RESUMO
In the past two decades, minimally invasive spine surgery (MISS) techniques have been developed for spinal surgery. Historically, minimizing invasiveness in decompression surgery was initially reported as a MISS technique. In recent years, MISS techniques have also been applied for spinal stabilization techniques, which were defined as minimally invasive spine stabilization (MISt), including percutaneous pedicle screws (PPS) fixation, lateral lumbar interbody fusion, balloon kyphoplasty, percutaneous vertebroplasty, cortical bone trajectory, and cervical total disc replacement. These MISS techniques typically provide many advantages such as preservation of paraspinal musculature, less blood loss, a shorter operative time, less postoperative pain, and a lower infection rate as well as being more cost-effective compared to traditional open techniques. However, even MISS techniques are associated with several limitations including technical difficulty, training opportunities, surgical cost, equipment cost, and radiation exposure. These downsides of surgical treatments make conservative treatments more feasible option. In the future, medicine must become "minimally invasive" in the broadest sense-for all patients, conventional surgeries, medical personnel, hospital management, nursing care, and the medical economy. As a new framework for the treatment of spinal diseases, the concept of minimally invasive spinal treatment (MIST) has been proposed.
Assuntos
Doenças da Coluna Vertebral , Fusão Vertebral , Humanos , Vértebras Lombares/cirurgia , Procedimentos Cirúrgicos Minimamente Invasivos/métodos , Procedimentos Neurocirúrgicos/métodos , Fusão Vertebral/métodos , Resultado do TratamentoRESUMO
INTRODUCTION: Vertebral fractures associated with ankylosing spinal disorders pose significant diagnostic and therapeutic challenges. Notably, the ankylosed spine remains in ankylosis after fracture treatment, and the underlying susceptibility to further fractures still remains. Nevertheless, information is scarce in the literature concerning patients with ankylosing spinal disorders who have multiple episodes of vertebral fractures. CASE REPORT: Case 1 involves an 83-year-old male patient with diffuse idiopathic skeletal hyperostosis (ankylosis from C2 to L4) who had three episodes of vertebral fractures. The first episode involved a C5-C6 extension-type fracture, which was treated with posterior segmental screw instrumentation. Five years later, the patient sustained a three-column fracture at the L1 vertebra following another fall. The fracture was managed with percutaneous segmental screw instrumentation. One year and two months postoperatively, the patient fell again and had a refracture of the healed L1 fracture. The patient was treated with a hard brace, and the fracture healed. Case 2 involves a 76-year-old female patient with ankylosing spondylitis (ankylosis from C7 to L2) who had two episodes. At the first episode, she suffered paraplegia due to a T8 vertebra fracture. The patient was treated with laminectomy and posterior segmental screw instrumentation. The patient recovered well and had all the hardware removed at 10 months postoperatively. Five years later, she had another fall and suffered a three-column fracture at L1. The patient underwent percutaneous segmental screw instrumentation. The patient required revision surgery with L1 laminectomy and L1 right pediclectomy for persistent right inguinal pain. At one-year follow-up, the patient recovered well, and the fracture healed. CONCLUSIONS: The abovementioned cases show that an age older than 75 years and a long spinal ankylosis from the cervical spine to the lumbar spine may serve as risk factors for the repetition of vertebral fractures associated with ankylosed spinal disorders.
RESUMO
Ewing family tumors (EFTs) are associated with a chromosomal translocation resulting in a fusion of the amino-terminus of EWS with the DNA-binding domain of an ETS transcription factor. Although previous reports suggested that these chimeric proteins would act as aberrant transcription factors, their downstream targets have not been fully elucidated. To identify downstream targets of these EWS-ETS fusion proteins, we introduced EWS-ETS fusion constructs into a human fibrosarcoma cell line, HT-1080, by retroviral transduction. Here we report that the LAMB3 gene encoding the beta3 chain of basement membrane protein laminin-5 is induced to a significantly higher level in cells expressing EWS-ETSs than in cells expressing normal ETSs. Additionally through use of an antisense oligonucleotide for EWS-ERG in the W-ES EFT cell line, laminin beta3 protein was reduced coordinately with EWS-ERG fusion protein expression. Furthermore, we found small mRNAs were preferentially transcribed from the LAMB3 gene in EFT cell lines. Molecular cloning of the entire coding region shows that the alternative transcripts from different promoter(s) located within the intron 14, which encode small proteins, likely are major products of the LAMB3 gene in EFT cells. We show that the small isoforms conferred increased anchorage-independent proliferation to NIH3T3 cells. Together with previous studies showing that laminin-5 is involved in the invasive and malignant phenotype of several tumor types, our data suggest that the oncogenic effect of EWS-ETS may be mediated in part by upregulation of LAMB3 expression.
Assuntos
Moléculas de Adesão Celular/genética , Proteínas de Fusão Oncogênica/genética , Proteínas Proto-Oncogênicas c-ets/genética , Proteína EWS de Ligação a RNA/genética , Sarcoma de Ewing/genética , Animais , Moléculas de Adesão Celular/metabolismo , Linhagem Celular Tumoral , Clonagem Molecular , Humanos , Camundongos , Células NIH 3T3 , Oligonucleotídeos Antissenso/farmacologia , Proteínas de Fusão Oncogênica/metabolismo , Isoformas de Proteínas/genética , Isoformas de Proteínas/metabolismo , RNA Mensageiro/metabolismo , Proteínas Recombinantes de Fusão/metabolismo , Retroviridae/genética , Sarcoma de Ewing/metabolismo , Sarcoma de Ewing/patologia , CalininaRESUMO
Ewing sarcoma (ES) and peripheral primitive neuroectodermal tumors (PNETs) are associated with a chromosomal translocation resulting in a fusion of the amino-terminus of EWS with the DNA-binding domain of an ETS transcription factor (most commonly FLI1 or ERG). Although previous reports suggested that these chimera proteins would act as aberrant transcription factors, their downstream targets have not been fully elucidated. To identify downstream targets of these EWS-ETS fusion proteins, we introduced EWS-ETS fusion constructs into a human fibrosarcoma cell line, HT-1080, by retroviral transduction. Here we report that Tenascin-C (TNC) is induced to a significantly higher level in cells expressing EWS-ETSs than in cells expressing normal ETSs. Furthermore, through use of an antisense cDNA expression vector we show that expression of endogenous TNC mRNA and protein were reduced coordinately with attenuation of EWS-FLI1 fusion protein expression. A chromatin immunoprecipitation assay showed direct interaction between the TNC promoter and the EWS-FLI1 fusion protein in vivo. In addition, a luciferase reporter assay revealed that EWS-ETSs upregulated the TNC gene through four ETS binding sites in the TNC promoter. High levels of TNC expression were observed in a subset of ES cell lines (3 of 6) and primary tumors (4 of 6). Together with previous studies showing that TNC expression is involved in the invasive and malignant phenotype of several tumor types, our data suggest that the oncogenic effect of EWS-ETS may be mediated in part by upregulating of TNC expression.