<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>22</volume><submitter>Li W</submitter><pubmed_abstract>Malignant melanoma cell-intrinsic PD-1:PD-L1 interaction thrusts tumorigenesis, angiogenesis, and radioresistance via mTOR hyperactivation to aggravate circumjacent aggression. Interdicting melanoma intrinsic growth signals, including the blockade of PD-L1 and mTOR signaling concurrently, cooperative with radiotherapy may provide a vigorous repertoire to alleviate the tumor encumbrance. Thence, we design a three-pronged platinum@polymer-catechol nanobraker to deliver mTOR inhibitor TAK228 and anti-PD-L1 antibody (aPD-L1) for impeding the melanoma-PD-1-driven aggression and maximizing the melanoma eradication. The aPD-L1 collaborated with TAK228 restrains melanoma cell-intrinsic PD-1: PD-L1 tumorigenic interaction via blocking melanoma-PD-L1 ligand and the melanoma-PD-1 receptor-driven mTOR</pubmed_abstract><journal>Bioactive materials</journal><pagination>34-46</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9513621</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>A platinum@polymer-catechol nanobraker enables radio-immunotherapy for crippling melanoma tumorigenesis, angiogenesis, and radioresistance.</pubmed_title><pmcid>PMC9513621</pmcid><pubmed_authors>Li W</pubmed_authors><pubmed_authors>Sang W</pubmed_authors><pubmed_authors>Yan J</pubmed_authors><pubmed_authors>Zhang Z</pubmed_authors><pubmed_authors>Tian H</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Wang G</pubmed_authors><pubmed_authors>Li B</pubmed_authors><pubmed_authors>Dai Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>A platinum@polymer-catechol nanobraker enables radio-immunotherapy for crippling melanoma tumorigenesis, angiogenesis, and radioresistance.</name><description>Malignant melanoma cell-intrinsic PD-1:PD-L1 interaction thrusts tumorigenesis, angiogenesis, and radioresistance via mTOR hyperactivation to aggravate circumjacent aggression. Interdicting melanoma intrinsic growth signals, including the blockade of PD-L1 and mTOR signaling concurrently, cooperative with radiotherapy may provide a vigorous repertoire to alleviate the tumor encumbrance. Thence, we design a three-pronged platinum@polymer-catechol nanobraker to deliver mTOR inhibitor TAK228 and anti-PD-L1 antibody (aPD-L1) for impeding the melanoma-PD-1-driven aggression and maximizing the melanoma eradication. The aPD-L1 collaborated with TAK228 restrains melanoma cell-intrinsic PD-1: PD-L1 tumorigenic interaction via blocking melanoma-PD-L1 ligand and the melanoma-PD-1 receptor-driven mTOR</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Apr</publication><modification>2025-04-04T09:25:15.821Z</modification><creation>2025-04-04T09:25:15.821Z</creation></dates><accession>S-EPMC9513621</accession><cross_references><pubmed>36203954</pubmed><doi>10.1016/j.bioactmat.2022.09.006</doi></cross_references></HashMap>