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Gastrointestinal Stromal Tumors: From Molecular Pathogenesis to Therapy
Published in Sherry X. Yang, Janet E. Dancey, Handbook of Therapeutic Biomarkers in Cancer, 2021
Joaquina Baranda, Stafinur Atay, Andrew K. Godwin
The true incidence of gastrointestinal stromal tumor is unclear. A report based on the SEER (Surveillance, Epidemiology, and End results) data of the National Cancer Institute in 1995 is believed to be an underestimation, as many cases were not captured in the SEER registries [34]. A 13-center cumulative tumor registry SEER database query from 1992 to 2002 determined a 25-fold age-adjusted increase in incidence of GIST, from 0.028 per 100,000 in 1992 to 0.688 per 100,000 in 2002. This increase was primarily because of the reclassification of “smooth-muscle tumors” as GISTs but also represented a 50% increase in population- and age-adjusted gastrointestinal mesenchymal tumor diagnosis since 1992 [35]. The report also suggested that the observed dramatic improvement in survival of patients with GIST coincided with the Food and Drug Administration (FDA) approval of imatinib in the treatment of advanced GIST [35].
Metastatic Gastrointestinal Stromal Tumor with Bleeding
Published in Savio George Barreto, Shailesh V. Shrikhande, Dilemmas in Abdominal Surgery, 2020
Inian Samarasam, K. Senthilnathan
Acute presentations such as gastrointestinal bleeding, perforation, and obstruction generally warrant surgical management. Acute gastrointestinal bleeding is not an uncommon presentation of a gastrointestinal stromal tumor. In the setting of a surgically resectable gastrointestinal stromal tumor, an emergency surgical resection may be performed. However, management of a patient with a locally advanced or a metastatic gastrointestinal stromal tumor, when associated with acute gastrointestinal bleeding, may pose a treatment dilemma since surgical resection of the primary tumor may be difficult or unlikley. This chapter deals with two such case scenarios – the first patient with a bleeding metastatic gastrointestinal stromal tumor and a potentially resectable primary, and the second one with a bleeding, non-resectable metastatic gastrointestinal stromal tumor.
Benign tumors
Published in Mohammad Ibrarullah, Atlas of Diagnostic Endoscopy, 2019
Gastrointestinal stromal tumor (GIST) is the commonest non-epithelial tumor of the GI tract. It arises from the interstitial cells of Cajal, a part of the autonomic nervous system located in the muscular propria. The stomach is the commonest site of its occurrence, followed by the small bowel, the esophagus and the colorectum. It commonly presents with bleeding. Mucosal biopsy is usually non-yielding; deeper biopsy may be required for diagnosis. The presence of spindle cells points to the diagnosis of GIST that is further confirmed on positive immunohistology for CD 117 (c-kit). Surgical excision is the preferred treatment. Tumor size <2 cm and a mitotic index <5/50 HPF suggest a low risk tumor.
Establishment of the prediction model and biological mechanism exploration for secondary imatinib-resistant in gastrointestinal stromal tumor
Published in Scandinavian Journal of Gastroenterology, 2022
Chao Wang, Zhanlong Shen, Kewei Jiang, Zhidong Gao, Yingjiang Ye
A gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor in the gastrointestinal tract, which is frequently driven by the auto-activated, mutant KIT receptor tyrosine kinase gene or by the platelet-derived growth factor receptor alpha (PDGFRA) [1]. Inhibition of KIT-signaling is the primary molecular target for GIST therapy, and imatinib is known as the first-line treatment for recurrent/metastatic/unresectable GIST. Unfortunately, more than half of advanced or metastatic GIST may develop secondary resistance to imatinib within 2 years after initiation of treatment [2]. One of the admitted mechanism is the acquisition of KIT or PDGFRA secondary mutations, which mostly occurs in exon 13, 14, or 17/18 mutation [3,4]. In addition, c-Kit/PDGFRA genomic alterations [5], downregulation of tumor suppressor genes expression (such as PTEN [6] and AXL [7], or abnormal activation of signaling pathways (such as PI3-K/AKT/MTOR [8] or JAK/STAT3 [9] are also potential hypotheses for secondary resistance to imatinib. Until now, the mechanism of acquired imatinib-resistant in GIST remains unclear.
Helicobacter Pylori Related Gastric Cancer Screening and Cost-Effectiveness Analysis: A Hospital-Based Cross-Sectional Study (SIGES)
Published in Nutrition and Cancer, 2022
Wen Xiang, Rui Wang, Dan Bai, Tian-Hang Yu, Xin-Zu Chen
The eligibility was assessed based on the electronic medical records reported by general practitioners, gastroenterologists, or gastrointestinal surgical oncologists. The healthy controls were collected from the health checkup in the Center of Health Checkup. The general practitioners recorded them as the asymptomatic status and cancer-free status. The gastric cancer patients were collected from the Department of Gastrointestinal Surgery. The diagnosis was proved by the ICD-10 code C16 and histology, regardless of TNM stage. Other kinds of malignancies were excluded, such as lymphoma and gastrointestinal stromal tumor. In addition, all the included observations should be tested by the 14-C UBT. For the gastric cancer patients, the UBT should be performed preoperatively, while the postoperative tests would not be considered.
Is the benefit of using adjuvant capecitabine in patients with residual triple-negative breast cancer related to pathological response to neoadjuvant chemotherapy?
Published in Expert Review of Anticancer Therapy, 2022
Özgecan Dülgar, Başak Bala Öven, Muhammed Mustafa Atcı, Rukiye Arıkan, Seval Ay, Murat Ayhan, Oğuzhan Selvi, Deniz Tataroglu Ozyukseler, Ertuğrul Bayram, Erkan Özcan, Ayşe İrem Yasin, Mahmut Gümüş
Hormone receptor status was defined as negative when immunohistochemistry test results for ER PR were negative and defined as weak positive when both tests’ results were 1–10% positive. Weak positive results were also included. HER2 expression was defined as negative when the immunohistochemistry results were negative or 1+ . When the results were 2+, we defined the negativity of HER2 according to the results of the fluorescence in situ hybridization test. The American Society of Clinical Oncology/College of American Pathologists guideline recommendations for immunohistochemical testing of ER, PR, and HER2 were used [10,11]. The ratio of stromal tumor-infiltrating lymphocyte [12] was measured in primary tumor specimen using visual assessment of standard hematoxylin and eosin (H&E) stained sections. TIL was classified in to four groups as none, low, moderate, and high. A point of 0 indicated none of sTIL; 1+, low sTIL (<30%); and 2+, moderate. The Miller-Payne grading system was used to evaluate the pathologic response. Patients with a Miller–Payne grade of V were classified as complete pathologic response, patients with a grade of IV have lost more than 90% of tumor cells, and a grade III was reduced 30% and 90% of tumor cells. Those with a grade II lost less than 30% of tumor cells, also cellularity still high, a grade I had no change malignant cells and no reduction in cellularity [2]. Patients with MPG score V were excluded. Tumors were classified according to pathological response as good pathologic response (MPG scores IV and III) and poor pathologic response (MPG scores I and II) [2].