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Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is considered to be an immune-mediated heterogeneous disease involving cellular and humoral immunity. In recent years, autoantibodies against nodal/paranodal protein neurofascin155 (NF155), neurofascin186 (NF186), contactin-1 (CNTN1), and contactin-associated protein 1 (CASPR1) have been identified in a small subset of patients with CIDP, which disrupt axo-glial interactions at nodes/paranodes. Although CIDP electrodiagnosis was made in patients with anti-nodal/paranodal component autoantibodies, macrophage-induced demyelination, the characteristic of typical CIDP, was not observed. Apart from specific histopathology, the pathogenic mechanisms and clinical manifestations of CIDP with autoantibody are also distinct. We herein compared pathogenesis, histopathology, clinical manifestations, and therapeutic response in CIDP with autoantibody vs. CIDP without autoantibody. CIDP with autoantibodies should be considered as an independent disease entity, not a subtype of CIDP due to many differences. They possibly should be classified as CIDP-like chronic nodo-paranodopathy, which can better characterize these disorders, help diagnose and make the most effective therapeutic decisions.BACKGROUND Spinocerebellar ataxias (SCAs) are rare dominantly inherited neurodegenerative disorders that lead to severe disability and premature death. OBJECTIVE To better characterize the natural history of the most common SCAs, SCA1, SCA2, SCA3 and SCA6, we performed a meta-analysis of literature to determine disease progression, provide data for sample-sizes calculations for interventional trials and study the impact of geographical locations and study follow-up on disease progression. METHODS A systematic literature search from MEDLINE and EMBASE databases for longitudinal natural history studies of SCA patients was conducted. Studies using the Scale for the Assessment and Rating Ataxia (SARA) as outcome measure were considered. Random-effect (RE) meta-analysis was applied to estimate pooled disease progression. RESULTS Six studies with 1215 SCA patients enrolled between 2005 and 2016 were finally selected. Annual pooled SARA score increase was 1.83 (1.46-2.20) in patients with SCA1, 1.40 (1.19-1.61) in pnd improve patient stratification in interventional trials.OBJECTIVE To evaluate the prognostic potential of vimentin, p53, EGFR, CK5/6, CK 14, and CK 17 in patients with triple-negative breast cancer (TNBC). MATERIAL AND METHODS Tumor specimens of 60 patients with histologically confirmed TNBC were retrospectively analyzed. Formalin-fixed paraffin-embedded blocks of the tumor tissue were used to prepare tissue microarrays (TMAs). After immune-histochemical staining, protein expression of vimentin, p53, EGFR, CK5/6, CK 14, and CK 17 was determined and the immunoreactive score (IRS) was calculated. The protein expression was correlated to overall (OS) and disease-free survival (DFS). RESULTS Ninety percent of patients suffered from an invasive ductal carcinoma T1 or T2, 66.7% were N0, and 70% had a G3 tumor with Ki67 of > 14%. Vimentin expression was found in 28/60 patients (46.7%), p53 expression in 30/60 patients (50%), and EGFR expression in 3/60 patients (5%). CK5/6, CK14, and CK17 expression was found in 60.0%, 63.3%, and 66.7%, respectively. Vimentin expression vs no expression was associated with significantly higher mean Ki67 values (52.5% vs. 31.1%; p = 0.0013) and significantly higher p53 expression (67.9% vs. 34.4%; p = 0.0097). No significant association between vimentin expression and OS (p = 0.7710) or DFS (p = 0.5558) was found during a mean follow-up of 92 months. CONCLUSION None of the six proteins proved to be suitable prognostic factors for OS and DSF in patients with TNBC.BACKGROUND An increasing number of studies have focused on the early diagnostic value of the methylation of RASSF1A and SHOX2 in lung cancer. However, the intricate cellular events related to RASSF1A and SHOX2 in lung cancer are still a mystery. For researchers and clinicians aiming to more profoundly understand the diagnostic value of methylated RASSF1A and SHOX2 in lung cancer, this review will provide deeper insights into the molecular events of RASSF1A and SHOX2 in lung cancer. METHODOLOGY We searched for relevant publications in the PubMed and Google Scholar databases using the keywords "RASSF1A", "SHOX2" and "lung cancer" etc. First, we reviewed the RASSF1A and SHOX2 genes, from their family structures to the functions of their basic structural domains. Then we mainly focused on the roles of RASSF1A and SHOX2 in lung cancer, especially on their molecular events in recent decades. Finally, we compared the value of measuring RASSF1A and SHOX2 gene methylation with that of the common methods for the diagnosis of lung cancer patients. RESULTS The RASSF1A and SHOX2 genes were confirmed to be regulators or effectors of multiple cancer signaling pathways, driving tumorigenesis and lung cancer progression. MZ-1 modulator The detection of RASSF1A and SHOX2 gene methylation has higher sensitivity and specificity than other commonly used methods for diagnosing lung cancer, especially in the early stage. CONCLUSIONS The RASSF1A and SHOX2 genes are critical for the processes of tumorigenesis, development, metastasis, drug resistance, and recurrence in lung cancer. MZ-1 modulator The combined detection of RASSF1A and SHOX2 gene methylation was identified as an excellent method for the screening and surveillance of lung cancer that exhibits high sensitivity and specificity.PURPOSE It is important for hepatocellular carcinoma (HCC) treatment that the targets related to its progression are identified. Clustered regularly interspaced short palindromic repeat (CRISPR)-associated nuclease 9 (Cas9)-based genetic screening is a powerful tool for identifying genes with loss-of-function mutations that are critical for tumour growth and metastasis. METHODS We transduced the human SMMC7721 HCC cell line expressing Cas9 with a human genome-scale CRISPR-Cas9 knockout (GeCKO) lentiviral library A (hGeCKOa) of 65,383 single-guide RNAs (sgRNAs) targeting 19,050 human genes; we then subcutaneously transplanted the transduced cells into nude mice. RESULTS The transduced cells were found to proliferate and metastasize faster than the untransduced cells. Through next-generation sequencing, the genes potentially related to HCC proliferation and metastasis were identified. The sgRNAs targeting the ADAMTSL3 and PTEN genes appeared twice on the list of genes related to HCC proliferation and metastasis, respectively.
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