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1.
World J Surg Oncol ; 6: 37, 2008 Apr 04.
Article in English | MEDLINE | ID: mdl-18394167

ABSTRACT

BACKGROUND: Gastrointestinal stromal tumors (GIST) of the esophagogastric junction might pose a major problem to surgical resection. If locally advanced, extended or multivisceral resection with relevant procedural-specific morbidity and mortality is often necessary. CASE PRESENTATION: We report a case of a patient with a locally advanced GIST of the esophagogastric junction who was treated by transhiatal resection of the lower esophagus and gastric cardia with reconstruction by interposition of segment of the jejunum (Merendino procedure). Prior to resection, downsizing of the tumor had successfully been achieved by treatment with imatinib mesylate for six months. Histological proof of GIST by immunohistochemical expression of c-KIT and/or PDGF alpha Receptor is crucial to allow embarking on this treatment strategy. CONCLUSION: A multimodal approach for an advanced GIST of the esophagogastric junction with preoperative administration of imatinib mesylate could avoid extended resection. The Merendino procedure might be considered as the reconstruction method of choice after resection of GIST at this location.


Subject(s)
Antineoplastic Agents/therapeutic use , Esophagogastric Junction/pathology , Gastrointestinal Stromal Tumors/drug therapy , Gastrointestinal Stromal Tumors/surgery , Neoadjuvant Therapy/methods , Piperazines/therapeutic use , Pyrimidines/therapeutic use , Antineoplastic Agents/administration & dosage , Benzamides , Chemotherapy, Adjuvant , Esophagogastric Junction/surgery , Gastrointestinal Stromal Tumors/pathology , Humans , Imatinib Mesylate , Male , Middle Aged , Piperazines/administration & dosage , Protein Kinase Inhibitors/administration & dosage , Protein Kinase Inhibitors/therapeutic use , Pyrimidines/administration & dosage
2.
J Gastrointest Surg ; 11(11): 1573-5, 2007 Nov.
Article in English | MEDLINE | ID: mdl-17436049

ABSTRACT

Gastric neuroendocrine tumors (carcinoids) are relatively uncommon neoplasms. Some 70 to 80% of these lesions occur in patients with autoimmune body gastritis. This disorder, however, is also a risk factor for the development of conventional gastric adenocarcinomas. We report a case of a patient with autoimmune body gastritis and a well-differentiated neuroendocrine tumor of the stomach, which was removed with endoscopic full-thickness resection in sano upon signs of invasive growth several years after its first diagnosis. Histological examination surprisingly showed a composite glandular-endocrine gastric carcinoma. We discuss the histopathological genesis of the tumor and provide evidence that endoscopic full-thickness resection might be an oncologically appropriate minimally invasive treatment for such gastric lesions.


Subject(s)
Adenocarcinoma/pathology , Neuroendocrine Tumors/pathology , Stomach Neoplasms/pathology , Adenocarcinoma/metabolism , Cell Differentiation , Chromogranin A/metabolism , Female , Humans , Immunohistochemistry , Male , Middle Aged , Neuroendocrine Tumors/metabolism , Stomach Neoplasms/metabolism
3.
Oncol Rep ; 16(4): 657-61, 2006 Oct.
Article in English | MEDLINE | ID: mdl-16969476

ABSTRACT

The nonoxidative pentose phosphate pathway allows glucose conversion to ribose for DNA or RNA synthesis and glucose degradation to lactate controlled by transketolase enzyme reactions. It has been postulated, that this pathway is of the utmost importance in tumors for the proliferation process. We detected a strong upregulation of the mutated transketolase transcript (TKTL1) in a considerable number of patients with gastric cancer (GC) or cancer of the gastroesophageal junction (GEJ). While only 10.8% of the cancer tissues revealed a significant mRNA upregulation, 36.9% of the cancer tissues demonstrated a protein overexpression. We propose that TKTL1 upregulation is a common phenomenon in GC and cancer of the GEJ leading to an enhanced, oxygen-independent glucose usage which might contribute to a more aggressive tumor growth. Since molecular targeted inhibition of transketolase enzyme reactions suppresses tumor growth and metastasis, TKTL1 could be a relevant target for anti-transketolase therapies in gastric cancer.


Subject(s)
Biomarkers, Tumor , Gene Expression Regulation, Neoplastic , Mutation , Stomach Neoplasms/metabolism , Transketolase/biosynthesis , Transketolase/genetics , Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Neoplasm Metastasis , Oxygen/metabolism , RNA, Messenger/metabolism
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