The association of neonatal intestinal obstruction with situs inversus totalis is extremely rare with only few cases reported in the literature to date. This association poses dilemmas in management. We presen...
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Κυριακή 17 Σεπτεμβρίου 2017
Neonatal intestinal obstruction associated with situs inversus totalis: two case reports and a review of the literature
Σάββατο 16 Σεπτεμβρίου 2017
Successful treatment with hyperbaric oxygen therapy for pneumatosis cystoides intestinalis as a complication of granulomatosis with polyangiitis: a case report
Although gastrointestinal involvement in patients with granulomatosis with polyangiitis is uncommon, it is associated with mild to severe life-threatening complications. We present a case of pneumatosis cystoi...
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Margin-free excision of small solid breast carcinomas using the Intact Breast Lesion Excision System ® : is it feasible?
Abstract
Background
The Breast Lesion Excision System® (BLES®) is a stereotactic vacuum-assisted breast biopsy device that utilizes radiofrequency in order to excise non-palpable mammographic lesions for pathologic diagnosis. The purpose of this study was to evaluate the efficacy of BLES® in performing complete, margin-free excisions of small solid carcinomas.
Methods
Our retrospective study of prospectively enrolled patients included 50 cases of non-palpable, BIRADS ≥ 4, solid by means of mammography and sonography, lesions. All these patients underwent a BLES® breast biopsy procedure from June 2010 to June 2014 and had a malignant diagnosis. According to each patient's pathologic diagnosis, appropriate surgical treatment was recommended. Postoperatively, surgical specimens were histologically analyzed, aiming to determine whether residual malignant disease was present in the specimen cavity formatted by BLES®.
Results
Ductal carcinoma in situ (DCIS) was diagnosed in 5 patients and invasive carcinoma (IC) in 45 patients, at primary BLES® pathology report. Tumor-free resection margins (< 0.5 and < 1 mm) were accomplished in only 8/24 subcentimeter cases (33.3%). Absence of residual disease upon surgical excision was confirmed in 23/24 subcentimeter cases (95.8%) and 2/26 of the cases measuring > 1 cm (7.69%). Statistical analysis revealed that mammographic size was the only significant prognostic factor for complete excision (i.e., with no residual disease in the biopsy cavity) of a malignant lesion.
Conclusions
Our results indicate that it is possible, when using the BLES® device, to completely excise small (≤ 10 mm) breast carcinomas that appear radiologically as solid lesions. This subset of patients should be investigated regarding the therapeutic potential of this method.
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Cancer-specific mortality of high-risk prostate cancer after carbon-ion radiotherapy plus long-term androgen deprivation therapy
Abstract
The treatment outcomes of patients with high-risk localized prostate cancer (PC) after carbon-ion radiotherapy (CIRT) combined with long-term androgen deprivation therapy (LTADT) were analyzed, and compared with those of other treatment modalities, focusing on PC-specific mortality (PCSM). A total of 1247 patients were enrolled in three phase II clinical trials of fixed-dose CIRT between 2000 and 2013. Excluding patients with T4 disease, 608 patients with high- or very-high-risk PC, according to the National Comprehensive Cancer Network classification system, who received CIRT with LTADT were evaluated.
The median follow-up was 88.4 months, and the 5-/10-year PCSM rates were 1.5%/4.3%, respectively. T3b disease, Gleason score of 9-10, and percentage of positive biopsy cores > 75% were associated with significantly higher PCSM on univariate and multivariate analyses. The 10-year PCSM rates of patients having all three (n=16), two (n=74), or one of these risk factors (n=217) were 27.1%, 11.6%, and 5.7%, respectively. Of the 301 patients with none of these factors, only 1 PCSM occurred over the 10-year follow-up (10-year PCSM rate, 0.3%), and significant differences were observed among the four stratified groups (p < 0.001).
CIRT combined with LTADT yielded relatively favorable treatment outcomes in patients with high-risk PC and very favorable results in patients without any of the three abovementioned factors for PCSM. Because a significant difference in PCSM among the high-risk PC patient groups was observed, new categorization and treatment intensity adjustment may be required for high-risk PC patients treated with CIRT.
This article is protected by copyright. All rights reserved.
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via IFTTT
The miR-203 inhibits cell proliferation, invasion, and migration of non-small cell lung cancer by downregulating RGS17
Abstract
The involvement of the RGS17 oncogene in promotion of non-small cell lung cancer (NSCLC) has been reported, but the regulation mechanism in NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand the role of microRNAs in RGS17-induced NSCLC, we showed that miR-203 was downregulated during tumorigenesis, and inhibited the proliferation and invasion of lung cancer cells. We then determined if miR-203 regulated NSCLC by targeting RGS17. To characterize the regulatory effect of miR-203 on RGS17, we used lung cancer cell lines, A549 and Calu-1, and the constructed miR-203 and RGS17 overexpression vectors. The CCK8 kit was used to determine the cell proliferation, and the Transwell® assay was used to measure cell invasion and migration. RT-PCR, western blots, and immunofluorescence were used to analyze the expression of miR-203 and RGS17, and the luciferase reporter assay was used to examine the interaction between miR-203 and RGS17. Nude mice were used to characterize in vivo tumor growth regulation. The expression of miR-203 inhibited the proliferation, invasion, and migration of lung cancer cell lines A549 and Calu-1 by targeting RGS17. The regulatory effect of miR-203 was inhibited after overexpression of RGS17. The luciferase reporter assay showed that miR-203 downregulated RGS17 by direct integration into the 3′-UTR of RGS17 mRNA. In vivo studies showed that the expression of miR-203 significantly inhibited the growth of tumors. Taken together, the results suggested that the expression of miR-203 inhibited tumor growth and metastasis by targeting RGS17.
This article is protected by copyright. All rights reserved.
from Cancer via ola Kala on Inoreader http://ift.tt/2xpusMl
via IFTTT
Cancer-specific mortality of high-risk prostate cancer after carbon-ion radiotherapy plus long-term androgen deprivation therapy
Abstract
The treatment outcomes of patients with high-risk localized prostate cancer (PC) after carbon-ion radiotherapy (CIRT) combined with long-term androgen deprivation therapy (LTADT) were analyzed, and compared with those of other treatment modalities, focusing on PC-specific mortality (PCSM). A total of 1247 patients were enrolled in three phase II clinical trials of fixed-dose CIRT between 2000 and 2013. Excluding patients with T4 disease, 608 patients with high- or very-high-risk PC, according to the National Comprehensive Cancer Network classification system, who received CIRT with LTADT were evaluated.
The median follow-up was 88.4 months, and the 5-/10-year PCSM rates were 1.5%/4.3%, respectively. T3b disease, Gleason score of 9-10, and percentage of positive biopsy cores > 75% were associated with significantly higher PCSM on univariate and multivariate analyses. The 10-year PCSM rates of patients having all three (n=16), two (n=74), or one of these risk factors (n=217) were 27.1%, 11.6%, and 5.7%, respectively. Of the 301 patients with none of these factors, only 1 PCSM occurred over the 10-year follow-up (10-year PCSM rate, 0.3%), and significant differences were observed among the four stratified groups (p < 0.001).
CIRT combined with LTADT yielded relatively favorable treatment outcomes in patients with high-risk PC and very favorable results in patients without any of the three abovementioned factors for PCSM. Because a significant difference in PCSM among the high-risk PC patient groups was observed, new categorization and treatment intensity adjustment may be required for high-risk PC patients treated with CIRT.
This article is protected by copyright. All rights reserved.
http://ift.tt/2fccHtl
The miR-203 inhibits cell proliferation, invasion, and migration of non-small cell lung cancer by downregulating RGS17
Abstract
The involvement of the RGS17 oncogene in promotion of non-small cell lung cancer (NSCLC) has been reported, but the regulation mechanism in NSCLC remains unclear. MicroRNAs (miRNAs) negatively regulate gene expression, and their dysregulation has been implicated in tumorigenesis. To understand the role of microRNAs in RGS17-induced NSCLC, we showed that miR-203 was downregulated during tumorigenesis, and inhibited the proliferation and invasion of lung cancer cells. We then determined if miR-203 regulated NSCLC by targeting RGS17. To characterize the regulatory effect of miR-203 on RGS17, we used lung cancer cell lines, A549 and Calu-1, and the constructed miR-203 and RGS17 overexpression vectors. The CCK8 kit was used to determine the cell proliferation, and the Transwell® assay was used to measure cell invasion and migration. RT-PCR, western blots, and immunofluorescence were used to analyze the expression of miR-203 and RGS17, and the luciferase reporter assay was used to examine the interaction between miR-203 and RGS17. Nude mice were used to characterize in vivo tumor growth regulation. The expression of miR-203 inhibited the proliferation, invasion, and migration of lung cancer cell lines A549 and Calu-1 by targeting RGS17. The regulatory effect of miR-203 was inhibited after overexpression of RGS17. The luciferase reporter assay showed that miR-203 downregulated RGS17 by direct integration into the 3′-UTR of RGS17 mRNA. In vivo studies showed that the expression of miR-203 significantly inhibited the growth of tumors. Taken together, the results suggested that the expression of miR-203 inhibited tumor growth and metastasis by targeting RGS17.
This article is protected by copyright. All rights reserved.
http://ift.tt/2xpusMl