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Cellular collusion: cracking the code of immunosuppression and chemo resistance in PDAC.
Musiu, Chiara; Lupo, Francesca; Agostini, Antonio; Lionetto, Gabriella; Bevere, Michele; Paiella, Salvatore; Carbone, Carmine; Corbo, Vincenzo; Ugel, Stefano; De Sanctis, Francesco.
Afiliación
  • Musiu C; Department of Medicine, University of Verona, Verona, Italy.
  • Lupo F; Department of Engineering for Innovation Medicine, University of Verona, Verona, Italy.
  • Agostini A; Medical Oncology, Department of Translational Medicine, Catholic University of the Sacred Heart, Rome, Italy.
  • Lionetto G; Medical Oncology, Department of Medical and Surgical Sciences, Fondazione Policlinico Universitario Agostino Gemelli Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy.
  • Bevere M; General and Pancreatic Surgery Unit, Pancreas Institute, University of Verona, Verona, Italy.
  • Paiella S; ARC-Net Research Centre, University of Verona, Verona, Italy.
  • Carbone C; General and Pancreatic Surgery Unit, Pancreas Institute, University of Verona, Verona, Italy.
  • Corbo V; Medical Oncology, Department of Medical and Surgical Sciences, Fondazione Policlinico Universitario Agostino Gemelli Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS), Rome, Italy.
  • Ugel S; Department of Engineering for Innovation Medicine, University of Verona, Verona, Italy.
  • De Sanctis F; Department of Medicine, University of Verona, Verona, Italy.
Front Immunol ; 15: 1341079, 2024.
Article en En | MEDLINE | ID: mdl-38817612
ABSTRACT
Despite the efforts, pancreatic ductal adenocarcinoma (PDAC) is still highly lethal. Therapeutic challenges reside in late diagnosis and establishment of peculiar tumor microenvironment (TME) supporting tumor outgrowth. This stromal landscape is highly heterogeneous between patients and even in the same patient. The organization of functional sub-TME with different cellular compositions provides evolutive advantages and sustains therapeutic resistance. Tumor progressively establishes a TME that can suit its own needs, including proliferation, stemness and invasion. Cancer-associated fibroblasts and immune cells, the main non-neoplastic cellular TME components, follow soluble factors-mediated neoplastic instructions and synergize to promote chemoresistance and immune surveillance destruction. Unveiling heterotypic stromal-neoplastic interactions is thus pivotal to breaking this synergism and promoting the reprogramming of the TME toward an anti-tumor milieu, improving thus the efficacy of conventional and immune-based therapies. We underscore recent advances in the characterization of immune and fibroblast stromal components supporting or dampening pancreatic cancer progression, as well as novel multi-omic technologies improving the current knowledge of PDAC biology. Finally, we put into context how the clinic will translate the acquired knowledge to design new-generation clinical trials with the final aim of improving the outcome of PDAC patients.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Resistencia a Antineoplásicos / Carcinoma Ductal Pancreático / Microambiente Tumoral Límite: Animals / Humans Idioma: En Revista: Front Immunol Año: 2024 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Suiza
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Resistencia a Antineoplásicos / Carcinoma Ductal Pancreático / Microambiente Tumoral Límite: Animals / Humans Idioma: En Revista: Front Immunol Año: 2024 Tipo del documento: Article País de afiliación: Italia Pais de publicación: Suiza