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      Recent Advancements in the Treatment of Rectal Gastrointestinal Stromal Tumor: In Era of Imatinib

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          Abstract

          Gastrointestinal stromal tumors (GIST) are the most common mesenchymal tumor of the gastrointestinal tract, with an annual incidence of 10–15 cases per million. However, rectal GIST has a low incidence, accounting for approximately 0.1% of all rectal tumors. The treatment of rectal GISTs is still controversial and the relative unified guidelines and consensus opinions are inadequate. Treatment is based primarily on the clinical experience of the physician. The widespread application of neoadjuvant imatinib therapy allows diversification of treatment, especially in the choice of surgical methods. Herein, we reviewed the most recent literature and summarized the new progress in rectal tumor treatment, with the aim of providing patients with more systematic and individualized therapeutic strategies.

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          Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors.

          George Demetri, Margaret von Mehren, Charles Blanke … (2002)
          Constitutive activation of KIT receptor tyrosine kinase is critical in the pathogenesis of gastrointestinal stromal tumors. Imatinib mesylate, a selective tyrosine kinase inhibitor, has been shown in preclinical models and preliminary clinical studies to have activity against such tumors. We conducted an open-label, randomized, multicenter trial to evaluate the activity of imatinib in patients with advanced gastrointestinal stromal tumor. We assessed antitumor response and the safety and tolerability of the drug. Pharmacokinetics were assessed in a subgroup of patients. A total of 147 patients were randomly assigned to receive 400 mg or 600 mg of imatinib daily. Overall, 79 patients (53.7 percent) had a partial response, 41 patients (27.9 percent) had stable disease, and for technical reasons, response could not be evaluated in 7 patients (4.8 percent). No patient had a complete response to the treatment. The median duration of response had not been reached after a median follow-up of 24 weeks after the onset of response. Early resistance to imatinib was noted in 20 patients (13.6 percent). Therapy was well tolerated, although mild-to-moderate edema, diarrhea, and fatigue were common. Gastrointestinal or intraabdominal hemorrhage occurred in approximately 5 percent of patients. There were no significant differences in toxic effects or response between the two doses. Imatinib was well absorbed, with pharmacokinetics similar to those reported in patients with chronic myeloid leukemia. Imatinib induced a sustained objective response in more than half of patients with an advanced unresectable or metastatic gastrointestinal stromal tumor. Inhibition of the KIT signal-transduction pathway is a promising treatment for advanced gastrointestinal stromal tumors, which resist conventional chemotherapy. Copyright 2002 Massachusetts Medical Society
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            Primary and secondary kinase genotypes correlate with the biological and clinical activity of sunitinib in imatinib-resistant gastrointestinal stromal tumor.

            Michael Heinrich, Robert G Maki, Christopher L Corless … (2008)
            Most gastrointestinal stromal tumors (GISTs) harbor mutant KIT or platelet-derived growth factor receptor alpha (PDGFRA) kinases, which are imatinib targets. Sunitinib, which targets KIT, PDGFRs, and several other kinases, has demonstrated efficacy in patients with GIST after they experience imatinib failure. We evaluated the impact of primary and secondary kinase genotype on sunitinib activity. Tumor responses were assessed radiologically in a phase I/II trial of sunitinib in 97 patients with metastatic, imatinib-resistant/intolerant GIST. KIT/PDGFRA mutational status was determined for 78 patients by using tumor specimens obtained before and after prior imatinib therapy. Kinase mutants were biochemically profiled for sunitinib and imatinib sensitivity. Clinical benefit (partial response or stable disease for > or = 6 months) with sunitinib was observed for the three most common primary GIST genotypes: KIT exon 9 (58%), KIT exon 11 (34%), and wild-type KIT/PDGFRA (56%). Progression-free survival (PFS) was significantly longer for patients with primary KIT exon 9 mutations (P = .0005) or with a wild-type genotype (P = .0356) than for those with KIT exon 11 mutations. The same pattern was observed for overall survival (OS). PFS and OS were longer for patients with secondary KIT exon 13 or 14 mutations (which involve the KIT-adenosine triphosphate binding pocket) than for those with exon 17 or 18 mutations (which involve the KIT activation loop). Biochemical profiling studies confirmed the clinical results. The clinical activity of sunitinib after imatinib failure is significantly influenced by both primary and secondary mutations in the predominant pathogenic kinases, which has implications for optimization of the treatment of patients with GIST.
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              Imatinib potentiates anti-tumor T cell responses in gastrointestinal stromal tumor through the inhibition of Ido

              Vinod P Balachandran, Michael J. Cavnar, Hai-shan Zeng … (2011)
              Imatinib mesylate targets mutated KIT oncoproteins in gastrointestinal stromal tumor (GIST) and achieves a clinical response in 80% of patients. The mechanism is believed to depend predominantly on the inhibition of KIT-driven signals for tumor cell survival and proliferation. Using a mouse model of spontaneous GIST, we found that the immune system contributes substantially to the anti-tumor effects of imatinib. Imatinib therapy activated CD8+ T cells and induced regulatory T cell (T reg) apoptosis within the tumor by reducing tumor cell expression of the immunosuppressive enzyme indoleamine 2,3-dioxygenase (Ido). Concurrent immunotherapy augmented the efficacy of imatinib in mouse GIST. In freshly obtained human GIST specimens, the T cell profile correlated with imatinib sensitivity and IDO expression. Thus, T cells are critical to the anti-tumor effects of imatinib in GIST and concomitant immunotherapy may further improve outcome in human cancers treated with targeted agents.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancer Manag Res
                Journal ID (iso-abbrev): Cancer Manag Res
                Journal ID (publisher-id): cmar
                Title: Cancer Management and Research
                Publisher: Dove
                ISSN (Electronic): 1179-1322
                Publication date (Electronic): 16 March 2022
                Publication date Collection: 2022
                Volume: 14
                Pages: 1141-1152
                Affiliations
                [1 ]Department of Hernia and Colorectal Surgery, The Second Hospital of Dalian Medical University , Dalian, 116023, People’s Republic of China
                [2 ]Dalian Medical University , Dalian, People’s Republic of China
                Author notes
                Correspondence: Xin Chen, Tel +86 17709872266, Email chenxincjz@gmail.com
                Author information
                http://orcid.org/0000-0002-5172-7029
                http://orcid.org/0000-0001-8122-4396
                Article
                Publisher ID: 352860
                DOI: 10.2147/CMAR.S352860
                PMC ID: 8934706
                PubMed ID: 35321404
                SO-VID: 064107de-9d59-4f39-9971-4a8ca77f5355
                Copyright © © 2022 Qu et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 22 December 2021
                Date accepted : 18 February 2022
                Page count
                Figures: 0, Tables: 8, References: 109, Pages: 12
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: gastrointestinal stromal tumors,gist,rectum,laparoscopy,surgery,neoadjuvant imatinib
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: gastrointestinal stromal tumors, gist, rectum, laparoscopy, surgery, neoadjuvant imatinib

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