Gastrointestinal stromal tumor最新文献

英文中文

A narrative review of imatinib-resistant gastrointestinal stromal tumors. 伊马替尼耐药胃肠道间质瘤综述。

Gastrointestinal stromal tumor

Pub Date : 2021-10-01 Epub Date: 2021-10-30 DOI: 10.21037/gist-21-10

Yujiro Hayashi, Vy Truong Thuy Nguyen

Objective: Review the studies that investigate the mechanisms underlying imatinib-resistant gastrointestinal stromal tumors (GIST).

Background: GIST are the most common mesenchymal tumors of the gastrointestinal (GI) tract and the most common sarcoma in humans. GIST are thought to be arise from interstitial cells of Cajal (ICC), pacemaker and neuromodulator cells in the GI tract, as well as "fibroblast"-like cells, which are another type of interstitial cells of the gut wall and also known as telocyte or platelet-derived growth factor-alpha (PDGFRA)-positive cells. The majority of GIST harbor gain-of-function mutations in either KIT or PDGFRA, and these gain-of-function mutations are mutually exclusive and most often heterozygous. GIST are responsive to the KIT/PDGFRA tyrosine kinase inhibitor (TKI), imatinib, the standard first-line drug for advanced and metastatic GIST. However, imatinib alone does not eradicate GIST despite an initial clinical benefit, and more than 90% of GIST harbor imatinib-resistance. Although second and third-generation TKIs have been developed and are currently in clinical use, they are not curative for refractory and metastatic GIST due to the emergence of clones with drug-resistant mutations. Eradication of drug-resistant GIST will cure patients with refractory GIST. Several mechanisms may contribute to refractory GIST. These mechanisms are secondary mutations in KIT and/or PDGFRA, alternative activation of tyrosine kinases, stem cells for GIST and cellular quiescence, a reversible nonproliferating state in which cells retain the ability to reenter cell proliferation.

Methods: We review our current optimal treatment approach for managing patients with advanced and refractory GIST.

Conclusions: This review explores the novel and potential therapeutic approaches to combat drug-resistant GIST.

目的：回顾有关伊马替尼耐药的胃肠道间质瘤（GIST）机制的研究：回顾有关伊马替尼耐药的胃肠道间质瘤（GIST）机制的研究：背景：胃肠道间质瘤是胃肠道最常见的间质肿瘤，也是人类最常见的肉瘤。GIST 被认为源于卡贾尔间质细胞（ICC）、胃肠道的起搏器细胞和神经调节细胞，以及 "成纤维细胞 "样细胞，后者是肠壁间质细胞的另一种类型，也被称为端粒细胞或血小板衍生生长因子-α（PDGFRA）阳性细胞。大多数 GIST 都携带 KIT 或 PDGFRA 的功能增益突变，这些功能增益突变是相互排斥的，且多为杂合突变。GIST 对 KIT/PDGFRA 酪氨酸激酶抑制剂（TKI）--伊马替尼（治疗晚期和转移性 GIST 的标准一线药物）有反应。然而，尽管伊马替尼能带来初步临床疗效，但单用伊马替尼并不能根除 GIST，超过 90% 的 GIST 对伊马替尼产生耐药性。虽然第二代和第三代 TKIs 已经开发出来并投入临床使用，但由于耐药突变克隆的出现，它们并不能根治难治性和转移性 GIST。根除耐药 GIST 将治愈难治性 GIST 患者。导致难治性 GIST 的机制有多种。这些机制包括 KIT 和/或 PDGFRA 的继发性突变、酪氨酸激酶的替代性激活、GIST 的干细胞和细胞静止（一种可逆的非增殖状态，细胞在这种状态下仍能保持重新进入细胞增殖的能力）：我们回顾了目前治疗晚期和难治性 GIST 患者的最佳方法：本综述探讨了抗药性 GIST 的新型和潜在治疗方法。

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引用次数: 0

A narrative review of surgical management of gastrointestinal stromal tumors 胃肠道间质瘤的外科治疗述评

Gastrointestinal stromal tumor

Pub Date : 2021-09-01 DOI: 10.21037/gist-21-2

I. Kalinowska, M. Zdzienicki, J. Skoczylas, P. Rutkowski

引用次数: 1

Adjuvant therapy for primary GIST: is longer really better? A narrative review 原发性GIST的辅助治疗:时间越长真的越好吗?叙述性回顾

Gastrointestinal stromal tumor

Pub Date : 2021-08-20 DOI: 10.21037/gist-21-4

Pamela W. Lu, C. Raut

引用次数: 0

Design your strategy, define your costs: third or subsequent-lines in advanced gastrointestinal stromal tumors (GIST) 设计策略，确定成本:晚期胃肠道间质瘤(GIST)的三线或后续治疗

Gastrointestinal stromal tumor

Pub Date : 2021-08-06 DOI: 10.21037/gist-21-5

J. Giuliani

引用次数: 0

Ripretinib—a new star in the firmament 雷普雷蒂尼——天空中的一颗新星

Gastrointestinal stromal tumor

Pub Date : 2021-07-30 DOI: 10.21037/GIST-21-3

A. Kollár

引用次数: 0

Dose escalation of ripretinib can lead to response in advanced gastrointestinal stromal tumor patients refractory to the standard dose: a report of two cases 利普雷替尼剂量递增可导致对标准剂量难治的晚期胃肠道间质瘤患者产生反应:两例报告

Gastrointestinal stromal tumor

Pub Date : 2021-05-31 DOI: 10.21037/GIST-21-1

P. A. Costa, Caroline Hana, N. Balaji, A. Skryd, Brianna Nicole Valdes, R. Minjares, Priscila Barreto-Coelho, Andrea P Espejo-Freire, Muhammad Hakim, Emily E. Jonczak, T. Subhawong, A. Livingstone, J. Trent, G. D'Amato

Despite an initial response, most metastatic gastrointestinal stromal tumor (GIST) patients will ultimately be refractory to all current therapies, including imatinib, sunitinib, and regorafenib. Ripretinib at 150 mg daily was recently approved as an additional line of treatment. Few options remain after ripretinib. Here we report two cases with responses to dose escalation of ripretinib after progressing on the standard dose. Case 1: A 25-year-old man was diagnosed with a kit exon 9 mutated small intestine GIST after presenting with abdominal pain. The tumor was resected, but a year later, he developed metastases to the liver and pelvis. Over the course of three years, he received multiple lines of therapies as his disease progressed, including imatinib, sunitinib, and regorafenib. He was then placed on ripretinib 150 mg daily. However, he had disease progression after two months. Ripretinib was increased to 150 mg twice a day, which he tolerated well. After three months, he had regression of his disease. Case 2: A 54-year-old male was diagnosed with an unresectable kit exon 11 mutated gastric GISTs after presenting with abdominal pain. Imatinib led to an 80% regression, allowing surgical excision. A year later, his disease recurred. Over the course of 5 years, due to multiple recurrences, he received two additional surgeries, with imatinib, sunitinib, regorafenib, and avapritinib on either the adjuvant or neoadjuvant setting. Ultimately, he developed a metastatic GIST to the left suprarenal region, retroperitoneum, and epigastric region. He was then started on ripretinib 150 mg daily, experiencing progression of his disease in three months. Ripretinib was escalated to 150 mg twice a day, which he tolerated well, and after three months, he had a regression. Dose escalation of ripretinib leads to response in patients that progressed after the standard dose, and it is well-tolerated, being a promising new treatment option in advanced GIST.

尽管最初有反应，但大多数转移性胃肠道间质瘤(GIST)患者最终对所有当前治疗都难以治愈，包括伊马替尼、舒尼替尼和瑞非尼。每日150毫克的利普雷替尼最近被批准作为一种额外的治疗方法。在利普雷替尼之后，几乎没有其他选择。在这里，我们报告了两个病例，在标准剂量进展后，对利普雷替尼剂量增加有反应。病例1:一名25岁的男子在出现腹痛后被诊断患有kit外显子9突变的小肠GIST。肿瘤被切除了，但一年后，他的肿瘤转移到了肝脏和骨盆。在三年中，随着病情的进展，他接受了多种治疗，包括伊马替尼、舒尼替尼和瑞戈非尼。然后给予每日150毫克的利普雷替尼。然而，他在两个月后病情恶化。利普雷替尼增加到150毫克，一天两次，他耐受良好。三个月后，他的病情有所好转。病例2:一名54岁男性在出现腹痛后被诊断为不可切除的kit外显子11突变胃gist。伊马替尼导致80%的消退，允许手术切除。一年后，他的病又复发了。在5年的时间里，由于多次复发，他接受了两次额外的手术，伊马替尼、舒尼替尼、瑞戈非尼和阿伐替尼作为辅助或新辅助治疗。最终，他发展为转移性间质瘤，转移至左肾上区、腹膜后和腹壁区域。随后，他开始服用每日150毫克的利普雷替尼，3个月后病情出现进展。利普雷替尼增加到150mg，每天两次，他耐受良好，三个月后，他的病情有所好转。利普雷替尼的剂量递增导致在标准剂量后进展的患者有反应，并且耐受性良好，是晚期GIST中有希望的新治疗选择。

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引用次数: 2

Avapritinib—a therapeutic breakthrough for PDGFRA D842V mutated gastrointestinal stromal tumors 阿伐替尼- PDGFRA D842V突变的胃肠道间质瘤的治疗突破

Gastrointestinal stromal tumor

Pub Date : 2021-01-01 DOI: 10.21037/gist-22-7

Evelyne Roets, N. Steeghs

引用次数: 0

The past, present, and future: the evolving role and challenges of surgery in the multimodal management of gastrointestinal stromal tumors 过去、现在和未来:手术在胃肠道间质瘤多模式治疗中的作用和挑战

Gastrointestinal stromal tumor

Pub Date : 2021-01-01 DOI: 10.21037/gist-22-10

R. Witt, Heather G Lyu, E. Keung

引用次数: 0

Resection of a giant gastrointestinal stromal tumor after failed imatinib treatment during the COVID-19 pandemic: a case report 新冠肺炎大流行期间伊马替尼治疗失败后切除巨大胃肠道间质瘤的病例报告

Gastrointestinal stromal tumor

Pub Date : 2021-01-01 DOI: 10.21037/gist-21-12

Katie Yusun Kwon, F. Iriarte, H. Hartman, Juhi Mittal, A. Di Carlo, A. Abbas

引用次数: 0

Dawn of immunotherapy treatment for gastrointestinal stromal tumors 免疫疗法治疗胃肠道间质瘤的曙光

Gastrointestinal stromal tumor

Pub Date : 2021-01-01 DOI: 10.21037/gist-22-4

S. Schuetze

© Gastrointestinal Stromal Tumor. All rights reserved. Gastrointest Stromal Tumor 2022 | https://dx.doi.org/10.21037/gist-22-4 Gastrointestinal stromal tumors (GIST) are characterized by pathogenic activating mutations in tyrosine kinases, or less commonly by loss of succinate dehydrogenase (SDH) complex activity through epigenetic silencing or loss of function mutation in one of the SDH subunits (1). A large majority of GIST contain activating mutations in KIT or platelet-derived growth factor receptor-alpha (PDGFRA) which are generally mutually exclusive. Very rarely, loss of neurofibromin-1, activation of RAS, translocation of neurotrophic receptor tyrosine kinase (NTRK) or cryptic genomic changes lead to development of GIST. A recent study suggests that spindle cell neoplasms of the gastrointestinal tract harboring translocations involving NTRK are distinct from GIST, and these malignancies respond to treatment with inhibitors of NTRK activity (2). The development of orally bioavailable small molecule inhibitors of KIT and PDGFRA substantively changed the treatment and survival of patients with locally advanced or metastatic GIST extending medial survival from less than 2 to more than 4 years with about 25% of patients surviving more than 10 years after the start of imatinib (3-5). However, secondary mutations in KIT or PDGFRA leading to resistance to kinase inhibition develop in many patients, and a minority have mutations in GIST that render primary resistance to imatinib. Once resistance to imatinib develops, the tumor progression-free interval generally is much shorter than with initial imatinib therapy (6-8). Moreover, SDH-deficient GISTs are resistant to treatment with imatinib although a minority may respond to treatment with sunitinib or other vascular growth factor receptor inhibitors. Few formal trials of non-tyrosine kinase inhibitor (TKIs) chemotherapy in treatment of advanced GIST have been conducted, but data collected prior to widespread incorporation of TKIs into the treatment of GIST suggests that GIST is resistant to conventional chemotherapy such as DNA-damaging agents (9,10). Thus, there is strong interest in developing alternative treatments for GIST in combination with TKIs in sensitive tumors, or in place of TKIs in resistant tumors. Much has been written about preclinical studies and biomarker analyses that suggests a role for immunotherapy in management of GIST (11-13). However, we are in the dawn of immunotherapy for GIST, and much needs to be learned to translate our understanding of GIST immunobiology into standard clinical care. A pilot study of imatinib combined with interferon-α2b in patients with imatinib-naïve GIST showed objective partial response in all patients treated (N=8); but, to my knowledge, a larger trial to confirm the high response rate has not been conducted (14). A pilot trial of lowdose metronomic oral cyclophosphamide combined with pembrolizumab in 10 patients with GIST produced no objective re

©胃肠道间质瘤。保留所有权利。2022年胃肠道间质瘤|https://dx.doi.org/10.21037/gist-22-4胃肠道间质瘤（GIST）的特征是酪氨酸激酶的致病性激活突变，或者不太常见的是通过表观遗传沉默或SDH亚基之一的功能缺失突变而丧失琥珀酸脱氢酶（SDH）复合物活性（1）。绝大多数GIST包含KIT或血小板衍生生长因子受体α（PDGFRA）的激活突变，这通常是互斥的。很少有神经纤维蛋白-1的缺失、RAS的激活、神经营养受体酪氨酸激酶（NTRK）的易位或神秘的基因组变化导致GIST的发展。最近的一项研究表明，含有NTRK易位的胃肠道梭形细胞肿瘤与GIST不同，这些恶性肿瘤对NTRK活性抑制剂的治疗有反应（2）。口服生物可利用的KIT和PDGFRA小分子抑制剂的开发极大地改变了局部晚期或转移性GIST患者的治疗和生存率，将中期生存期从不到2年延长到4年以上，约25%的患者在伊马替尼开始治疗后生存超过10年（3-5）。然而，KIT或PDGFRA的二次突变导致许多患者对激酶抑制产生耐药性，少数患者的GIST突变导致对伊马替尼产生原发耐药性。一旦对伊马替尼产生耐药性，肿瘤无进展间隔通常比初始伊马替尼治疗短得多（6-8）。此外，SDH缺陷型GIST对伊马替尼治疗具有耐药性，尽管少数患者可能对舒尼替尼或其他血管生长因子受体抑制剂治疗有反应。非酪氨酸激酶抑制剂（TKIs）化疗治疗晚期GIST的正式试验很少，但在将TKIs广泛纳入GIST治疗之前收集的数据表明，GIST对传统化疗（如DNA损伤剂）具有耐药性（9，10）。因此，人们对开发GIST与TKIs联合治疗敏感肿瘤或替代TKIs治疗耐药肿瘤的替代疗法非常感兴趣。关于临床前研究和生物标志物分析，已经有很多文章表明免疫疗法在GIST管理中的作用（11-13）。然而，我们正处于GIST免疫疗法的黎明，需要学习很多东西才能将我们对GIST免疫生物学的理解转化为标准的临床护理。伊马替尼联合干扰素-α2b治疗伊马替尼幼稚GIST患者的一项初步研究显示，所有接受治疗的患者都有客观的部分反应（N=8）；但是，据我所知，还没有进行更大规模的试验来证实高应答率（14）。一项针对10名GIST患者的低剂量节拍口服环磷酰胺联合pembrolizumab的试点试验没有产生客观反应（尽管1名患者的GIST略有降低），中位PFS为1.4个月（15）。节拍环磷酰胺的免疫刺激作用将为编辑评论提供最佳环境的假设

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Gastrointestinal stromal tumor

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