Results 51 to 60 of about 4,624,933 (258)

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

open access: yesMolecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis   +3 more
wiley   +1 more source

Restoration of Sensitivity in Chemo [PDF]

open access: yes, 2013
Glioblastoma (GBM) is the most common and aggressive brain tumor in adults. Despite multimodal treatments including surgery, chemotherapy and radiotherapy the prognosis remains poor and relapse occurs regularly.
Schäfer, Andrea   +10 more
core   +1 more source

The noncoding RNA LINC00152 conveys contradicting effects in different glioblastoma cells

open access: yesScientific Reports, 2021
Glioblastoma multiforme (GBM) is an extremely aggressive brain tumor, characterized by its high genetic heterogeneity. In search of novel putative therapeutic RNA targets we investigated the role of the oncogenic long noncoding RNA LINC00152 (CYTOR, and ...
Stefanie Binder   +11 more
doaj   +1 more source

A novel quinazolinone insulin receptor inhibitor and its synergy with an EGFR inhibitor in glucose‐driven glioblastoma

open access: yesMolecular Oncology, EarlyView.
The novel styrylquinazolinone‐based molecule W1B effectively suppresses glioblastoma by inhibiting IGF1R and EGFR. In high‐glucose microenvironments driving tumor resistance, W1B acts synergistically with the EGFR inhibitor dacomitinib. This combination safely blocks compensatory survival signaling in zebrafish xenograft models. Showcasing promising in
Patryk Rurka   +9 more
wiley   +1 more source

A combinatorial preclinical in vitro strategy against human glioblastoma cells. specific targeting of protein kinases, histone deacetylases and glycolysis [PDF]

open access: yes, 2009
Effective treatment of malignant gliomas remains one of the great challenges in neurooncology. The incidence of malignant gliomas is 5 to 10 per 100.000 persons, and the outcome is always fatal with a mean survival of less than one year.
Egler, Viviane
core   +1 more source

Nanos3, a cancer-germline gene, promotes cell proliferation, migration, chemoresistance, and invasion of human glioblastoma

open access: yesCancer Cell International, 2020
Background Radiotherapy, chemotherapy, and surgery have made crucial strides in glioblastoma treatment, yet they often fail; thus, new treatment and new detection methods are needed.
Fengyu Zhang   +4 more
doaj   +1 more source

Phosphorylation of ERK-Dependent NF-κB Triggers NLRP3 Inflammasome Mediated by Vimentin in EV71-Infected Glioblastoma Cells

open access: yesMolecules, 2022
Enterovirus 71 (EV71) is a dominant pathogenic agent that may cause severe central nervous system (CNS) diseases among infants and young children in the Asia-pacific. The inflammasome is closely implicated in EV71-induced CNS injuries through a series of
Zelong Gong   +6 more
doaj   +1 more source

Epigenetic heterogeneity and plasticity in therapy‐induced tumor states through single‐cell multi‐omics

open access: yesMolecular Oncology, EarlyView.
Single‐cell multi‐omics reveals epigenetic heterogeneity across therapy‐adaptive tumor states, including quiescent/dormant, drug‐tolerant persister, and EMT‐like phenotypes. By linking regulatory features with state‐associated biomarkers, these approaches inform biomarker‐guided therapeutic strategies for evolving tumors.
Hee Jung Kim   +3 more
wiley   +1 more source

Hypoxia helps glioma to fight therapy [PDF]

open access: yes, 2009
Despite major improvements in the surgical management the prognosis for patients bearing malignant gliomas is still dismal. Malignant gliomas are notoriously resistant to treatment and the survival time of patients is between 3-8 years for low-grade and
Amberger-Murphy, Verena   +1 more
core   +2 more sources

Translating whole‐genome doubling into precision medicine in cancer

open access: yesMolecular Oncology, EarlyView.
Whole‐genome doubling creates a WGD‐positive tumor state characterized by persistent chromosomal instability, karyotypic diversification, and cellular stress. These same biological pressures drive aggressive tumor evolution while exposing therapeutic vulnerabilities, providing a rationale for WGD‐informed precision medicine. Whole‐genome doubling (WGD)
Sejung Lee, Junghyeok Lim, Jinhyuk Bhin
wiley   +1 more source

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