Mucoid degeneration of the ACL can be suspected in patients with posterior knee pain associated with a thickened ACL. Associated findings such as an intraosseous tibial or ganglion cyst help to rule out differential diagnosis.
Renal cell carcinoma (RCC) is the major cause of death among patients with von Hippel-Lindau (VHL) disease. Resistance to therapies targeting tumor angiogenesis opens the question about the underlying mechanisms. Previously we have described that RWDD3 or RSUME (RWD domain-containing protein SUMO Enhancer) sumoylates and binds VHL protein and negatively regulates HIF degradation, leading to xenograft RCC tumor growth in mice. In this study, we performed a bioinformatics analysis in a ccRCC dataset showing an association of RSUME levels with VHL mutations and tumor progression, and we demonstrate the molecular mechanism by which RSUME regulates the pathologic angiogenic phenotype of VHL missense mutations. We report that VHL mutants fail to downregulate RSUME protein levels accounting for the increased RSUME expression found in RCC tumors. Furthermore, we prove that targeting RSUME in RCC cell line clones carrying missense VHL mutants results in decreased early tumor angiogenesis. The mechanism we describe is that RSUME sumoylates VHL mutants and beyond its sumoylation capacity, interacts with Type 2 VHL mutants, reduces HIF-2α-VHL mutants binding, and negatively regulates the assembly of the Type 2 VHL, Elongins and Cullins (ECV) complex. Altogether these results show RSUME involvement in VHL mutants deregulation that leads to the angiogenic phenotype of RCC tumors.
Introduction In the present study, we aim to provide more evidence about benefits of salvage radical prostatectomy (SRP). Our main objective is to assess prostatic-specific antigen control and postoperative urinary incontinence in open and robotic approaches as primary outcomes. Materials and methods After the Institutional Review Board approval (IRB00010193), we retrospectively analyzed 76 consecutive patients who underwent open or robot-assisted SRP for locally relapsed prostate cancer between 2004 and 2019 at the Urology Department of Hospital Italiano de Buenos Aires, Argentina. Data were collected from our electronic medical record and prospective database. Postoperative variables, such as urinary incontinence, erectile function preservation, and vesicourethral anastomosis stricture development, were analyzed. Results Before SRP, 59 patients (76.6%) were treated with 3D external beam radiotherapy, 11 (14.3%) with brachytherapy, and 6 (7.8%) with intensity-modulated radiotherapy. Fifty patients underwent open SRP, and 26, robot-assisted SRP. Comparing surgical approaches, the global incontinence rate was 34.2% versus 9.1% in open versus robot-assisted approach, respectively (p: 0.01). Vesicourethral anastomosis stricture occurred in six patients (8.7%), all in the open approach group (p: 0.07). Five patients of 69 (7.2%) preserved erectile function with/without use of phosphodiesterase 5 inhibitors. Two patients in the open approach group needed blood transfusion. Estimated 2-year biochemical recurrence–free survival rate in the open approach group and robot-assisted group was 67% (95% confidence interval: 53.7–80.3) and 60.9% (95% confidence interval: 40.5–81.3), respectively, with no statistical difference (log-rank test p: 0.873). Conclusions Robot-assisted SRP is a reliable procedure to treat local recurrences after external beam radiotherapy or brachytherapy, reducing the risk of anastomotic strictures and blood loss and improving continence outcomes.
We report the usefulness of a technique called direct-MDCT venography in the diagnostic workup of a patient with an inferior vena cava leiomyosarcoma. The technique consists in the injection of contrast agent through both lower limbs achieving maximum enhancement in the inferior vena cava. Images are similar to those of the gold standard conventional cavography. To our knowledge, this is the first description of the direct-MDCT imaging appearance of an inferior vena cava leiomyosarcoma.
Bladder cancer (BC) is the ninth most common cancer worldwide, but molecular changes are still under study. During tumor progression, Epithelial cadherin (E-cadherin) expression is altered and β-catenin may be translocated to the nucleus, where it acts as co-transcription factor of tumor invasion associated genes. This investigation further characterizes E-cadherin and β-catenin associated changes in BC, by combining bioinformatics, an experimental murine cell model (MB49/MB49-I) and human BC samples. In in silico studies, a DisGeNET (gene-disease associations database) analysis identified CDH1 (E-cadherin gene) as one with highest score among 130 BC related-genes. COSMIC mutation analysis revealed CDH1 low mutations rates. Compared to MB49 control BC cells, MB49-I invasive cells showed decreased E-cadherin expression, E-to P-cadherin switch, higher β-catenin nuclear signal and lower cytoplasmic p-Ser33-β-catenin signal, higher Ephrin-B1 ligand and EphB2 receptor expression, higher Phospho-Stat3 and Urokinase-type Plasminogen Activator (UPA), and UPA receptor expression. MB49-I cells transfected with Ephrin-B1 siRNA showed lower migratory and invasive capacity than control cells (scramble siRNA). By immunohistochemistry, orthotopic MB49-I tumors had lower E-cadherin, increased nuclear β-catenin, lower pSer33-β-catenin cytoplasmic signal, and higher Ephrin-B1 expression than MB49 tumors. Similar changes were found in human BC tumors, and 83% of infiltrating tumors depicted a high Ephrin-B1 stain. An association between higher Ephrin-B1 expression and higher stage and tumor grade was found. No association was found between abnormal E-cadherin signal, Ephrin-B1 expression or clinical-pathological parameter. This study thoroughly analyzed E-cadherin and associated changes in BC, and reports Ephrin-B1 as a new marker of tumor aggressiveness.
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