PurposeMany studies have revealed that diabetes mellitus (DM) increases a person's lifetime risk of colorectal cancer and that DM is associated with a worse outcome of colon cancer, but this association is controversial. In this study, we intended to examine the relationship between DM and the long-term outcomes of colorectal cancer.MethodsA retrospective analysis was conducted on 657 patients who underwent surgery due to colorectal cancer between 1997 and 2004 at Korea Cancer Center Hospital. The operations were done by a single surgeon. With a median follow-up of 4.7 years, we analyzed differences in recurrence-free survival (RFS) and overall survival (OS) between patients with DM and those without DM.ResultsOf the 657 patients, 374 (57%) were males and 67 (10%) had DM. There was no difference in age at diagnosis, sex and pathologic stage of colorectal cancer according to the presence of DM. There were no difference in the RFS and the OS of colon cancer between the patients with DM and those without DM. At 5 years, the RFS was 71.3% in diabetic patients vs. 70.4% in non-diabetic patients (P = 0.480), and the OS was 68.8% in diabetic patients vs. 75.0% in non-diabetic patients (P = 0.498). There was no difference in the median survival between the groups (9.6 years in the diabetic group vs. 10.6 years in the non-diabetic group; P = 0.495).ConclusionIn this study, we did not find any relation between the presence of DM and either the recurrence or the survival in cases of colorectal cancer. More studies to elucidate whether the influence of DM is directly related to a higher rate of cancer recurrence or survival are needed.
Background/AimsSilibinin, the main component of silymarin, is used as a hepatoprotectant and exhibits anticancer effects against various cancer cells. This study evaluated the effects of a combination of silibinin with either gefitinib or sorafenib on hepatocellular carcinoma (HCC) cells.MethodsSeveral different human HCC cell lines were used to test the growth-inhibiting effects and cell toxicity of silibinin both alone and in combination with either gefitinib or sorafenib. The cell viability and growth inhibition were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, trypan blue staining, and a colony-forming assay. Furthermore, changes in epidermal growth factor receptor (EGFR)-related signals were evaluated by Western blot analysis.ResultsGefitinib, sorafenib, and silibinin individually exhibited dose-dependent antiproliferative effects on HCC cells. Combined treatment with silibinin enhanced the gefitinib-induced growth-inhibiting effects in some HCC cell lines. The combination effect of gefitinib and silibinin was synergistic in the SNU761 cell line, but was only additive in the Huh-BAT cell line. The combination effect may be attributable to inhibition of EGFR-dependent Akt signaling. Enhanced growth-inhibiting effects were also observed in HCC cells treated with a combination of sorafenib and silibinin.ConclusionsCombined treatment with silibinin enhanced the growth-inhibiting effects of both gefitinib and sorafenib. Therefore, the combination of silibinin with either sorafenib or gefitinib could be a useful treatment approach for HCC in the future.
Close surveillance may be suggested as an option for EGC patients for whom a surgical approach is difficult, who exhibit a positive vertical margin after ESD, and who have no lymphovascular or deep submucosa invasion after ESD.
abbreviations as in Fig 1). A cardiac malignant tumor was suggested. Extensive diagnostic work-up yielded no evidence of extracardiac neoplastic manifestations. Because of the highly compromised conditions of the patient, surgery was considered not feasible. Chemotherapy and supportive treatment were initiated, but patient's conditions rapidly deteriorated with refractory right-sided heart failure. A second CT, performed 9 days after the first one, showed further increase in mass dimensions (9.2 ϫ 7.0 ϫ 8.5 cm; volume 287 cm 3 ; relative increase 24%; mean growth rate 6.1 cm 3 /d). On day 25 after admission in our laboratory, the patient died. Autopsy (Fig 3, panels A-B) confirmed the presence of a large and vascularized right atrial mass (asterisks) characterized by friable and hemorrhagic consistency, thrombotic extension into the SVC (white arrows) and encasement of both electrodes. Histology showed extensive lymphocyte infiltration (Fig 3, panel C), and immunohistochemical analysis revealed staining for CD 20 (Fig 3, panel D), showing the mass to be a large B-cell primary cardiac lymphoma (PCL).PCL represents 1.3% of primary cardiac tumors and 0.5% of extranodal lymphomas. 1 It occurs more commonly in immunocompromised patients, particularly in HIV-positive individuals, whereas its detection in immunocompetent subjects is exceedingly rare. 2,3 Clinical presentations may depend on flow obstruction, infiltration of adjacent tissues, or tumor embolization, and include heart failure, arrhythmias, atrioventricular disturbances, pericardial effusion, SVC syndrome, and stroke. 4,5 Sick sinus syndrome has been reported as a complication of lymphomas with secondary myocardial involvement, 6 but its occurrence as first presentation of PCL is exceptional. The prognosis depends on tumor stage and location, comorbidities, and the immunological status of the patient, but early diagnosis is fundamental to allow prompt initiation of aggressive treatment. 7 Although in most cases this may be achieved by transthoracic echocardiography, the nonspecific clinical presentations often lead to diagnostic delay. In this view, tumor growth rate represents a key aspect in affecting the feasibility of early diagnosis. These images illustrate the massive growth of a PCL characterized by unusual presentation and fatal evolution over less than 24 weeks. Because neither transesophageal echocardiography nor chest CT was performed at the time of pacemaker implantation, the effective stage of tumor mass at that time cannot be established. Nonetheless, the following elements support the hypothesis of an extremely high growth rate: (1) the absence of right atrial masses by transthoracic echocardiography immediately before implantation; (2) the evidence of no
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