosensitivity and cellular adaptation in glioblastoma cells. Eurasian J Med. 2026, 58(2), 1207, doi: 10.5152/eurasianjmed.2026.251207.

The patient received various treatment regimens, including toripalimab monotherapy, combination therapy with anlotinib, and combination therapy with temozolomide. Ultimately, surgical resection of the pancreatic and spleen metastases revealed a BRAF V600 mutation, permitting successful transition to targeted therapy with dabrafenib plus trametinib...This case report, along with the subsequent literature review, emphasizes the need for continued treatment and vigilance of molecular monitoring in patients with advanced melanoma, as well as the critical role of multidisciplinary team collaboration in managing complex metastases. Surgical resection and targeted therapy might yield favorable outcomes for select patients with melanoma and pancreatic and splenic metastases.

Background: Acquired tolerance to temozolomide (TMZ) remains one of the main obstacles to enduring therapeutic success in glioblastoma (GBM)... Current data uncover an intercellular signaling network driven by vesicular circ_0050688, which functions as a mobile oncogene to reshape the TMZ-refractory microenvironment. Targeting this exosomal circ_0050688/miR-508-5p/MDM2 network to suppress P-gp and Ki-67 expression represents a highly promising therapeutic strategy for refractory GBM.

[This retracts the article DOI: 10.2147/OTT.S243833.].

Ferroptosis represents a biologically plausible and therapeutically promising target in glioma. Improved understanding of ferroptosis regulation, tumor microenvironment interactions, and biomarker-guided therapeutic strategies may support the future development of more effective treatments for GBM.

SLC44A4 overexpression also increased sensitivity to DNA-damaging agents, including temozolomide, doxorubicin, cisplatin, olaparib, and etoposide, while decreasing sensitivity to 5-fluorouracil. Together, these findings identify SLC44A4 as a potential tumor-suppressive factor in NPC and suggest that SLC44A4 may serve as a biomarker for metabolic state, B-cell/TLS-associated immune features, and vulnerability to DNA damage-based therapies.

Glioblastoma (GBM) is a highly invasive brain cancer arising from astrocytes, and current treatments are often ineffective, limiting patient five-year survival to <5%, despite maximal safe resection, temozolomide (TMZ) chemotherapy, and radiotherapy...By synthesizing available NGFR and GBM data, this review identifies p75NTR as the primary NGFR implicated in GBM progression and positions it as a rationally supported therapeutic target for GBM. This review also identifies key questions warranting further investigation into p75NTR's molecular mechanisms.