Targeting SRC Family Kinases in Mesothelioma: Time to Upgrade.

Malignant mesothelioma (MM) is a deadly tumor mainly caused by exposure to asbestos. Unfortunately, no current treatment is able to change significantly the natural history of the disease, which has a poor prognosis in the majority of patients. The non-receptor tyrosine kinase SRC and other SRC fami...

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Publicado en:Cancers Vol. 12; no. 7; pp. 1866 - 1867
Autores principales: Indovina, Paola, Forte, Iris Maria, Pentimalli, Francesca, Giordano, Antonio
Formato: review tables/charts Journal Article
Publicado: MDPI Jul2020
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Jul2020
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      pub: MDPI
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        10.3390/cancers12071866
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        atl: Targeting SRC Family Kinases in Mesothelioma: Time to Upgrade.
      aug:
        au:
          Indovina, Paola
          Forte, Iris Maria
          Pentimalli, Francesca
          Giordano, Antonio
        affil: Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA
      sug:
        subj:
          Mesothelioma, Malignant Drug Therapy
          Protein-Tyrosine Kinases Therapeutic Use
          Antineoplastic Agents
          Mesothelioma, Malignant Prognosis
          Cell Proliferation Drug Effects
          Survival
          Cell Movement
          Disease Progression
          Pathology, Molecular
          Cell Line, Tumor Drug Effects
      ab: Malignant mesothelioma (MM) is a deadly tumor mainly caused by exposure to asbestos. Unfortunately, no current treatment is able to change significantly the natural history of the disease, which has a poor prognosis in the majority of patients. The non-receptor tyrosine kinase SRC and other SRC family kinase (SFK) members are frequently hyperactivated in many cancer types, including MM. Several works have indeed suggested that SFKs underlie MM cell proliferation, survival, motility, and invasion, overall affecting multiple oncogenic pathways. Consistently, SFK inhibitors effectively counteracted MM cancerous features at the preclinical level. Dasatinib, a multi-kinase inhibitor targeting SFKs, was also assessed in clinical trials either as second-line treatment for patients with unresectable MM or, more recently, as a neoadjuvant agent in patients with resectable MM. Here, we provide an overview of the molecular mechanisms implicating SFKs in MM progression and discuss possible strategies for a more successful clinical application of SFK inhibitors. Our aim is to stimulate discussion and further consideration of these agents in better designed preclinical and clinical studies to make the most of another class of powerful antitumoral drugs, which too often are lost in translation when applied to MM.
      pubtype: Academic Journal
      doctype:
        review
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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