Abstract
Simple SummarySunitinib has been approved as the second-line targeted treatment for gastrointestinal stromal tumor (GIST) after imatinib failure. It is thus necessary to effectively assess prognosis after sunitinib use. However, the current assessment remains insufficient for the contemporary period. We examined prognostic factors influencing progression-free survival. Furthermore, we constructed a prognostic nomogram model using these significant pre-treatment and post-treatment variables.The present study aimed to construct a prognostic nomogram incorporating pre-treatment and post-treatment factors to predict progression-free survival (PFS) after use of sunitinib in patients with metastatic gastrointestinal stromal tumors (GISTs) following imatinib intolerance or failure. From 2007 to 2018, 109 metastatic GIST patients receiving sunitinib at Chang Gung Memorial Hospital, Taiwan, were enrolled. A prognostic nomogram to predict PFS was developed. Sixty-three male and forty-six female metastatic GIST patients, with a median age of 61 years (range: 15–91 years), received sunitinib. The median PFS for 109 patients is 9.93 months. For pre-treatment factors, male gender, body mass index more than 18.5 kg/m2, no sarcopenia status, higher lymphocyte count, lower platelet/lymphocyte ratio, good performance status, higher sunitinib dose, and non-liver metastasis were significantly associated with favorable PFS. For post-treatment factors, adverse events with hypertension, hand–foot skin reaction, and diarrhea were significantly associated with favorable PFS. However, only eight clinicopathological independent factors for PFS prediction were selected for prognostic nomogram establishment. The calibration curve for probability of PFS revealed good agreement between the nomogram prediction and actual observation. High risk patients will experience the lowest PFS. A prognostic nomogram integrating eight clinicopathological factors was constructed to assist prognostic prediction for individual patients with advanced GIST after sunitinib use.
Highlights
Gastrointestinal stromal tumors (GISTs) arise from mesenchymal tissue in the gastrointestinal (GI) tract and peritoneum, accounting for the most common mesenchymal malignancy of the GI tract [1]
GISTs have been reported to originate from the interstitial cells of Cajal, expressing transmembranous KIT receptor with tyrosine kinase activity [3]
We retrospectively reviewed 299 patients with recurrent, unresectable, or metastatic GISTs, which were histologically confirmed by expression of CD117 or DOG1
Summary
Gastrointestinal stromal tumors (GISTs) arise from mesenchymal tissue in the gastrointestinal (GI) tract and peritoneum, accounting for the most common mesenchymal malignancy of the GI tract [1]. Curative surgical resection provides chance of cure and remains the standard of treatment for GISTs. postoperative recurrence is not uncommon [2]. GISTs have been reported to originate from the interstitial cells of Cajal, expressing transmembranous KIT receptor with tyrosine kinase activity [3]. Gain-of-function mutations of KIT in GISTs lead to constitutive and persistent activation of KIT signaling, leading to aberrant cell proliferation and resistance to apoptosis [4]. Imatinib mesylate (IM) is a selective tyrosine kinases inhibitor, including KIT and platelet-derived growth factors (PDGFRs), showing a promising clinical outcome for a patient with an advanced GIST [5] and has been established as the standard first-line therapy [5,6,7,8,9]. Progression of GIST upon IM treatment inevitably develops within two to three years [8,9]
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