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PubMed1992

[Septic arthritis due to Streptococcus bovis].

A 47-year-old man presented with arthritis of the right shoulder and spondylodiscitis by Streptococcus bovis. This microorganism is a frequent cause of endocarditis and has been associated with gastrointestinal neoplasm, mainly carcinoma of the colon; however up to the present it had not been described as an causal agent of septic arthritis. The studies carried out on the patient permitted the exclusion of the existence of a digestive neoplasm and endocarditis. Despite a prolonged evolution prior to treatment with elevated doses of penicillin G and not requiring surgical drainage, the evolution was good and no destructive lesions were produced in the shoulder joint. Hematogenous infections (in this case septic arthritis) by Streptococcus bovis may present in patients without gastrointestinal diseases or endocarditis, possibly have a low damage to skeletal structures and respond adequately to conventional treatment with penicillin G.

Arthritis, Infectious↗

PubMedDate not supplied

Long-term follow-up of patients with familial adenomatous polyposis undergoing pancreaticoduodenal surgery.

Adenomatous polyps and adenocarcinomas of the periampullary region are the most common upper gastrointestinal neoplasms encountered in familial adenomatous polyposis (FAP) patients. Tumors arising from the liver, biliary tract, and pancreas have also been reported. The purpose of this study was to review the clinical outcome of FAP patients after pancreaticoduodenal surgery for periampullary neoplasms. Of the 61 individuals participating in our prospective FAP registry, 8 underwent surgical resection of periampullary neoplasms between 1987 and 1998. The charts of these individuals were reviewed for clinical indications, type of pancreaticoduodenal surgery, postoperative complications, and outcome. Of the 8 patients identified, 7 had pancreaticoduodenectomy and 1 had duodenotomy with ampullectomy. The indications for surgery were periampullary cancer (3), severe dysplasia within a duodenal villous tumor (4), and solid-pseudopapillary tumor of the pancreas (1). At the time of pancreaticoduodenal surgery, patients ranged in age from 29-65 years, and all but one had undergone colorectal surgery, on average 16 years beforehand. Pancreatic ascites after a pylorus-sparing pancreaticoduodenectomy was the only surgical complication. At a median follow-up of 70.5 months (range 37-162), 2 patients had died, neither from their periampullary neoplasm. The patient treated by local excision subsequently developed gastric cancer arising from a polyp and went on to gastrectomy. Another patient developed confluent benign jejunal adenomas just beyond the gastroenteric anastomosis almost 12 years after pancreaticoduodenectomy for severe dysplasia of a duodenal villous adenoma. Pancreaticoduodenectomy is a safe and appropriate surgical option for FAP patients with duodenal villous tumors containing severe dysplasia or carcinoma. Postoperative morbidity was minimal and there was no perioperative mortality. Good long-term prognosis can be expected in completely resected patients although subsequent proliferative and/or neoplastic lesions may still be detected in the gastrointestinal tract with prolonged follow-up.

Adenoma↗

PubMed2005

[A case of giant gastric villous tumor with carcinomatous change].

Villous tumors of the stomach are somewhat rare with approximately 100 cases only reported in the literatures and have tendency to undergo malignant transformation as high as 72%. They are frequently multiple and associated with other gastrointestinal neoplasm. Thirty percent of them are associated with an independent gastric carcinoma. Gastric villous tumor has certain radiologic characteristics that may permit a preoperative diagnosis and also some distinctive clinicopathologic features which make early diagnosis and proper treatment possible. We experienced a 64-year-old man who complained of prolonged general weakness, weight loss for several months and left upper quadrant pain for four days. Esophagogastroduodenoscopy and barium study of upper gastrointestinal tract demonstrated typical, irregular, frond-like surfaced villous tumor occupying nearly whole gastric lumen and located eccentrically along the lesser curvature side. Endoscopic biopsy of the tumor revealed a gastric villous tumor with carcinomatous change.

Adenoma, Villous↗

PubMed1993

A new tumor-associated antigen defined by a monoclonal antibody directed to gastric adenocarcinoma.

BACKGROUND: To develop useful markers for the gastrointestinal neoplasms, the authors have established a new monoclonal antibody (MoAb), FU-MK-1, directed to gastric adenocarcinoma. METHODS: The MoAb was produced by a mouse hybridoma technique by immunizing a BALB/c mouse with cancerous ascites derived from a poorly differentiated adenocarcinoma of the stomach. RESULTS: FU-MK-1 did not react with the normal adult gastric mucosa, but did react with most carcinomas of the gastrointestinal tract. In addition, the MoAb recognized cholangiocarcinomas (CC), but it did not react with hepatocellular carcinomas (HCC). Furthermore, in the combined type tumor consisting of a mixture of HCC and CC, the MoAb react only with CC element, but not with pseudoglandular structures in the HCC areas. These results indicate that FU-MK-1 is a useful antigenic marker for distinguishing HCC from CC in the liver. Furthermore, because this MoAb retains its reactivity with formalin-fixed paraffin-embedded material, it may become a useful reagent for routine or retrospective immunohistologic studies. The molecular weight of the FU-MK-1 antigen was estimated to be ca. 41,000 dalton by the Western blot analysis. Periodic acid and trypsin treatment on the antigen suggested that the antigenic determinant is a glycoprotein. CONCLUSIONS: This MoAb may contribute to the histopathologic and immunologic studies of the digestive system.

Adenocarcinoma↗

PubMed2005

Analysis of prognostic and immunohistochemical factors in gastrointestinal stromal tumors with malignant potential.

The aim of this study was to analyze 37 patients with malignant primary gastrointestinal stromal tumors and to compare the findings and their therapeutic implications with those previously reported. The medical records of 37 patients who were diagnosed and operated on between January 1996 and December 2002 were retrospectively reviewed. The patients' age, tumor size, type of surgery, histologic type, mitotic counts, presence of necrosis, Ki-67 proliferative index, National Institutes of Health 2001 consensus classification, immunohistochemical staining, and recurrence were examined to analyze factors affecting survival. Overall actuarial survival for all patients was 46%. When analyzed by type of resection, the complete resection group (R0 resection) had a mean overall survival of 48.2 +/- 6.18 months compared with the patients with incomplete resection (R1-R2) who survived a mean of 10.8 +/- 3.2 months (P=0.00). Univariate analysis showed development of recurrence (P=0.00), tumor size of 8 cm or greater (P=0.05), Ki-67 proliferative index greater than 0.82 (P=0.0448), desmin staining (P=0.0076), age younger than 49 years (P=0.0009), and incomplete resection (P=0.00) to be significantly correlated with a poor survival. In multivariate analysis, desmin staining (P=0.031), tumor size (P=0.033), age (P=0.01), recurrence (P=0.038), and R0 resection (P=0.02) were significant independent prognostic factors. We recommend that more careful preoperative and more frequent postoperative follow-up examinations be performed for patients with large tumors, age of younger than 49 years, and Ki-67 proliferative index greater than 0.82.

Adolescent↗

PubMed2006

Cyclooxygenase-2 expression and clinical outcome in gastrointestinal stromal tumors.

The significance of cyclooxygenase-2 (COX-2) expression in mesenchymal tumors has not been completely described. We analyzed clinicopathologic variables and COX-2 protein expression in all mesenchymal tumors of the GI tract that were treated at our institution between 1990 and 2002. Paraffin-embedded specimens were immunohistochemically stained for KIT and COX-2 protein. KIT-positive tumors were diagnosed as gastrointestinal stromal tumors (GIST). Among 42 available specimens, 38 tumors were diagnosed as GIST and four were non-GIST mesenchymal GI tumors (KIT negative). The median overall survival for the GIST patients was 34 months. Ninety-two percent of GIST expressed COX-2 protein. COX-2 protein was not expressed in any of the non-GIST tumors. GIST patients with negative or low COX-2 expression developed disease recurrence and/or died of their disease in 37% of the cases, compared with 18% for GIST patients with high COX-2 expression (difference not statistically significant). The vast majority of mesenchymal tumors of the GI tract are GIST that express COX-2 protein. As opposed to known predictors of GIST behavior such as tumor size and mitotic count, levels of COX-2 protein expression did not correlate with clinical outcome.

Biomarkers, Tumor↗

PubMedDate not supplied

Efficacy of STI571 for a patient with metastatic gastrointestinal stromal tumor.

A 65-year-old man was referred to our hospital for evaluation of his huge abdominal tumor. He was diagnosed as having a gastrointestinal stromal tumor arising from the stomach. Seven months after surgery, multiple liver metastases and mesenteric dissemination occurred. He was medicated with STI571, which works by blocking proliferation of malignant cells with expression of c-kit. The tumors shrank and serum lactate dehydrogenase and alkaline phosphatase concentrations fell to below the normal limit three months later. STI571 was effective medicine for the metastatic gastrointestinal stromal tumor for six months in this case.

Aged↗

PubMed2001

Estrogens and colorectal cancer.

In recent years, several lines of epidemiologic, clinical and experimental evidences have been reported showing that estrogen hormones may be involved in malignant colorectal tumors. The sex differences in site-specific incidence, the increased incidence of colonic cancer in women with breast cancer, the protective effect of increasing parity and the reduced risk among women taking postmenopausal hormones, are all elements suggesting that sex hormones may play a role. Male rats experimentally exposed to the carcinogen dimethylhydrazine, have twice the risk of developing colon cancer and significantly shorter survival times than their female counterparts. Along with the clinical, experimental and epidemiologic findings there are also biologic reasons why estrogen may be protective. Most estrogen action appears to be exerted via the estrogen receptors (ERs) on target cells. ERs have been reported in several solid tumors including gastrointestinal neoplasms such as esophageal, gallbladder, gastric and colorectal cancer. At the end of 1995, a second ER (ER-beta) was cloned from the rat prostate cDNA library and subsequently, the human and mouse homologs. Its demonstration in normal and neoplastic human colorectal tissues and "in vitro" in colonic epithelial cells, has renewed interest in investigating the existence of two ER subtypes. The presence of two ERs could explain the selective actions of estrogens on different target tissues and, particularly, on the gastrointestinal tract. Finally, our studies suggest that estrogens and their receptors play an important role in the growth and progression of colorectal tumors, by interacting with other molecules required for cell proliferation like growth factors and polyamines.

Animals↗

PubMed2006

Surgical treatment of patients with initially inoperable and/or metastatic gastrointestinal stromal tumors (GIST) during therapy with imatinib mesylate.

BACKGROUND: The aim of the study was to analyze the surgical possibilities of unresectable and/or metastatic GIST CD117(+) patients during imatinib treatment. METHODS: We analyzed the results of surgery in 141 patients treated with imatinib for initially inoperable and/or metastatic GIST CD117(+). Median follow-up time was 12 months (range: 3-26). RESULTS: Surgery was performed as subsequent treatment in 24 patients (Group I, 17%) for resection of residual disease after complete/partial response and lack of further response to imatinib and as salvage therapy in eight patients (Group II, 6%), who progressed on initially successful imatinib therapy. In Group I, the viable GIST cells were not detected histologically in only three resection specimens. The first five patients in Group I did not receive imatinib further and we observed four recurrences. In next 19 patients, continuing imatinib after surgery, we observed only one relapse. In Group II, we continued imatinib therapy after high-risk surgical procedures, but in five patients we observed subsequent progression. CONCLUSIONS: Surgical removal of residual disease during imatinib treatment may allow for complete remission in selected GIST patients after response to therapy, theoretically prolonging durable remission, but it is necessary to continue imatinib for its maintenance.

Adult↗

PubMedDate not supplied

Surgical interventions during STI 571 treatment of metastatic GIST: experience in six patients.

Gastrointestinal stromal tumours (GIST), previously classified as smooth muscle tumours, are the most common mesenchymal tumours of the digestive tract. Since the discovery of KIT (CD 117) expression, these tumours can be diagnosed confidently by pathology. Until recently, surgery was the only treatment available because these tumours were not sensitive to chemotherapy nor radiation therapy. In the long run most of these tumours recurred in the abdominal cavity or in the liver. Recently a new drug STI 573 (Glivec) showed very promising results in metastatic disease with response rates of about 65%. In six patients treated at our center, surgery was indicated during STI therapy because of subobstruction, skin necrosis, abdominal distention, bleeding. Surgery proved to be safe and efficient, allowing continuation of STI therapy in much better circumstances.

Adult↗

PubMed2004

Gastrointestinal stromal tumours in a single institute: is there an association to other gastrointestinal malignancies?

Our knowledge of Gastrointestinal Stromal Tumours (GIST) has been broadened in the last few years by the discovery of the key function of c-kit tyrosine kinase mutation in their pathogenesis. A single institution database is presented and a hypothesis is examined regarding probable connection between GIST and other gastrointestinal malignancies. Between 2000 and 2004 20 patients were admitted to our department with GIS tumour. With the addition of three cases detected between 1991 and 2000, and proved to be GIST retrospectively, 23 cases are followed. Mean age was 64.52 years, male to female ratio 11:12. Ten tumours originated from the stomach, ten from small bowel, one from rectum and two from mesenterium. All patients underwent surgery, 16 operations were completed with R0 radicality, one R1 and four R2 resections were performed. Follow-up ranged from 1 to 157 months. Five out of 23 patients died (21.7%), six patients live with metastatic disease, twelve are disease free. Amongst patient-, tumour- and treatment-related factors the prognostic significance of Fletcher's risk and radicality of resection was demonstrated (p<0.05). Significantly more synchronous or metachronous gastrointestinal malignancies were found is this population of GIST patients, when compared to the prevalence of malignancies in normal Hungarian population (p<0.001).

Aged↗

PubMed2004

Some lessons learned from imatinib mesylate clinical development in gastrointestinal stromal tumors.

Imatinib mesylate is a molecular-targeted agent, shown to be effective in chronic myeloid leukemia and gastrointestinal stromal tumors (GIST). The latter may currently serve as a model on which speculating how the future of molecular-targeted therapy in solid tumors will be. So far, some lessons have been learnt. 1) Molecular-targeted therapy can be effective in the advanced disease setting, resulting in major tumor responses. 2) Patterns of tumor responses may be peculiar, radiologically and pathologically. 3) Anti-tumor activity may be highly predictable by assessing tumor molecular biology. 4) The methodology of clinical development of molecular-targeted agents may differ from standard chemotherapy in some respects, because, say, the preclinical rationale may be stronger, thus increasing the Bayesian prior probability of efficacy, or the optimal dose cannot be determined separately from the assessment of activity and efficacy. 5) Molecular-targeted agents will hardly remain "orphan drugs", if effective. 6) While an obvious impact on survival in the advanced disease setting has been clearly demonstrated, the biologic and clinical impact of molecular-targeted therapy still needs to be elucidated. Its eradicating capabilities, as well as the implications of secondary resistance, are to be understood. 7) Integrated, multimodality approaches, including surgery, may still be of value in the molecular-targeted therapy era.

Benzamides↗

PubMed2006

Fine-needle aspiration of pancreatic serous cystadenoma: cytologic features and diagnostic pitfalls.

BACKGROUND: The preoperative diagnosis of pancreatic serous cystadenoma (SCA) is important because as a typically benign tumor it can be treated expectantly, whereas many other cystic tumors require excision. This study examines the cytology, clinical and radiologic features, diagnostic accuracy of fine-needle aspiration (FNA), and potential pitfalls associated with this rare tumor. METHODS: Cytomorphologic features were retrospectively reviewed from 28 FNAs of SCA from 21 patients. FNA biopsies were guided by percutaneous computed tomographic or ultrasonographic imaging in 10 cases and by endoscopic ultrasonographic imaging in 18 cases. Corresponding histology (14 tumors) and clinical/imaging findings were also evaluated. RESULTS: Patients typically presented with upper abdominal discomfort or asymptomatically. Radiologically, a well-demarcated, multiloculated cystic mass involving the pancreatic head or uncinate process was common. Aspirates were sparsely cellular against a clean or granular, proteinaceous background. Tumor cells formed loose clusters or monolayered sheets composed of cuboidal cells with indistinct cell borders and granular or clear cytoplasm that was often stripped from the nucleus. Nuclei were small, round, with fine chromatin and indistinct nucleoli and devoid of mitotic activity. Seven (25%) of the aspirates were initially classified as "consistent with SCA," 6 (21%) as "no malignant cells," 3 (11%) as "nondiagnostic specimen," 3 (11%) as "suspicious for malignancy," 3 (11%) as "rare atypical cells," and 6 (21%) as "probably or consistent with mucinous cystic neoplasm." Features causing diagnostic difficulty were scant cellularity, papillary groups, nuclear atypia, and columnar cells mimicking those of mucinous neoplasms. Gastrointestinal (GI) epithelium and mucin also caused confusion. The detection of intracytoplasmic glycogen (3 of 6 cases) and cyst fluid analysis (2 of 2 cases) showing low viscosity and low or undetectable levels of carcinoembryonic antigen, CA 19.9, and amylase enhanced diagnostic confidence. CONCLUSIONS: Diagnosing SCA by FNA is challenging. Familiarity with its morphologic spectrum, use of ancillary studies, and correlation with clinical/radiologic findings greatly improves diagnostic accuracy. Contaminating GI epithelium and mucin should be distinguished from components of a mucinous neoplasm.

Adult↗

PubMed1994

The natural history of surgically treated primary adenocarcinoma of the appendix.

OBJECTIVE: The aim of this investigation was to determine the prognostic variables and optimal surgical procedure for patients with adenocarcinoma of the appendix. SUMMARY BACKGROUND DATA: Primary adenocarcinoma of the appendix is a rare malignancy that constitutes less than 0.5% of all gastrointestinal neoplasms. However, the prognostic factors and the preferred surgical procedure and outcome are poorly understood. METHODS: The authors reviewed their institutional experience from 1976 to 1992 in treating 94 consecutive patients with primary adenocarcinoma of the appendix. Patients with carcinoid tumors or those in whom the diagnosis of primary cecal cancer could not be ruled out were excluded from the study. RESULTS: Fifty-two (55%) patients had the mucinous variety, of which 22 had pseudomyxoma peritonei; the other 45% had the colonic and adenocarcinoid types of tumor. The most common presentation was that of acute appendicitis. Interestingly, in no patients was the correct diagnosis made before surgery, and it was entertained intraoperatively in only 30 patients (32%). The cure 5-year survival rate was 55%, but it varied with stage (A, 100%; B, 67%; C, 50%; and D, 6%; p < 0.01) and with grade (I, 68%, and III, 7%; p < 0.01). Patients with the mucinous type had a better prognosis than those with the colonic type (p < 0.01). The survival rate was superior after right hemicolectomy versus appendectomy alone (68% vs. 20%, p < 0.001). Right hemicolectomy performed as a secondary procedure resulted in the upstaging of 38% of the patients' tumors. A second primary malignancy occurred in 33 patients (35%), of which 17 were located in the gastrointestinal tract. CONCLUSIONS: Primary adenocarcinoma of the appendix should be treated by right hemicolectomy, even if it is a secondary procedure. Surveillance for synchronous or metachronous tumors, especially in the gastrointestinal tract, is warranted.

Actuarial Analysis↗

PubMed2004

Epidermal growth factor receptor tyrosine kinase inhibition represses cyclin D1 in aerodigestive tract cancers.

PURPOSE: Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are active in cancer therapy. Mechanisms engaged during these clinical responses need to be determined. We reported previously that epidermal growth factor stimulation markedly increased cyclin D1 protein expression in human bronchial epithelial (HBE) cells, and this was opposed by chemoprevention with all-trans-retinoic acid. The current study sought to determine whether the EGFR TKI erlotinib repressed cyclin D1 protein expression in immortalized HBE cells, lung cancer cell lines, and clinical aerodigestive tract cancers. EXPERIMENTAL DESIGN: The BEAS-2B immortalized HBE cell line was exposed to varying concentrations of erlotinib, and effects on proliferation, cell cycle distribution, G1 cyclin expression, and cyclin D1 reporter activity were measured. Non-small-cell lung cancer cell lines were also evaluated for changes in proliferation and cyclin protein expression after erlotinib treatments. A proof of principle clinical trial was conducted. During this study, patients underwent a 9-day course of erlotinib treatment. Pretreatment and posttreatment tumor biopsies were obtained, and changes in candidate biomarkers were determined by immunostaining. Plasma pharmacokinetics and tumor tissue erlotinib concentrations were measured. RESULTS: Erlotinib, at clinically achievable dosages, repressed BEAS-2B cell growth, triggered G1 arrest, and preferentially reduced cyclin D1 protein expression and transcriptional activation. Erlotinib also preferentially repressed proliferation and cyclin D1 protein expression in responsive, but not resistant, non-small-cell lung cancer cell lines. This occurred in the presence of wild-type EGFR sequence at exons 18, 19, and 21. Five patients were enrolled onto an erlotinib proof of principle clinical trial, and four cases were evaluable. Pharmacokinetic studies established therapeutic erlotinib plasma levels in all patients, but tissue levels exceeding 2 micromol/L were detected in only two cases. Notably, these cases had pathological evidence of response (necrosis) in posttreatment biopsies as compared with pretreatment biopsies. In these cases, marked repression of cyclin D1 and the proliferation marker Ki-67 was detected by immunohistochemical assays. Cases without pathological response to erlotinib did not exhibit changes in cyclin D1 or Ki-67 immunohistochemical expression and had much lower erlotinib tissue levels than did responding cases. CONCLUSIONS: Taken together, these in vitro and in vivo findings provide direct evidence for repression of cyclin D1 protein as a surrogate marker of response in aerodigestive tract cancers to erlotinib treatment. These findings also provide a rationale for combining an EGFR TKI with an agent that would cooperatively repress cyclin D1 expression in clinical trials for aerodigestive tract cancer therapy or chemoprevention.

Biomarkers, Tumor↗

PubMed2007

Surgical resection of gastrointestinal stromal tumors after treatment with imatinib.

BACKGROUND: Surgical resection of gastrointestinal stromal tumors (GISTs) has been the most effective therapy for these rare tumors. Imatinib has been introduced as systemic therapy for locally advanced and metastatic GIST. In this study, the surgical resection rates and long-term outcomes of patients treated with preoperative imatinib for locally advanced primary, recurrent, or metastatic GISTs were evaluated. METHODS: Patients were retrospectively assessed for completeness of surgical resection and for disease-free and overall survival after resection. RESULTS: Forty-six patients underwent surgery after treatment with imatinib. Eleven were treated for locally advanced primary GISTs for a median of 11.9 months, followed by complete surgical resection. All eleven were alive at a median of 19.5 months, and ten were free of disease. Thirty-five patients were treated for recurrent or metastatic GIST. Of these, eleven underwent complete resection. Six of the eleven patients had recurrent disease at a median of 15.1 months. All eleven patients were alive at a median of 30.7 months. Patients with a partial radiographic tumor response to imatinib had significantly higher complete resection rates than patients with progressive disease (91% vs. 4%; P < .001). Of the 24 patients with incomplete resection, 18 initially responded to imatinib but were unable to undergo complete resection after they progressed before surgery. CONCLUSIONS: Preoperative imatinib can decrease tumor volume and is associated with complete surgical resection in locally advanced primary GISTs. Early surgical intervention should be considered for imatinib-responsive recurrent or metastatic GIST, since complete resection is rarely achieved once tumor progression occurs.

Adult↗

PubMed2005

[Gastrointestinal stromal tumors: definition, histological, immunohistochemical, and molecular features, and diagnostic strategy].

Gastrointestinal stromal tumors (GISTs) are the most frequent mesenchymal tumors of the gastrointestinal tract. Major advances in their definition and classification and the understanding of their molecular mechanisms have recently been made. These advances have resulted in the delineation of a treatment that has become a model of targeted therapy in oncology. GISTs are defined as tumors of the gastrointestinal tract, but also of the mesentery and peritoneum, constituted by a proliferation of usually spindle-shaped, rarely epithelioid cells, usually, but not consistently expressing the KIT protein. Most GISTs are associated with molecular abnormalities in two target genes: KIT (which encodes the KIT protein) and PDGFRA (which encodes the A chain of the PDGF receptor). The diagnosis of GIST relies on histological arguments (proliferation of spindle-shaped cells in 70% of cases, of epithelioid cells in 20%; histological variants are rare and sometimes misleading) and on immunohistochemical arguments (expression of KIT in 95%, usually associated with CD34 expression in 60%-70% of cases). The demonstration of mutations in target genes is required only in cases that are histologically suggestive but KIT-negative; beyond this indication, this is only undertaken in research protocols. The differential diagnosis of GIST includes the other mesenchymal tumors of the gastrointestinal tract, such as leiomyomas and leiomyosarcomas, and the digestive locations of some sarcomas; it relies on both histological and immunohistochemical arguments. The evaluation of the prognosis is essential. According to the current concept, every GIST carries a risk of malignancy, which may vary from very low to very high. Prognosis is based on a simple algorithm using two histoprognostic parameters, i.e., tumor size and mitotic index. The treatment of localized GIST is surgical resection, which must be complete; that of advanced or unresectable GIST is based on the use of a targeted therapy, imatinib, which is a pharmacological antagonist of the KIT protein. Proper understanding and utilisation of the diagnostic criteria and classification of GIST by pathologists are essential for good patient management.

Adult↗

PubMed2006

Endoscopic submucosal dissection for early gastric cancer: results and degrees of technical difficulty as well as success.

BACKGROUND AND STUDY AIMS: Endoscopic submucosal dissection (ESD) is a new method for the curative treatment of early gastrointestinal neoplasms, which was developed in order to increase the en bloc and R0 resection rate, especially for lesions larger than 20 mm in diameter. Drawbacks of ESD include the fact that it is technically a substantially more difficult procedure and that it is associated with a higher perforation rate. A retrospective study was therefore carried out to analyze cases in relation to the procedure time and resection success, and these factors were correlated with the characteristics of the lesions. PATIENTS AND METHODS: From January 2002 to November 2005, 196 lesions in 185 patients with early gastric cancer were treated using ESD in our hospital. The rates of curative en bloc resection, the incidence of perforation, and the procedure times were analyzed in relation to lesion size (small, 20 mm or less in diameter; large, over 20 mm), location (upper, middle, or lower third of the stomach) and the presence or absence of ulceration. RESULTS: The rate of curative en bloc resection was 84 % (93 % of the lesions overall were resected in one piece), with a perforation rate of 6.1 % (all perforations were managed endoscopically) and a mean procedure time of 68 min. The rate of curative en bloc resection differed significantly depending on the location of the lesion (upper vs. middle vs. lower, 74 % vs. 77 % vs. 91 %; P < 0.05), as well as on the size of the lesion (> 20 mm vs. 20 mm or less, 59 % vs. 89 %; P < 0.0001). There were also significant differences in the mean procedure times in relation to the location of the lesion (upper vs. middle vs. lower, 105 min vs. 81 min vs. 45 min; P < 0.0001) and the size of the lesion (> 20 mm vs. 20 mm or less, 124 min vs. 55 min; P < 0.0001), as well as the presence of ulceration (positive vs. negative, 97 min vs. 65 min; P < 0.05). With regard to perforation rates, significant differences were also observed in relation to the location of the lesion (upper vs. middle vs. lower, 22.6 % vs. 2.8 % vs. 3.2 %; P < 0.0005) and size of the lesion (> 20 mm vs. 20 mm or less, 16.2 % vs. 3.8 %; P < 0.005). No local recurrences of curatively resected lesions (n = 119) were observed after a follow-up period of 1 year. CONCLUSIONS: The difficulty of ESD depends on the location and size of the lesion, as well as on the presence of ulceration. We would recommend that trainees should begin by carrying out ESD on lesions with a diameter of less than 20 mm without ulceration that are located in the lower third of the stomach.

Adult↗