A new mutation affecting the ATP pocket of kit receptor in patients with GIST showing acquired resistance to Imatinib: a coupled experimental and modeling investigation

نویسندگان

  • S. Pricl
  • A. Coslanich
  • M. Fermeglia
  • M. Ferrone
  • M. S. Paneni
  • E. Tamborini
  • S. Pilotti
  • M. A. Pierotti
چکیده

Computer-aided System Laboratory – MO.S:E., Department of Chemical, Environmental and Raw Materials Engineering, University of Trieste – Piazzale Europa 1, 34127 Trieste, Italy; Experimental Molecular Pathology, Department of Pathology, Istituto Nazionale per lo Studio e la Cura dei Tumori, Via Venezian 1, 20133 Milano, Italy; Department of Experimental Oncology, Istituto Nazionale per lo Studio e la Cura dei Tumori, Via Venezian 1, 20133 Milano, Italy

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

RACK1 overexpression is linked to acquired imatinib resistance in gastrointestinal stromal tumor

Although treatment with imatinib, which inhibits KIT and PDGFR, controls advanced disease in about 80% of gastrointestinal stromal tumor (GIST) patients, resistance to imatinib often develops. RACK1 (Receptor for Activated C Kinase 1) is a ribosomal protein that contributes to tumor progression by affecting proliferation, apoptosis, angiogenesis, and migration. Here, we found that c-KIT binds t...

متن کامل

Acquired resistance to imatinib in gastrointestinal stromal tumor occurs through secondary gene mutation.

Most gastrointestinal stromal tumors (GIST) have an activating mutation in either KIT or PDGFRA. Imatinib is a selective tyrosine kinase inhibitor and achieves a partial response or stable disease in about 80% of patients with metastatic GIST. It is now clear that some patients with GIST develop resistance to imatinib during chronic therapy. To identify the mechanism of resistance, we studied 3...

متن کامل

Cancer Therapy: Preclinical Mechanisms of Sunitinib Resistance in Gastrointestinal Stromal Tumors Harboring KIT Mutation: An In vitro Mutagenesis Screen for Drug Resistance

Purpose: Although tyrosine kinase inhibitors have improved survival in advanced gastrointestinal stromal tumor (GIST), complete response is rare and most patients eventually fail the first-line treatment with imatinib. Sunitinib malate is the only approved second-line therapy for patients with imatinib-resistant or imatinib-intolerant GIST. The clinical benefit of sunitinib is genotype-dependen...

متن کامل

The potential value of F-18 FDG PET in comparison to ct in early prediction of response to Imatinib (STI571) therapy in patients with gastrointestinal stromal tumors

  Introduction: Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. GIST has been shown to over-express c-KIT (CD117), the receptor tyrosine kinase. Imatinib (STI571 or Glivec) is a new type of tyrosine kinase inhibitor that selectively inhibits various tyrosine kinases and has been successfully used to trea...

متن کامل

Crosstalk between KIT and FGFR3 Promotes Gastrointestinal Stromal Tumor Cell Growth and Drug Resistance.

Kinase inhibitors such as imatinib have dramatically improved outcomes for patients with gastrointestinal stromal tumor (GIST), but many patients develop resistance to these treatments. Although in some patients this event corresponds with mutations in the GIST driver oncogenic kinase KIT, other patients develop resistance without KIT mutations. In this study, we address this patient subset in ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2004