gastrointestinal tumors

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Ligation-assisted endoscopic enucleation for the diagnosis and resection of small gastrointestinal tumors originating from the muscularis propria: a preliminary study

Ligation-assisted endoscopic enucleation for the diagnosis and resection of small gastrointestinal tumors originating from the muscularis propria: a preliminary study

Gastrointestinal tumors of muscularis propria origin in- clude leiomyomas, GISTs, neural tumors, and others. GISTs are the most common mesenchymal tumors of the gastrointestinal tract. Large GISTs with high mitotic rates are often associated with malignant behavior and display higher rates of recurrence and metastasis [14-18]. Therefore, the presence of such lesions can become a psy- chological burden to patients, even if the lesions are very small. For these reasons, some patients with such lesions prefer to undergo resection, although the management of small, incidentally discovered GISTs of <2 cm is contro- versial [19,20]. A histologic diagnosis of these lesions is sometimes needed [19-21]. EUS-guided sampling, deep bi- opsy, and endoscopic partial resection with the unroofing technique are feasible and effective procedures with which
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Molecular Diagnosis of Gastrointestinal Tumors

Molecular Diagnosis of Gastrointestinal Tumors

Juxtamembrane domain (exon 11) Juxtamembrane domain (exon 12) Extracellular domain (exon 9) Ligand-binding domain Tyrosine kinse II domain (exon 18) Imatinib (Gleevec) snsitive mut Gleev[r]

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Non-Coding RNAs and Resistance to Anticancer Drugs in Gastrointestinal Tumors.

Non-Coding RNAs and Resistance to Anticancer Drugs in Gastrointestinal Tumors.

In this review we summarise the role of non-coding RNAs for different mechanisms resulting in drug resistance (e.g. drug transport, drug metabolism, cell cycle regulation, regulation of [r]

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Role of intravenous iron in the treatment of anemia in patients with gastrointestinal tract tumors undergoing chemotherapy: a single-center, observational study

Role of intravenous iron in the treatment of anemia in patients with gastrointestinal tract tumors undergoing chemotherapy: a single-center, observational study

The study included 30 adults (n = 30), 18 men and 12 women with gastrointestinal tumors undergoing palliative or adjuvant chemotherapy diagnosed with iron-deficiency anemia. Inclusion criteria were Hb ≤ 11 g/dL or a reduction ≥ 2 g/dL since the start of the current chemotherapy regimen, and ferritin < 30 ng/mL and transferrin saturation (TSAT) < 20% or ferritin 30–800 ng/mL, and TSAT < 50%. Patients who needed to receive red blood cell transfusion, were being treated with ESAs, and received any oral iron formulation within 1 week before the screening or any intravenous iron
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Synchronous gastrointestinal cancer and gastrointestinal stromal tumors: a single institution experience

Synchronous gastrointestinal cancer and gastrointestinal stromal tumors: a single institution experience

Multiple studies showed that among patients with pri- mary GISTs, 14–27 % have synchronous gastrointestinal neoplasms. By contrast, only 3–5 % of the general popu- lation may have the gastrointestinal tumors, which re- veals a conspicuous discrepancy between the two groups. Currently, various hypotheses attempt to explain the synchronous existence of GISTs with other gastro- intestinal tumors. These hypotheses include the relations to genetic predisposition, environmental risk factors, mutagenic effect from previous radiation or chemother- apy, Helicobacter pylori infection, chronic atrophic gas- tritis, and coincidental findings [21–24]. Whether the synchronicity is a simple incidental association or a legit- imate causal relationship between the occurrences of the two tumors is still unknown. Tada et al. [23] believed that a stomach harboring a leiomyosarcoma may have a tendency to develop malignant epithelial lesions. On the basis of accumulated reports, Maiorana et al. [24] pro- posed that in cases of synchronicity, a single carcino- genic agent may have interacted with two neighboring tissues and induced the development of tumors of differ- ent origins in the same organ, such as the gene mutation of KIT or PDGFRA. However, Ponti et al. [25] specu- lated that a small subset of GISTs that are negative for the KIT- and PDGFRA-activating mutations may be inherited and may occur as part of a multi-neoplastic disease. Some researchers believe in the existence of a
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Role of Immunohistochemical Studies in Neuroendocrine Tumors of Gastrointestinal Tract.

Role of Immunohistochemical Studies in Neuroendocrine Tumors of Gastrointestinal Tract.

Incidence of neuroendocrine differentiation is common in carcinomas arising in organs that normally contain neuroendocrine cells such as the gastrointestinal tract [25]. Neuroendocrine cell expression in large intestinal adenocarcinomas was found to be more when compared with adenocarcinomas at other gastrointestinal sites (stomach) and extraintestinal sites like prostate and breast. The number of hormone products was also more in gastrointestinal tumors with neuroendocrine differentiation, upto five different hormone products have been noted in these tumors [26]. neuroendocrine cells were observed at the metastatic sites of these tumors. Chromogranin A was the most reliable marker to detect neuroendocrine expression in adenocarcinomas [25]
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Management of hemorrhage in gastrointestinal stromal tumors: a review

Management of hemorrhage in gastrointestinal stromal tumors: a review

The causes of gastrointestinal bleeding in GIST The causes of intraluminal hemorrhage of GISTs may be related to mucosal and submucosal destruction by tumor growth, invasion of nutrient vessels leading to vascular rup- ture, tumor necrosis, and the joint action of digestive juices, gastrointestinal peristalsis, and fecal transmission. GISTs are relatively fragile and more vascularized, compared with other common gastrointestinal tumors. In general, by the time symptoms of gastrointestinal bleeding appear, the tumor would already have attained a relatively large size. 44 Studies
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Pattern of Upper Gastrointestinal Malignancies as Seen at Endoscopy in Ekiti State University Teaching Hospital, Ado Ekiti, Nigeria

Pattern of Upper Gastrointestinal Malignancies as Seen at Endoscopy in Ekiti State University Teaching Hospital, Ado Ekiti, Nigeria

Gastric cancer remains the world’s third most common malignancy and the second leading cause of cancer mortality in the world [5]. A 2005 analysis of the global incidence and cancer related mortality revealed that 934,000 cases of gastric cancer occurred in 2002 and approximately 700,000 patients died annually from this problem [6]. In industrialized countries, mortality from gastric cancer has declined steadily over the years whe- reas gastric cancer remains a leading cause of death from cancer in the developing world. Geographical resi- dence and dietary habits may play a part in the pathogenesis of gastric cancer. Social class and socioeconomic conditions of the inhabitants confer a significantly increased risk of developing gastric cancer. The pattern of upper GI cancer differs in different regions of the world depending upon the genetic, cultural, dietary and so- cioeconomic factors [7]. The aim of this study was to determine the prevalence, type, pattern and the histologic characteristics of upper gastrointestinal tumors seen in patients who underwent upper gastrointestinal endoscopy at the Ekiti State University Teaching Hospital, Ado-Ekiti, Nigeria.
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Non-Hodgkin lymphoma and GIST: molecular pathways and clinical expressions

Non-Hodgkin lymphoma and GIST: molecular pathways and clinical expressions

A diffuse large-cell lymphoma (DLCL) of B-cell origin is a lymphoid neoplasm with diverse clinical manifestations. These neoplasms present as masses and grow rapidly, and cause symptoms when they infiltrate tissues or obstruct organs. These neoplasms can present either with B symptoms (fever, drenching night sweats, and weight loss) or pain when the lymphomatous mass enlarges rapidly. 1 Gastrointestinal stromal tumors (GISTs)

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Management Colorectal Gastrointestinal Stromal Tumors (Gists) in Surabaya

Management Colorectal Gastrointestinal Stromal Tumors (Gists) in Surabaya

Immunohistochemically, GISTs are usually positive for KIT (CD117), a transmembrane receptor that is nor- mally expressed on the myenteric plexus of the normal adult, among others tissues. All our cases immunocyto- chemical staining for CD117 is Positive. Approximately 70% of GISTs coexpress CD34, and they also may be positive for smooth muscle actin and rarely for desmin and S-100 protein. However, the term GIST is only ap- plied to gastrointestinal mesenchymal neoplasms witch are c-kit positive, with rare exceptions. Approximately 95% of GISTs are positive for expression of the KIT (CD117, stem cell factor receptor) protein and as well as 70% - 80% of GISTs expressing CD34, the human progenitor cell antigen [1]-[3]. Risk of malignancy is based on the primary tumor diameter and the mitotic count. A mitotic index over 5 per 50 high-power field (HPF)
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Motesanib inhibits Kit mutations associated with gastrointestinal stromal tumors

Motesanib inhibits Kit mutations associated with gastrointestinal stromal tumors

Motesanib is an orally administered small-molecule antagonist of vascular endothelial growth factor recep- tors (VEGFR) 1, 2, and 3; PDGFR and Kit [9,10]. In clini- cal studies, motesanib has shown encouraging efficacy in the treatment of patients with advanced solid tumors [10- 13]. In biochemical assays, motesanib potently inhibits the activity of both Kit (50% inhibitory concentration [IC 50 ] = 8 nM) and PDGFR (IC 50 = 84 nM) [9], suggesting that it may have direct antitumor activity in GIST [14,15]. The aim of this study was to characterize the ability of motesanib to inhibit the activity of wild-type Kit in vitro and in vivo, and to investigate differences in the potency of motesanib and imatinib against clinically important primary activating Kit mutants and mutants associated with secondary imatinib resistance. The results suggest that motesanib has inhibitory activity against primary Kit muta- tions and some imatinib-resistant secondary mutations.
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Prognostic impact of gastrointestinal bleeding and expression of PTEN and Ki 67 on primary gastrointestinal stromal tumors

Prognostic impact of gastrointestinal bleeding and expression of PTEN and Ki 67 on primary gastrointestinal stromal tumors

AFIP: Armed Forces Institute of Pathology; CI: confidence interval; DAB: 3,3 ′ -diaminobenzidine; EDTA: ethylenediaminetetraacetic acid; FFPE: formalin-fixed paraffin-embedded; GI: gastrointestinal; GIST: gastrointestinal stromal tumor; H & E: hematoxylin and eosin; ICC: interclass correlation coefficient; IgG: immunoglobulin G; IHC: immunohistochemistry; IM: imatinib mesylate; LI: labeling index; NIH: National Institutes of Health; NJPH: Northern Jiangsu People ’ s Hospital; PBS: phosphate-buffered saline; PDGFRA: platelet derived growth factor receptor α ; PIP3: phosphoinositol 3,4,5-triphosphate; PTEN: phosphatase and tensin homolog deleted from chromosome 10; RFS: relapse-free survival; ROC: receiver operator characteristic; TMA: tissue microarray.
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Ménétrier disease and gastrointestinal stromal tumors: hyperproliferative disorders of the stomach

Ménétrier disease and gastrointestinal stromal tumors: hyperproliferative disorders of the stomach

Ménétrier disease and gastrointestinal stromal tumors (GISTs) are hyperproliferative disorders of the stomach caused by dysregulated receptor tyrosine kinases (RTKs). In Ménétrier disease, overexpression of TGF-a, a ligand for the RTK EGFR, results in selective expansion of surface mucous cells in the body and fundus of the stomach. In GISTs, somatic mutations of the genes encoding the RTK KIT (or PDGFRA in a minority of cases) result in constitutive kinase activity and neoplastic transformation of gut pacemaker cells (interstitial cells of Cajal). On the basis of the involvement of these RTKs in the
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Collision tumors in the gastrointestinal tract: a rare case series

Collision tumors in the gastrointestinal tract: a rare case series

Due to the lack of any large series with long-term follow-up, the prognosis of such tumors has not been properly clarified. However, it seems that the survival rate is similar to that of patients with gastric adenocarcinoma but worse than that of patients with MALT-type lymphoma without gastric adenocarcinoma. 21 The incidence of a carci-

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Update on imatinib for gastrointestinal stromal tumors: duration of treatment

Update on imatinib for gastrointestinal stromal tumors: duration of treatment

Abstract: Gastrointestinal stromal tumors (GISTs) are the most common sarcoma of the gastrointestinal tract, with transformation typically driven by activating mutations of c-KIT and less commonly platelet-derived growth factor receptor alpha (PDGFRA). Successful targeting of c-KIT and PDGFRA with imatinib, a tyrosine kinase inhibitor (TKI), has had a major impact in advanced GIST and as an adjuvant and neoadjuvant treatment. If treatment with imatinib fails, further lines of TKI therapy have a role, but disease response is usually only measured in months, so strategies to maximize the benefit from imatinib are paramount. Here, we provide an overview of the structure and signaling of c-KIT coupled with a review of the clinical trials of imatinib in GIST. In doing so, we make recommendations about the duration of imatinib therapy and suggest how best to utilize imatinib in order to improve patient outcomes in the future. Keywords: adjuvant, c-KIT, mutations, resistance, treatment, gastrointestinal stromal tumors, imatinib
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Update on the treatment of gastrointestinal stromal tumors (GISTs): role of imatinib

Update on the treatment of gastrointestinal stromal tumors (GISTs): role of imatinib

possible. Patients were categorized based on response to TKI at the time of surgery (stable disease which included patients initially with unresectable or metastatic GIST who achieved a drug response to render all disease resectable and whose tumors were not growing at the time of surgery, limited disease progression or generalized disease progression) and surgical result (no evidence of disease, minimal residual disease or bulky residual disease). Results of this single center study sug- gested that response to TKI was significantly associated with surgical outcome. Seventy-eight percent of patients with stable disease at the time of surgery were rendered radiographically disease-free post-operatively, as compared to 25% and 7% of patients with limited progression and generalized progression respectively. Conversely bulky residual disease remained after surgery in 4%, 16%, and 43% of these patients respectively. One-year progression-free survival in patients with stable dis- ease, limited progression and generalized progression was 80%, 33%, and 0%. The median time to progression for patients with limited and generalized disease progression was 7.7 months and 2.9 months respectively, while the median time to progression for patients with stable disease has not been reached after a median follow-up of 14.6 months (range, 0.5 to 36.4 months). One-year overall survival was 95%, 86%, 0% respectively. The authors concluded that patients with advanced GISTs exhibiting stable disease or limited progression on TKI have prolonged survival after debulking procedures while surgery has little to offer in the setting of generalized progression. While it is clear that patients with generalized disease progression are unlikely to benefit from surgery, it is unclear from this study whether the improved progression-free and overall survival seen in patients with stable disease and limited disease progression was a result of surgical intervention or inherent tumor biology and response to TKI.
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Epidemiology, survival, and costs of localized gastrointestinal stromal tumors

Epidemiology, survival, and costs of localized gastrointestinal stromal tumors

sensitivity analyses using different algorithms to identify recurrence. First, we shortened the time interval between initial surgical resection and detection of a recurrence from 90 to 60 days using the original surgical procedures to iden- tify recurrence. Second, keeping the days between the index date and identification of a recurrence fixed at 90 days, we added the following: 1) additional procedure/HCPCS codes for biopsy (32405), excision (11642, 22900, 49201), radiation (77413, 77300), chemotherapy (96408, 96410– 96412, 96549, Q0085), and other surgical procedures (88172, 88305, 43235, 43239); 2) a surgical procedure coupled with an ICD-9 cancer diagnosis (140–239 excluding benign tumors) on the same date; and 3) identification of inpatient hospitalization with an ICD-9 cancer diagnosis (140–239 excluding benign tumors).
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Adding trans-abdominal elastography to the diagnostic tool for an ileal gastrointestinal stromal tumor: a case report

Adding trans-abdominal elastography to the diagnostic tool for an ileal gastrointestinal stromal tumor: a case report

Gastrointestinal stromal tumors (GISTs), although rare, are the most common submucosal tumors (SMTs) of the gastrointestinal (GI) tract [1]. GISTs may arise from any- where throughout the digestive tract, with 50–70% in the stomach and 30–45% in the small bowel (SB) [2, 3]. Tumor size, mitotic count, and tumor site of origin are the three key predictors of aggressive behavior and recurrence [4]. SB GISTs exhibit worse prognosis, especially in the ileum, compared to those arising in the stomach or colon [3, 5].

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Molecular subtypes of gastrointestinal stromal tumors and their prognostic and therapeutic implications.

Molecular subtypes of gastrointestinal stromal tumors and their prognostic and therapeutic implications.

In the Multinational European ConticaGIST Database analysis KIT p.W557_K558del mutants equally segregated in gastric and nongastric sites (55 vs 45%). KIT p.W557_K558del was more frequently identified in patients younger than 60 years of age (59 vs 42.4%), in tumors’ >5 cm (84.5 vs 57.7%), with MI >5/50 HPF (68.9 vs 39.4%), and classified as high risk (70.2 vs 38.9%), when compared with other KIT exon 11 mutated tumors. It was an important obser- vation that the clinicopathologic characteristics of tumors bearing KIT p.W557_K558del were comparable with the group of tumors with KIT delinc557/558, within which tumor size, mitotic rate and fraction of high-risk tumors were also significantly higher than in tumors with other KIT exon 11 mutants. KIT delinc557/558 was associated with an increased risk for tumor pro- gression with a hazard ratio (HR) of 1.45 and an inferior disease-free survival (DFS; median DFS 45.5 months; 5-year DFS 33.1%). The relatively high number of KIT del-inc557/558 mutants equally distributed in gastric and nongastric sites enabled the researchers to analyze the pos- sible impact of this genotype on DFS, depend- ing on the anatomical site of GISTs. In clear contrast with other KIT exon 11, KIT exon 9 and PDGFRA exon 18 mutations, the poor prog- nostic impact of KIT del-inc557/558 on patients’ survival was only significant in GIST localized to the stomach (p < 0.001), but not in tumors’ with nongastric origin (p < 0.26). The same asso- ciations were also evident when comparing KIT del-inc557/558 mutants with other exon11 KIT mutations, overall (p < 0.0001; or comparing gastric (p < 0.0001) and nongastric (p < 0.599) GIST. This phenomenon might be related to the observation that gastric GIST with KIT del-inc557/558 had a larger size (7 vs 5.8 cm) and a higher mitotic rate (6 vs 4/50 HPF) when Table 2. KIT and PDGFRA ‘hot spot’ mutation landscape.
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Aims and Objectives: To study the tumours of stomach with respect to etiology, site and histological types. Material and Methods: This Histopathological study of tumors of stomach and intestines’ was carried out

Aims and Objectives: To study the tumours of stomach with respect to etiology, site and histological types. Material and Methods: This Histopathological study of tumors of stomach and intestines’ was carried out

Tumors of the gastrointestinal tract show a wide variation in the histological type making the histopathological examination a must in the diagnosis of these tumors. Early diagnosis and treatment is beneficial for better management and is imperative in providing better quality of life to the patient. The result of a careful and systematic examination of surgical specimens from patients with tumors of the gastrointestinal tract play an important role in patient care and the assessment of prognosis. Despite promising findings with molecular and immunohistochemical analysis, tumor stage is still regarded as the most important prognostic factor in colorectal cancer. The other stage independent prognostic factors include histologic grade, vascular invasion, perineural invasion and tumor border configuration.
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