Recurrent advanced colonic cancer occurring 11 years after initial endoscopic piecemeal resection: a case report

<p>Abstract</p> <p>Background</p> <p>The high frequency of local recurrence occurring after endoscopic piecemeal resection (EPMR) for large colorectal tumors is a serious problem. However, almost all of these cases of local recurrence can be detected within 1 year and cured by additional endoscopic resection. We report a rare case of recurrent advanced colonic cancer diagnosed 11 years after initial EPMR treatment.</p> <p>Case presentation</p> <p>A 65-year-old male was diagnosed with a sigmoid colon lesion following a routine health check-up. Total colonoscopy revealed a 12 mm type 0-Is lesion in the sigmoid colon, which was diagnosed as an adenoma or intramucosal cancer and treated by EPMR in 1996. The post-resection defect was closed completely using metallic endoclips to avoid delayed bleeding. In 2007, at the third follow up, colonoscopy revealed a 20 mm submucosal tumor (SMT) like recurrence at the site of the previous EPMR. The recurrent lesion was treated by laparoscopic assisted sigmoidectomy with lymph node dissection.</p> <p>Conclusion</p> <p>When it is difficult to evaluate the depth and margins of resected tumors following EPMR, it is important that the defect is not closed in order to avoid tumor implantation, missing residual lesions and to enable earlier detection of recurrence. It is crucial that the optimal follow-up protocol for EPMR cases is clarified, particularly how often and for how long they should be followed.</p

Prognostic analysis of salvage esophagectomy after definitive chemoradiotherapy for esophageal squamous cell carcinoma: The importance of lymphadenectomy

ObjectivesThe objective of this study was to review the prognostic factors for increased survival after salvage esophagectomy after definitive chemoradiotherapy for esophageal squamous carcinoma and determine the importance of lymphadenectomy from a prognostic view.MethodsClinical data for all patients from January 1999 to December 2012 who underwent salvage esophagectomy for residual tumor or tumor recurrence after definitive chemoradiotherapy were retrospectively collected. Survival was determined and prognostic factors were analyzed with univariate and multivariate analyses.ResultsSurvival after 1, 3, and 5 years postoperatively was 74.4%, 39.8%, and 29.5%, respectively. The independent predictive factors for increased postoperative survival were tumor recurrence rather than residual tumor as the indication for salvage surgery (P < .001; odds ratio [OR], 0.292); complete tumor resection (P < .001; OR, 4.520); N category (P = .089; OR, 1.304); M category (P = .081; OR, 2.215), and total mediastinal dissection with 15 or more dissected mediastinal lymph nodes (P = .034; OR, 0.546).ConclusionsSalvage indications of recurrence, earlier disease, and complete tumor resection are related to longer survival. The total area of mediastinal dissection with a sufficient number of dissected mediastinal lymph nodes improves survival. Additional neck dissection does not add benefit. The optimal procedure for lymph node dissection in salvage esophagectomy should be established in future studies

A solitary fibrous tumor in the pelvic cavity of a patient with Doege-Potter syndrome: a case report

Abstract Background A solitary fibrous tumor (SFT) is a mesenchymal lesion, which commonly develops in the thorax. Non-islet cell hypoglycemia is a rare paraneoplastic phenomenon caused by an extra-pancreatic tumor. We report a rare case of a pelvic SFT with severe hypoglycemia, which was considered to be Doege-Potter syndrome. Case presentation A 72-year-old man was referred to our hospital for treatment of hypoglycemia and a large pelvic tumor. His blood glucose level was 52 mg/dl; serum insulin level, 1.0 μIU/ml; C-peptide level, 0.2 ng/ml; and insulin-like growth factor-I (IGF-I) level, 31 ng/ml. Contrast-enhanced computed tomography (CT) showed a 13-cm mass in the pelvic cavity. Magnetic resonance imaging (MRI) revealed a lobulated tumor with iso- and high-intensity areas combined in T2-weighted images. No clear invasion to any adjacent organs was identified. The tumor was resected, and hypoglycemic symptoms disappeared immediately. Pathological diagnosis was an SFT with malignant potential that secreted IGF-II and caused hypoglycemia. There has been no tumor recurrence during the 1 year of follow-up. Conclusion Non-islet cell tumor hypoglycemia should be considered in the differential diagnosis of patients presenting with tumors and hypoglycemia

Esophageal cancer associated with a sarcoid-like reaction and systemic sarcoidosis in lymph nodes: supportive findings of [18F]-fluorodeoxyglucose positron emission tomography–computed tomography during neoadjuvant therapy

Abstract Background In patients with esophageal cancer, differentiation between lymph node metastasis and lymphadenopathies from sarcoidosis or sarcoid-like reactions of lymph nodes is clinically important. Herein, we report two esophageal cancer cases with lymph node involvement of sarcoid-like reaction or sarcoidosis. Case presentation One patient received chemotherapy and the other chemoradiotherapy as initial treatments. In both cases, [18F]-fluorodeoxyglucose positron emission tomography–computed tomography (FDG-PET/CT) was performed before and after chemo(radio)therapy. After the treatment, FDG uptake was not detected in the primary tumor, but it was slightly reduced in the hilar and mediastinal lymph nodes in both cases. These non-identical responses to chemo(radio)therapy suggest the presence of sarcoid-like reaction of lymph nodes associated with squamous cell carcinoma of the esophagus. Curative surgical resection was performed as treatment. Conclusions These FDG-PET/CT findings may be helpful to distinguish between metastasis and sarcoidosis-associated lymphadenopathy in esophageal cancer

Early-Stage Induction of SWI/SNF Mutations during Esophageal Squamous Cell Carcinogenesis

<div><p>The SWI/SNF chromatin remodeling complex is frequently inactivated by somatic mutations of its various components in various types of cancers, and also by aberrant DNA methylation. However, its somatic mutations and aberrant methylation in esophageal squamous cell carcinomas (ESCCs) have not been fully analyzed. In this study, we aimed to clarify in ESCC, what components of the SWI/SNF complex have somatic mutations and aberrant methylation, and when somatic mutations of the SWI/SNF complex occur. Deep sequencing of components of the SWI/SNF complex using a bench-top next generation sequencer revealed that eight of 92 ESCCs (8.7%) had 11 somatic mutations of 7 genes, <i>ARID1A</i>, <i>ARID2</i>, <i>ATRX</i>, <i>PBRM1</i>, <i>SMARCA4</i>, <i>SMARCAL1</i>, and <i>SMARCC1</i>. The <i>SMARCA4</i> mutations were located in the Forkhead (85Ser>Leu) and SNF2 family N-terminal (882Glu>Lys) domains. The <i>PBRM1</i> mutations were located in a bromodomain (80Asn>Ser) and an HMG-box domain (1,377Glu>Lys). For most mutations, their mutant allele frequency was 31–77% (mean 61%) of the fraction of cancer cells in the same samples, indicating that most of the cancer cells in individual ESCC samples had the SWI/SNF mutations on one allele, when present. In addition, a BeadChip array analysis revealed that a component of the SWI/SNF complex, <i>ACTL6B</i>, had aberrant methylation at its promoter CpG island in 18 of 52 ESCCs (34.6%). These results showed that genetic and epigenetic alterations of the SWI/SNF complex are present in ESCCs, and suggested that genetic alterations are induced at an early stage of esophageal squamous cell carcinogenesis.</p></div