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Palabras clave – provistas por la editorial

actin cytoskeletal reorganization; breast cancer; CD99 agonist; EGFR dimerization; endocytosis; FAK dephosphorylation; PTPN12; Rac1; RhoA; tripeptide; OMD; PRELP; tumor suppression gene; bladder cancer initiation; tight junction; partial EMT; tousled-like kinase (TLK); NIMA-related kinase 1 (NEK1); yes-associated protein 1 (YAP1); thioridazine (THD); MS-determined phosphopeptides; human immunodeficiency virus type 1; epithelial cells; carcinogenicity; oxidative stress; reactive oxygen species; gp120; Tat; Nef; matrix protein p17; reverse transcriptase; mitochondria; metastasis; OXPHOS; cancer; Warburg effect; cancer therapeutics; myeloproliferative neoplasms; signaling pathways; JAK2; CALR; MPL; TPOR; DUSP1; MAPK; Snail; prostate cancer; migration and invasion; patient survival; biomarkers; pBRD4; SET; PP2A; prognosis; triple negative breast cancer; resistance; anti-receptor therapy; trastuzumab; PI3K; mTOR; TAK-228; epigenetic; methylation; acetylation; non-coding RNA; small-cell lung cancer; triple-negative breast cancer; pancreatic ductal adenocarcinoma; glioblastoma; metastatic melanoma; advanced ovarian cancer; hepatocellular carcinoma; immune evasion; immunotherapy; immune checkpoint inhibitors; oncogenic signaling pathway; molecular targeted agents; genome; epigenome; tumor immune microenvironment; ovarian cancer; adaptive immunity; innate immunity; complement system; cancer immunology; tumor microenvironment; splicing pathway; luminal breast cancer; BET inhibitors; n/a