Granular cell tumors are relatively uncommon benign laryngeal lesions thought to originate from Schwann cells. The granular cell tumor occurs everywhere in the body, especially in the oral cavity. Most oral cases are located in the tongue. It has no preference for race, sex, and age. Because pseudoepitheliomatous hyperplasia is frequently associated with granular cell tumors, it should be differentiated from squamous cell tumors. Confirmative diagnosis should be made histopathologically and supported by immunohistochemical staining using S-100. Treatment of a granular cell tumor consists of a wide local excision by the endoscopic, transoral or laryngofissure methods. Recently, CO2 laser has been used to remove granular cell tumor with clear resection margin. We have recently experienced a granular cell tumor of larynx, so we report it with a review of literatures.
Continental Population Groups ; Diagnosis ; Granular Cell Tumor* ; Humans ; Hyperplasia ; Larynx* ; Lasers, Gas ; Mouth ; Schwann Cells ; Tongue

A 27-year-old woman presented with epigastric pain. Abdominal computed tomography revealed an irregular ulcer with circumferential thickening of the gastric antral wall. An endoscopy suggested advanced gastric cancer or gastric lymphoma. Biopsy of the lesion showed an inclusion body of the cytomegalovirus and positive immunohistochemical staining of the infected cell for cytomegalovirus. A thorough evaluation of her immune system revealed no abnormality. General supportive treatment for gastric ulcer did not relieve her symptoms. Intravenous infusion of ganciclovir improved her symptoms and healed the ulcer. We report a case of cytomegalovirus-associated gastric ulcer mimicking malignancy in an immunocompetent woman.
Adult ; Biopsy ; Cytomegalovirus* ; Endoscopy ; Female ; Ganciclovir ; Humans ; Immune System ; Inclusion Bodies ; Infusions, Intravenous ; Lymphoma ; Stomach Neoplasms* ; Stomach Ulcer* ; Ulcer

PURPOSE: Chemotherapy is the treatment of choice for small-cell lung cancer (SCLC). Despite the high response rates with first-line therapy, most patients eventually experience disease progression, and finally become candidates for second-line therapy. Topotecan is the only single agent currently approved in the United States for the treatment of a recurrent disease. The aim of this study was to evaluate its efficacy in patients with of previously treated, but relapsed and refractory, SCLC. MATERIALS AND METHODS: Twenty-five patients, who had taken topotecan as a second-line therapy, between March 1999 and October 2002, were reviewed. The patients were divided into two groups: (1) One group were the patients that had failed the first-line treatment within 3 months from end of the chemotherapy (refractory group, RG); and (2) the other group were those that responded to the first-line treatment, but who progressed 3 months after the end of the chemotherapy (sensitive group, SG). Topotecan was administered, intravenously, at a dose of 1.5 mg/m2, within 30 minutes, for five consecutive days every 3 weeks. RESULTS: There was only one partial response in the SG (3.8%), but there were 9 stable diseases, 4 in the SG and 5 in the RG; 15.4 and 19.2%, respectively. The median survivals were 6.9 and 5.2 months in SG and RG, respectively (p=0.162). There were ninety-nine chemotherapy cycles. The toxicities were mainly hematological. There were 26 incidences of Grades III and IV neutropenia, and the non hematological toxicities were mild. CONCLUSION: It was concluded that topotecan is not so effective in the treatment of patients with relapsed and refractory SCLC, despite its predictable and manageable toxicity. The incorporation of topotecan in combination chemotherapy regimens for treatment of SCLC is now warranted.
Disease Progression ; Drug Therapy ; Drug Therapy, Combination ; Humans ; Incidence ; Lung Neoplasms* ; Lung* ; Neutropenia ; Retrospective Studies* ; Topotecan* ; United States

BACKGROUND: Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis, including stimulating the proliferation and migration of vascular smooth muscle cells (VSMCs). It has been known that diabetes is associated with accelerated cellular proliferation via VEGF, as compared to that under a normal glucose concentration. We investigated the effects of selective blockade of a VEGF receptor by using anti-Flt-1 peptide on the formation and hyperplasia of the neointima in balloon injured-carotid arteries of OLETF rats and also on the in vitro VSMCs' migration under high glucose conditions. MATERIAL AND METHOD: The balloon-injury method was employed to induce neointima formation by VEGF. For 14 days beginning 2 days before the ballon injury, placebo or vascular endothelial growth factor receptor-1 (VEGFR-1) specific peptide (anti-Flt-1 peptide), was injected at a dose of 0.5 mg/kg daily into the OLETF rats. At 14 days after balloon injury, the neointimal proliferation and vascular luminal stenosis were measured, and cellular proliferation was assessed by counting the proliferative cell nuclear antigen (PCNA) stained cells. To analyze the effect of VEGF and anti-Flt-1 peptide on the migration of VSMCs under a high glucose condition, transwell assay with a matrigel filter was performed. And finally, to determine the underlying mechanism of the effect of anti-Flt-1 peptide on the VEGF-induced VSMC migration in vitro, the expression of matrix metalloproteinase (MMP) was observed by performing reverse transcription-polymerase chain reaction (RT-PCR). RESULT: Both the neointimal area and luminal stenosis associated with neointimal proliferation were significantly decreased in the anti-Flt-1 peptide injected rats, (0.15+/-0.04 mm2 and 36.03+/-3.78% compared to 0.24+/-0.03 mm2 and 61.85+/-5.11%, respectively, in the placebo-injected rats (p<0.01, respectively). The ratio of PCNA(+) cells to the entire neointimal cells was also significantly decreased from 52.82+/-4.20% to 38.11+/-6.89% by the injected anti-Flt-1 peptide (p<0.05). On the VSMC migration assay, anti-Flt-1 peptide significantly reduced the VEGF-induced VMSC migration by about 40% (p<0.01). Consistent with the effect of anti-Flt-1 peptide on VSMC migration, it also obviously attenuated the induction of the MMP-3 and MMP-9 mRNA expressions via VEGF in the VSMCs. CONCLUSION: Anti-Flt-1 peptide inhibits the formation and hyperplasia of the neointima in a balloon-injured carotid artery model of OLETF rats. Anti-Flt-1 peptide also inhibits the VSMCs' migration and the expressions of MMP-3 and MMP-9 mRNA induced by VEGF under a high glucose condition.
Animals ; Arteries ; Carotid Arteries ; Cell Proliferation ; Constriction, Pathologic ; Endothelial Growth Factors* ; Glucose ; Hyperplasia ; Muscle, Smooth, Vascular* ; Neointima* ; Phenobarbital ; Rats* ; Rats, Inbred OLETF ; Receptors, Vascular Endothelial Growth Factor ; RNA, Messenger ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factor Receptor-1