Results 231 to 240 of about 775,220 (247)

Investigating the interaction of ACKR1 and c-Myc in the breast carcinoma tumor microenvironment modulation. [PDF]

open access: yesDiscov Oncol
Talukdar J   +7 more
europepmc   +1 more source

TriCON: A Carbon‐Based Triple‐Modal Nanoplatform for Pancreatic Cancer Therapy

open access: yesAdvanced Science, EarlyView.
We developed TriCON, a triple‐modality nanotherapeutic platform, to treat pancreatic ductal adenocarcinoma (PDAC) by synergizing gene editing, chemotherapy, and immunotherapy. TriCON utilizes CRISPR/Cas9 to target the poliovirus receptor (PVR), combined with nano‐encapsulated doxorubicin and checkpoint blockade. This approach achieved significant tumor
Xinyu Peng   +9 more
wiley   +1 more source

[18F]FDG PET/CT Radiomics in Untreated Breast Carcinoma: A Review of the Current State and Future Directions. [PDF]

open access: yesDiagnostics (Basel)
Mitoi A   +5 more
europepmc   +1 more source

Proteogenomic Characterization Reveals Subtype‐Specific Therapeutic Potential for HER2‐Low Breast Cancer

open access: yesAdvanced Science, EarlyView.
Multiomic profiling of HER2‐low breast cancer identifies three proteomic subtypes with distinct therapeutic strategies: endocrine, antiangiogenic, and anti‐HER2 therapies. Genomic and lactate modification landscapes are detailed, providing insights for precise management.
Shouping Xu   +20 more
wiley   +1 more source

GLUL Confers Perivascular Cancer‐Associated Fibroblasts With Pro‐Angiogenic Capacity to Promote Glioma Progression

open access: yesAdvanced Science, EarlyView.
Schematic illustration of the proposed model. Primary CAFs are isolated from fresh human GBM specimens according to established protocols. GLUL is essential for pro‐angiogenic capacity of CAFs through its impact on the PI3K/AKT pathway. GLUL enhances the pro‐angiogenic capacity of CAFs, driving aberrant tumor vasculature that fuels tumor growth ...
Qing Zhang   +4 more
wiley   +1 more source

Dual Targeting of Mutant p53 and SNRPD2 via Engineered Exosomes Modulates Alternative Splicing to Suppress Ovarian Cancer

open access: yesAdvanced Science, EarlyView.
Mutant p53 drives oncogenic splicing to promote the progression of ovarian cancer by partnering with the spliceosome factor SNRPD2. Therefore, it is engineered iRGD‐exosomes to co‐deliver siRNAs against both targets. This approach restored tumor‐suppressive mRNA isoforms, effectively enhanced sensitivity to cisplatin, and ultimately blocked tumor ...
Wei Zhao   +14 more
wiley   +1 more source

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