E on the tyrosine kinase, thus preventing its function. The firstE on the tyrosine kinase,

E on the tyrosine kinase, thus preventing its function. The first
E on the tyrosine kinase, thus preventing its function. The first report of imatinib in the treatment of GIST was published in 2001 by Joensuu et al [6]. Since then, multiple studies have confirmed the usefulness of imatinib therapy in treating GISTs, leading to FDA approval of imatinib in the treatment of metastatic and/or unresectable GISTs [7]. Notably, Demetri et al conducted a study of 147 patients who received either 400 or 600 mg of imatinib daily. They reported a 54 radiographic response in their patient population [2]. The most common side effects of imatinib are fluid retention, diarrhea, nausea, fatigue, muscle cramps, abdominal pain, and rash. Extremity a facial edema (the latter was experienced by the patient in this case) were the most frequent adverse effects in the Demetri study. A new approach is evolving that relies on neoadjuvant imatinib to down-stage the tumor in cases of advanced GISTs. Prior studies have described patients with inoperable or metastatic GISTs who underwent treatment with imatinib and had a BMS-214662 web dramatic response allowing surgical resection [8,9]. The median time for an objective response to imatinib is four months, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28212752 but maximal response is reported to take six months or longer [10]. Response is defined as absence of progression at the time of first follow-up, generally two-DiscussionGISTs are the most common sarcoma of the gastrointestinal tract. GISTs are characterized by the expression of the cell surface marker CD117, which is found in 95?00 of GISTs [3]. CD117 is a receptor tyrosine kinase, coded for by the c-kit proto-oncogene. Overexpression of this gene is most commonly caused by an activating mutation of exon 11 and is hypothesized to be responsible for GIST oncogenesis [4]. Historically, GISTs have responded very poorly to radiation and cytotoxic chemotherapy, making surgical resection the only effective treatment. Imatinib, a receptor tyrosine kinase inhibitor, was first used in the treatment of chronic myelogenous leukemia, which is characterized by the constitutive activation of the Bcr-Abl tyrosine kinasePage 2 of(page number not for citation purposes)World Journal of Surgical Oncology 2009, 7:http://www.wjso.com/content/7/1/three months after starting therapy. The patient in our case was believed to have achieved sufficient response to allow for an uncomplicated, successful resection of the GIST. While most patients respond to imatinib, many eventually develop resistance. Initial (primary) resistance is defined as progression of disease at the time of first follow up after start of therapy [11]. These patients are not responsive to imatinib. Late (secondary) resistance is seen in a patient who experiences disease progression after a period of response. Patients who respond should be followed with serial imaging. Ideally, resection should be performed before the development of resistance. The role of imatinib in the neoadjuvant setting is illustrated in this case. While the GIST found in this patient may not have been inoperable before imatinib treatment, the procedure may have required a multi-visceral resection. Neoadjuvant imatinib was given and after dramatic radiographic response, a simple wedge gastric resection was needed. Surgeons should consider the use of neoadjuvant imatinib therapy in patients with marginally resectable GISTs. A response to imatinib can allow for a less extensive though still therapeutic oncologic resection.7.8.9.10.11.Dagher R, Cohen M, Williams G, Rothmann M,.