Results 101 to 110 of about 111,871 (303)

Posttranscriptional regulation of PARG mRNA by HuR facilitates DNA repair and resistance to PARP inhibitors [PDF]

open access: yes, 2017
The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRNA stability factor HuR (ELAV-L1) to drive cancer growth and progression. Here, we show that CRISPR-Cas9–mediated silencing of the HuR locus increases the relative sensitivity of PDAC
Brody, Jonathan R.   +17 more
core   +1 more source

Targeting of Prosurvival Pathways as Therapeutic Approaches against Primary Effusion Lymphomas: Past, Present, and Future [PDF]

open access: yes, 2015
Constitutively activated prosurvival pathways render cancer cells addicted to their effects. Consequently they turn out to be the Achilles’ heels whose inhibition can be exploited in anticancer therapy.
CIRONE, Mara   +6 more
core   +4 more sources

Single‐Cell Computational Frameworks for Quantifying BET Bromodomain Inhibitor Resistance and Screening Re‐Sensitizer Drugs in Triple‐Negative Breast Cancer

open access: yesAdvanced Science, EarlyView.
To combat BET inhibitor resistance in triple‐negative breast cancer, we developed two single‐cell computational frameworks. FR20 quantifies resistance by integrating ferroptosis‐related gene signatures, while D‐FR20 screens for potential re‐sensitizers.
Haizhou Liu   +6 more
wiley   +1 more source

Efficacy and safety of PARP inhibitors in advanced or recurrent endometrial cancer: a systematic review and meta-analysis

open access: yesFrontiers in Immunology
ObjectiveSeveral clinical trials have explored the efficacy and safety of Poly (ADP-ribose) polymerase (PARP) inhibitors in endometrial cancer (EC). However, evidence supporting PARP inhibitors alone or in combination with other medications in advanced ...
Huanhuan Zhang   +7 more
doaj   +1 more source

Understanding and Overcoming Antibody‐Drug Conjugate Resistance: Biological Mechanisms and Emerging Analytical Frameworks in Breast Cancer

open access: yesAdvanced Science, EarlyView.
Antibody–drug conjugates (ADCs) transform breast cancer therapy, yet resistance limits their durability. Emerging evidence reveals that ADC failure is not solely tumor‐intrinsic but shaped by dynamic tumor–microenvironment interactions that alter drug delivery, processing, and response.
Minji Seo, Jangsoon Lee, Naoto T. Ueno
wiley   +1 more source

Combination of triapine, olaparib, and cediranib suppresses progression of BRCA-wild type and PARP inhibitor-resistant epithelial ovarian cancer.

open access: yesPLoS ONE, 2018
PARP inhibitors target BRCA mutations and defective homologous recombination repair (HRR) for the treatment of epithelial ovarian cancer (EOC). However, the treatment of HRR-proficient EOC with PARP inhibitors remains challenging.
Z Ping Lin   +9 more
doaj   +1 more source

Halofuginone is a Molecular Glue Degrader of Integrin β4

open access: yesAdvanced Science, EarlyView.
Integrin β4 overexpression is linked to aggressive tumors and poor prognosis, but targeted therapies are lacking. We identified halofuginone (HF) as a molecular glue degrader that promotes integrin β4 degradation via the CRL4BWDR18 E3 ligase. HF suppresses tumor progression in vitro and in vivo, offering a new strategy for targeting oncogenic ...
Wei Gong   +8 more
wiley   +1 more source

Selective targeting of HDAC1/2 elicits anticancer effects through Gli1 acetylation in preclinical models of SHH Medulloblastoma. [PDF]

open access: yes, 2017
SHH Medulloblastoma (SHH-MB) is a pediatric brain tumor characterized by an inappropriate activation of the developmental Hedgehog (Hh) signaling. SHH-MB patients treated with the FDA-approved vismodegib, an Hh inhibitor that targets the transmembrane ...
Bufalieri, Francesca   +18 more
core   +2 more sources

PARP Inhibitors for Cancer Therapy

open access: yesCell, 2017
Rucaparib is an inhibitor of nuclear poly (ADP-ribose) polymerases (inhibition of PARP-1 > PARP-2 > PARP-3), following a similar drug, Olaparib. It disrupts DNA repair and replication pathways (and possibly transcription), leading to selective killing of cancer cells with BRCA1/2 mutations.
Ken Y, Lin, W Lee, Kraus
openaire   +2 more sources

SLC2A3‐Mediated Lactate Metabolism Promotes Lung Cancer Bone Metastasis by Modulating P53 Lactylation and Immune Evasion

open access: yesAdvanced Science, EarlyView.
SLC2A3 derived lactate promotes metastasis through p53 lactylation at K120 and osteoclast differentiation. Pharmacological inhibition of SLC2A3 upregulates PD‐1 expression on CD8+ T cells via lactate induced p53 lactylation, which modulates immune evasion. ABSTRACT Bone metastasis is a devastating consequence of lung cancer.
Yi Ding   +10 more
wiley   +1 more source

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