International journal of gastrointestinal cancer最新文献

{"title":"Aberrant p16 methylation, a possible epigenetic risk factor in familial esophageal squamous cell carcinoma.","authors":"Mohammad Reza Abbaszadegan,&nbsp;Hamid Reza Raziee,&nbsp;Kamran Ghafarzadegan,&nbsp;Mohammad Taghi Shakeri,&nbsp;Sima Afsharnezhad,&nbsp;Mohammad Reza Ghavamnasiry","doi":"10.1385/IJGC:36:1:047","DOIUrl":"https://doi.org/10.1385/IJGC:36:1:047","url":null,"abstract":"<p><strong>Aim: </strong>Detection of methylation in the p16 gene, an inhibitor of cyclin D-dependent protein kinase, as a new tumor marker for early detection of esophageal squamous cell carcinoma (ESCC) in DNA derived from blood and serum.</p><p><strong>Method: </strong>A large family with clustering of ESCC was assessed in Khorasan province in northeastern Iran. The family had three histologically proven cases of ESCC in two consecutive generations and several other deceased cases with histories of ESCC. DNA from blood of 28 living family members in three consecutive generations, 30 sporadic ESCC cases (from serum, blood, and tumor tissues), and 30 healthy volunteers (from blood) were examined for the methylation status of p16 promoter using methylation-specific PCR (MSP).</p><p><strong>Results: </strong>Aberrant p16 promoter methylation was found in 64.3% (n = 28) of ESCC family members and none (n = 30) of our normal volunteers. Five of the 28 family members with esophageal cancer symptoms had negative endoscopy results for ESCC, while four of these members had p16 hypermethylation in their blood. The family members with negative endoscopy and positive p16 promoter methylation are being monitored closely for signs of ESCC development through regular check-ups and chromoendoscopies. In sporadic ESCC in northeastern Iran, 73.3% (n = 30) of tumor tissue samples had p16 hypermethylation. Serum and blood samples from the same patients showed p16 hypermethylation in 26.6% and 43.3% of the samples, respectively.</p><p><strong>Conclusion: </strong>Aberrant p16 methylation may be a valuable diagnostic tool as a tumor marker for the early identification of individuals in high risk ESCC families.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"36 1","pages":"47-54"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:36:1:047","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25637788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metastasis to appendix from lung adenocarcinoma.","authors":"Kunihiko Miyazaki,&nbsp;Hiroaki Satoh,&nbsp;Kiyohisa Sekizawa","doi":"10.1385/IJGC:36:1:059","DOIUrl":"https://doi.org/10.1385/IJGC:36:1:059","url":null,"abstract":"<p><p>We previously read with interest the case report by Filik et al. (International Journal of Gastrointestinal Cancer, 2003;34:55-58) on appendicular metastases from pancreatic adenocarcinoma. We would like to share our recent experience.A 64-yr-old man presented with a 2-d history of progressively increasing colicky abdominal pain and fever. His past medical history included a pneumonectomy of the left lung for locally advanced lung adenocarcinoma 9 mo previously. TNM stage of the original lung cancer was T2N2M0. On examination, his abdomen was slightly distended and he had an intermittent metallic bowel sound. Abdominal CT scan showed a low-density mass, 3 cm in diameter, in the right pelvic cavity. Endoscopic evaluation revealed no obstruction, but failed to identify mucosal abnormalities in the ileocecal region. Chest CT scan prior to surgery did not show any evidence of pulmonary recurrence or metastasis. He underwent a laparotomy, and tumor of the appendix, 3 x 3 cm in diameter, adhered to the surrounding tissue, but no perforation was seen. The mass was excised in combination with an ileocecal resection, followed by ileocolic anastomosis. Hisotologically, the neoplastic tumor cells infiltrated the submucosa, muscularis, and serosa, but mucosa of the appendix was intact, unremarkable, with no precursor lesion. The tumor was morphologically similar to the lung primary tumor. The patient had an uneventful postoperative course. He was examined at regular periodic follow-ups, but died from lung cancer 12 mo after the resection of the metastatic tumor to the appendix.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"36 1","pages":"59-60"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:36:1:059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25637790","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of apoptosis and cell cycle arrest by imexon in human pancreatic cancer cell lines.","authors":"Robert T Dorr,&nbsp;Mary Ann Raymond,&nbsp;Terry H Landowski,&nbsp;Nicholas O Roman,&nbsp;Shoji Fukushima","doi":"10.1385/IJGC:36:1:015","DOIUrl":"https://doi.org/10.1385/IJGC:36:1:015","url":null,"abstract":"<p><p>Imexon is an aziridine-containing small molecule currently in Phase I clinical trials. This agent has been shown to bind to thiols and increase intracellular oxidants, inducing apoptosis in hematologic cancer cells. Pancreatic cancers are known to be sensitive to oxidation, suggesting this disease may be an appropriate target for this agent. The current report examines the activity of imexon in pancreatic cells. Imexon induced concentration-dependent and time-dependent apoptosis in a panel of six human pancreatic carcinoma cell (PCC) lines. The mean IC50 (SD) for growth inhibition by the SRB assay was 200 (101) microM for a 48 h exposure with a range of 64-358 microM. Cell killing was schedule-dependent, favoring exposure times > or =48 h. Imexon-treated MiaPaCa-2 cells underwent non-lethal growth arrest following exposure to concentrations < or =200 microM for 48 h. When concentrations were increased to 300 microM for > or =48 h, the MiaPaCa-2 cells arrested in G2 phase and activated caspases 3, 8, and 9 were detected. After a 72 h exposure to the IC80 concentration of imexon, cells exhibited a loss of mitochondrial membrane potential detected by CMXRos staining. However, there was no loss of reduced cellular thiols unless very high concentrations of > or =400 microM were used. In contrast, reactive oxygen species (ROS) were elevated in a dose-dependent fashion, starting at very low imexon concentrations. Imexon also significantly inhibited MiaPaCa-2 tumor growth in SCID mice at 100 mg/kg/d for 9 d. The tumor growth inhibition (% T/C) was 27% of control, and the tumor growth delay was 21 d, indicating an active agent by NCI standards. The levels of imexon that are cytotoxic in human PCC's are achievable based on the preliminary results of the ongoing Phase I trial. Imexon appears to be active against PCCs in vitro and has an entirely novel mechanism of action involving G2 arrest, accumulation of ROS, and the induction of apoptosis.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"36 1","pages":"15-28"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:36:1:015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25637839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary malignant fibrous histiocytoma of the small bowel: a report of an additional case in duodenum.","authors":"Ze-sheng Wang,&nbsp;Cheng-long Xiong,&nbsp;Na Zhan,&nbsp;Guo-sheng Xiong,&nbsp;Hui Li,&nbsp;Hong Hu","doi":"10.1385/IJGC:36:2:105","DOIUrl":"https://doi.org/10.1385/IJGC:36:2:105","url":null,"abstract":"<p><strong>Aims: </strong>We report herein an additional case of primary malignant fibrous histiocytoma (MFH) in the duodenum and provide a review of the existing literature.</p><p><strong>Methods and results: </strong>A 61-yr-old Chinese man was admitted to our hospital with symptoms of melena, anorexia, and weight loss. An abdominal computed tomography (CT) and gastrointestinal barium meal examination demonstrated a tumor of the duodenum suggestive of primary malignancy. The tumor was successfully treated by pancreaticoduodenectomy. It was histopathologically and immunohistochemically diagnosed to be a storiform-type primary MFH of the duodenum. There have been a total of 40 cases of primary malignant fibrous histiocytoma of the small bowel documented in the literature including our Chinese cases.</p><p><strong>Conclusion: </strong>Primary malignant fibrous histiocytoma of the small bowel, especially in the duodenum is extremely rare. The final diagnosis is made only after pathological and immunopathological examination of the tumor. The malignant potential of such tumors is high. The prognosis may be mainly dependent on the invasion and metastasis of tumor, while tumor size is irrelevant. The treatment should be surgery if possible. Early surgical intervention may be the best form of management that may offer the patient good result.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"36 2","pages":"105-12"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:36:2:105","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26437204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aberrant expression of maspin in idiopathic inflammatory bowel disease is associated with disease activity and neoplastic transformation.","authors":"Dengfeng Cao,&nbsp;Robb E Wilentz,&nbsp;James L Abbruzzese,&nbsp;Linus Ho,&nbsp;Anirban Maitra","doi":"10.1385/IJGC:36:1:039","DOIUrl":"https://doi.org/10.1385/IJGC:36:1:039","url":null,"abstract":"<p><strong>Background: </strong>Maspin is both overexpressed in tumors and inflammation, implicating a possible role in bridging inflammation and neoplasia. Idiopathic inflammatory bowel disease (IBD) and IBD-associated dysplasias and carcinomas represent a prototype for studying the relationship between chronic inflammatory states and neoplasia.</p><p><strong>Aim of study: </strong>To investigate expression of maspin in IBD and IBD-associated dysplasia and colorectal carcinoma.</p><p><strong>Methods: </strong>Immunohistochemical labeling of maspin was examined using tissue microarrays constructed from archival biopsy and resection tissue from 90 patients with 125 histologically defined lesions including 30 with inactive chronic IBD, 51 with active chronic IBD, 4 IBD-associated foci with epithelial changes indefinite for dysplasia (IFD), 7 with IBD-associated low-grade epithelial dysplasia (LGD), 8 with IBD-associated high grade epithelial dysplasia (HGD), and 25 with IBD-associated invasive colorectal adenocarcinomas.</p><p><strong>Results: </strong>Maspin was expressed in 47/51 (92%) active chronic IBD lesions, which was significantly higher than both inactive chronic IBD (13/30, 43%) and normal mucosa (1 of 9, 11%) (p < 0.01); in particular, the diffuse pattern of maspin expression was significantly higher in active IBD (41/51, 80%), compared with inactive IBD (5/30, 17%) and normal mucosa (0%) (p < 0.01). In the multistage progression model of colitis-associated neoplasia, aberrant labeling was observed at the earliest stages, with 3/4 (75%) IFD foci, 6/7 (86%) LGD, and 8/8 (100%) HGD specimens expressing maspin, virtually always in a diffuse pattern. Expectedly, 22/25 (88%) of invasive IBD-associated cancers overexpressed maspin, including 21 with diffuse labeling.</p><p><strong>Conclusions: </strong>Maspin is significantly overexpressed in both active IBD and colitis-associated dysplasia compared to either inactive IBD or normal colonic mucosa, suggesting a potential role in disease \"flare\" as well as neoplastic progression. Targeting maspin for control of disease activity and cancer prophylaxis may be a promising novel therapeutic strategy for IBD.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"36 1","pages":"39-46"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:36:1:039","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25637787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zollinger-Ellison phenotype in the absence of hypergastrinemia and islet-cell tumor.","authors":"Anish A Desai,&nbsp;James E McGuigan,&nbsp;Peter Draganov","doi":"10.1385/IJGC:35:2:157","DOIUrl":"https://doi.org/10.1385/IJGC:35:2:157","url":null,"abstract":"<p><p>Patients with the Zollinger-Ellison syndrome are characterized by islet-cell tumors, striking gastric acid hypersecretion, and peptic ulcer disease. They often experience severe abdominal pain, diarrhea, and gastrointestinal bleeding with potentially life-threatening consequences. It is a rare syndrome caused by non-beta cell islet-cell tumors (gastrinomas) located in or in proximity to the pancreas. These tumors freely secrete gastrin, a peptide hormone that serves as a powerful stimulant of gastric acid secretion. Exuberant secretion of gastrin from the gastrinomas produces severe gastric acid hypersecretion that often leads to impressive peptic ulcer disease and the constellation of symptoms listed above. We describe a patient presenting with clinical manifestations characteristic of the ZES with strikingly elevated gastric acid secretion,multiple ulcers in the first and second portions of the duodenum and diarrhea, but in absence of islet-cell tumor and/or hypergastrinemia.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"35 2","pages":"157-61"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:35:2:157","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25098108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Do the progesterone receptors have a role to play in gallbladder cancer?","authors":"V Baskaran,&nbsp;U Vij,&nbsp;P Sahni,&nbsp;R K Tandon,&nbsp;S Nundy","doi":"10.1385/IJGC:35:1:061","DOIUrl":"https://doi.org/10.1385/IJGC:35:1:061","url":null,"abstract":"<p><strong>Background: </strong>Gallstone disease as well as gallbladder cancer are more common in women and female sex hormones may be involved in their etiology.</p><p><strong>Aim and methods: </strong>To determine whether female sex hormones have a role in the pathogenesis, of gallbladder carcinoma and in its prognosis, we estimated, by enzyme immunoassay, the estrogen and progesterone receptors (ER and PgR) in the gallbladders of 21 patients with gallbladder cancer, 19 patients with cholelithiasis, and 6 patients who underwent incidental removal of essentially normal gallbladder as a component of wider resection.</p><p><strong>Results: </strong>ER were present in the gallbladder mucosa in all the three groups in proportions which were not significantly different (9/21 in carcinoma, 4/19 in gallstones, and 1/6 normal), whereas the expression of PgR was greater in carcinomas (13/18), less in cholelithiasis (4/12), and absent in normal gallbladders. PgR expression was higher in tumors of lower stage (7/7) and lower in advanced disease stage IV tumors (6/11). PgR expression was associated with better disease stage (p=0.05) and significantly longer overall survival (median survival of 301 d vs 54 d) as well as better survival within the same stage (269 d vs 54 d for stage IV disease, p=0.011). Cox's regression analysis showed that PgR was an independent risk factor (R=0.2283, p=0.0035).</p><p><strong>Conclusions: </strong>Our findings suggest that the female sex hormones may have a role in the pathogenesis of gallbladder cancer and that PgR expression has a prognostic significance. We believe that when this relationship is reaffirmed by larger studies, gallbladder cancer may be treated with appropriate sex hormonal manipulation.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"35 1","pages":"61-8"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:35:1:061","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25136188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pancreatic endocrine neoplasm can mimic serous cystadenoma.","authors":"Hiroshi Imaoka,&nbsp;Kenji Yamao,&nbsp;Ahmed A S Salem,&nbsp;Akira Sawaki,&nbsp;Kuniyuki Takahashi,&nbsp;Nobumasa Mizuno,&nbsp;Hiroki Kawai,&nbsp;Masahiro Tajika,&nbsp;Toshifumi Isaka,&nbsp;Yasuyuki Okamoto,&nbsp;Yasuhiro Shimizu,&nbsp;Akio Yanagisawa","doi":"10.1385/IJGC:35:3:217","DOIUrl":"https://doi.org/10.1385/IJGC:35:3:217","url":null,"abstract":"<p><p>A 57-yr-old female patient was referred to our hospital with a cystic lesion of the head of the pancreas that had been noted on abdominal computed tomography (CT). Endoscopic ultrasonography (EUS) showed a 3.0 cm rounded mass in the head of the pancreas. EUS images showed that the tumor had a solid component consisting of multiple microcysts separated by septae and a cystic component consisting of a macrocystic lesion. Thus, the tumor was suspected of being a serous cystadenoma (SCA). However, the histopathological diagnosis based on endoscopic ultrasound- guided fine-needle-aspiration biopsy (EUS-FNAB) was that of a pancreatic endocrine neoplasm (PEN). Surgical resection was performed. Despite having very similar macroscopic findings to SCA, microscopic examination revealed that the patient's tumor was definitely a PEN. This case suggests that it is very difficult to distinguish PENs from SCAs based solely on imaging methods. EUS-FNAB is essential for determining the appropriate therapeutic strategy, as it provides the histopathological diagnosis.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"35 3","pages":"217-20"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:35:3:217","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25256275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of a family history of colorectal cancer on age at diagnosis, anatomic location, and clinical characteristics of colorectal cancer.","authors":"Williamson B Strum","doi":"10.1385/IJGC:35:2:121","DOIUrl":"https://doi.org/10.1385/IJGC:35:2:121","url":null,"abstract":"<p><strong>Background: </strong>Among the risk factors for colorectal cancer (CRC) is a family history of colorectal cancer. Reliable evidence is needed regarding the clinical characteristics of cancer in patients with this history to determine if a change in the diagnostic approach is needed.</p><p><strong>Aim of the study: </strong>This study set out to determine specific clinical outcomes in patients with CRC with a family history of one first-degree relative with sporadic colorectal cancer compared to control patients with colorectal cancer but without the family history.</p><p><strong>Methods: </strong>We designed a case-control study of colorectal cancer registry data between 1988 and 1999. Patients with a family history of one first-degree relative with colorectal cancer were compared to those without the history with regard to four characteristics: age at cancer diagnosis, anatomic location of the cancer, presence of distal adenomas with proximal cancer, and stage of disease at diagnosis.</p><p><strong>Results: </strong>Nine hundred and twenty-one patients met the inclusion criteria. Family history was positive in 124 patients. The demography of the populations was similar, except for mean age, which was 65 yr for men with a family history and proximal cancer compared to 70 yr for their counterparts without the family history (p = 0.03). The anatomic location of the cancer, presence of distal benign neoplasia when the cancer was proximal, and disease stage at diagnosis were not different between the groups.</p><p><strong>Conclusions: </strong>Men with a family history of sporadic colorectal cancer and proximal colon cancer were younger than men without the family history and proximal colon cancer. The overall results do not indicate that a change in the diagnostic approach is needed.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"35 2","pages":"121-6"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:35:2:121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25270211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asymptomatic familial colon cancer with FDG-PET scanning for recurrent disease.","authors":"Hugh J Freeman","doi":"10.1385/IJGC:36:3:163","DOIUrl":"https://doi.org/10.1385/IJGC:36:3:163","url":null,"abstract":"<p><p>A 57-yr-old female was referred for screening colonoscopy because of a positive family history of colon cancer. A lobulated tumor mass was detected in the sigmoid colon. The resected specimen showed an invasive adenocarcinoma without lymph node involvement. Later colonoscopic evaluations and CT imaging failed to reveal definite evidence of recurrent disease but a late rising carcinoembryonic antigen level led to FDG-PET scanning and the detection of suspect lymph nodes in the retroperitoneum. Further histopathological and immunohistochemical evaluation of resected lymph nodes confirmed metastatic carcinoma from the primary colon carcinoma with extra-nodal spread. This case underscores the ongoing need for additional evidence-based studies on evolving imaging modalities used in the diagnosis and management of colonic cancer.</p>","PeriodicalId":84927,"journal":{"name":"International journal of gastrointestinal cancer","volume":"36 3","pages":"163-9"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1385/IJGC:36:3:163","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26041860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}