Results 121 to 130 of about 6,610,213 (244)

TREX1, a predator for treating MSI‐H tumors?

open access: yesMolecular Oncology, EarlyView.
Immunotherapy benefits many patients; yet, some with MSI‐H tumors remain unresponsive despite their high immunogenicity. Xu et al. reveal that TREX1 enables immune evasion by degrading cytosolic DNA and suppressing cGAS–STING–IFN‐I signaling. TREX1 loss restores DNA sensing, increases CD8+ T and NK cell infiltration, and boosts antitumor immunity ...
Elena Benidovskaya   +2 more
wiley   +1 more source

LINC01116, a hypoxia‐lncRNA marker of pathological lymphangiogenesis and poor prognosis in lung adenocarcinoma

open access: yesMolecular Oncology, EarlyView.
The LINC01116 long noncoding RNA is induced by hypoxia and associated with poor prognosis and high recurrence rates in two cohorts of lung adenocarcinoma patients. Here, we demonstrate that besides its expression in cancer cells, LINC01116 is markedly expressed in lymphatic endothelial cells of the tumor stroma in which it participates in hypoxia ...
Marine Gautier‐Isola   +12 more
wiley   +1 more source

ATF4‐mediated stress response as a therapeutic vulnerability in chordoma

open access: yesMolecular Oncology, EarlyView.
We screened 5 chordoma cell lines against 100+ inhibitors of epigenetic and metabolic pathways and kinases and identified halofuginone, a tRNA synthetase inhibitor. Mechanistically halofuginone induces an integrated stress response, with eIF2alpha phosphorylation, activation of ATF4 and its target genes CHOP, ASNS, INHBE leading to cell death ...
Lucia Cottone   +11 more
wiley   +1 more source

Developing evidence‐based, cost‐effective P4 cancer medicine for driving innovation in prevention, therapeutics, patient care and reducing healthcare inequalities

open access: yesMolecular Oncology, EarlyView.
The cancer problem is increasing globally with projections up to the year 2050 showing unfavourable outcomes in terms of incidence and cancer‐related deaths. The main challenges are prevention, improved therapeutics resulting in increased cure rates and enhanced health‐related quality of life.
Ulrik Ringborg   +43 more
wiley   +1 more source

PARP inhibition and pharmacological ascorbate demonstrate synergy in castration‐resistant prostate cancer

open access: yesMolecular Oncology, EarlyView.
Pharmacologic ascorbate (vitamin C) increases ROS, disrupts cellular metabolism, and induces DNA damage in CRPC cells. These effects sensitize tumors to PARP inhibition, producing synergistic growth suppression with olaparib in vitro and significantly delayed tumor progression in vivo. Pyruvate rescue confirms ROS‐dependent activity.
Nicolas Gordon   +13 more
wiley   +1 more source

Plecstatin inhibits hepatocellular carcinoma tumorigenesis and invasion through cytolinker plectin

open access: yesMolecular Oncology, EarlyView.
The ruthenium‐based metallodrug plecstatin exerts its anticancer effect in hepatocellular carcinoma (HCC) primarily through selective targeting of plectin. By disrupting plectin‐mediated cytoskeletal organization, plecstatin inhibits anchorage‐dependent growth, cell polarization, and tumor cell dissemination.
Zuzana Outla   +10 more
wiley   +1 more source

Therapeutic strategies for MMAE‐resistant bladder cancer through DPP4 inhibition

open access: yesMolecular Oncology, EarlyView.
We established monomethyl auristatin E (MMAE)‐resistant bladder cancer (BC) cell lines by exposure to progressively increasing concentrations of MMAE in vitro. RNA sequencing showed DPP4 expression was increased in MMAE‐resistant BC cells. Both si‐DPP4 and the DPP4 inhibitor sitagliptin suppressed the viability of MMAE‐resistant BC cells.
Gang Li   +10 more
wiley   +1 more source

Recurrent cancer‐associated ERBB4 mutations are transforming and confer resistance to targeted therapies

open access: yesMolecular Oncology, EarlyView.
We show that the majority of the 18 analyzed recurrent cancer‐associated ERBB4 mutations are transforming. The most potent mutations are activating, co‐operate with other ERBB receptors, and are sensitive to pan‐ERBB inhibitors. Activating ERBB4 mutations also promote therapy resistance in EGFR‐mutant lung cancer.
Veera K. Ojala   +15 more
wiley   +1 more source

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