Results 231 to 240 of about 84,228 (303)
Activatable nanoflytrap achieves synergistic "Capture-Block-Regulate" therapy of pancreatic ductal adenocarcinoma. [PDF]
Guo K +9 more
europepmc +1 more source
Cancer pain: current practice and emerging targets
Cancer pain (CP) arises from a complex interplay between the tumour and its microenvironment. Many patients experience a mixed pain phenotype that encompasses nociceptive, neuropathic and neuroinflammatory mechanisms, and vary across tumour type and disease stage. Despite decades of intensive research, the mainstay of cancer pain treatment is still non‐
Yi Ye +5 more
wiley +1 more source
Futility of resection after neoadjuvant therapy in pancreatic ductal adenocarcinoma. [PDF]
Luo HT +6 more
europepmc +1 more source
BLURB FOR ETOC: The J‐TAIL‐2 study (NCT04501497) evaluated the efficacy and safety of atezolizumab, an anti‐programmed death‐ligand 1, plus chemotherapy in patients with non‐small cell lung cancer (NSCLC) and extensive‐stage small cell lung cancer (ES‐SCLC) in real‐world settings.
Yasushi Goto +19 more
wiley +1 more source
Explainable multi-omics modeling for risk stratification in pancreatic ductal adenocarcinoma. [PDF]
Chen B +8 more
europepmc +1 more source
Corresponding Author and colleagues identify a pancreas‐enriched microRNA, miR‐216b‐5p, that suppresses PTBP1 and its downstream effector TYMS. Their findings reveal a novel miR‐216b‐5p/PTBP1/TYMS regulatory axis driving pancreatic cancer progression and establish PTBP1 as a central molecular regulator of tumor biology beyond its metabolic role ...
Shigenori Suzuki +14 more
wiley +1 more source
Treating Pancreatic Ductal Adenocarcinoma: The Targeted Revolution is Here. [PDF]
May MS, Park W, O'Reilly EM.
europepmc +1 more source
RASD2 Drives Renal Clear Cell Carcinoma Progression via RAF1 (Ser338) Phosphorylation
RASD2 drives clear cell renal cell carcinoma (ccRCC) progression by physically interacting with RAF1 to induce its Ser338 phosphorylation, which subsequently activates the P38/ERK–MAPK signaling pathway to promote malignant tumor phenotypes and poor prognosis.
Jingxuan Yu +10 more
wiley +1 more source
MTAP Deficiency as a Metabolic Vulnerability in Cancer: Implications for Synthetic Lethal Therapy
MTAP deletion creates a therapeutically actionable metabolic vulnerability through MTA accumulation and PRMT5 dependency. This review summarizes the biochemical basis of MTAP‐directed synthetic lethality, emerging PRMT5/MAT2A inhibitors, clinicogenomic features of MTAP‐deleted tumors, and future strategies for precision oncology.
Hiroaki Ikushima, Hidenori Kage
wiley +1 more source

