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Objective:To evaluate the safety and efficacy of single incision apocrine gland excision in the treatment of children and adult patients with axillary osmidrosis.Methods:Medical records and follow-up results were reviewed for 164 patients who underwent surgical treatment in our department by the same surgeon from January 2013 to December 2016. There were 54 males and 110 females, aged 8-61 years. with a median age of 22 years. The patients were divided into the children group ( n=31) and the adults group ( n=133), and differences between the two groups were compared. Results:The end point of follow-up was December 2019, the cure and overall satisfaction rates in the third year after surgery were 77.6% (125/161) and 88.2% (142/161) for the total population, including 87.5% (27/31) and 93.5% (29/31) for the children, respectively. There were no significantly differences in the cure rate, scar, pigmentation and the patients' satisfaction between two groups during the follow-up. The cure rate, significantly improved rate and satisfaction rate in patients who became adult during the follow-up were 80.0% (20/25), 92.0% (23/25) and 96.0% (24/25), respectively.Conclusions:Single incision apocrine gland excision could be performed for children patients. Our procedure is safe, reliable and consistant, and worthy of clinical application.
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Objective:To investigate the expression and clinical relevance of micro RNA (miR)-324-5p in pancreatic cancer tissues, and to explore the effects and potential mechanisms of miR-324-5p on the proliferation and migration of pancreatic cancer cells.Methods:Real-time quantitative PCR was used to detect the expression of miR-324-5p in 34 pairs of pancreatic cancer and adjacent normal tissues resected at Peking University First Hospital from October 2018 to September 2019. The correlations between miR-324-5p expression and clinicopathological characteristics and prognosis of pancreatic cancer were analyzed using data from the Cancer Genome Atlas (TCGA) database. Real-time PCR was used to detect the expression of miR-324-5p in pancreatic cancer cell lines, and PANC-1 cell was used for functional study by overexpressing miR-324-5p via mimic transfection. CCK8 assay was used to evaluate cell proliferation. Both transwell and scratch wound healing assay were used to assess the cancer cell migration ability. Related proteins were detected by Western blot. The potential downstream target genes of miR-324-5p were selected using data from miRNA target genes predicted webs, in combination with functional analysis and their expressional correlation with miR-324-5p.Results:Data from TCGA database showed that the expression of miR-324-5p in tumor tissues was significantly lower than that in normal pancreatic tissues. And low level of miR-324-5p in pancreatic cancer was correlated with poor prognosis. Analysis of 34 pairs pancreatic cancer and adjacent normal tissues showed that miR-324-5p expression in tumor tissues (11.7±2.0) was significantly lower than that in adjacent normal tissues (70.9±14.4), and the pancreatic cancer patients who had the nerve invasion cancer showed low level of miR-324-5p (82.1%, 23/28) was significantly higher than that patients with high level of miR-324-5p (33.3%, 2/6). The expression of miR-324-5p in human pancreatic cancer cell line was also significantly lower than that in normal pancreatic ductal cells. CCK-8 assay showed that the proliferation ability of PANC-1 cell was significantly decreased when miR-324-5p was overexpressed. Transwell and wound healing assays showed that the capabilities of vertical migration and the horizontal movement were significantly inhibited in PANC-1 cell with miR-324-5p overexpressed [(30.11±5.2) and (174.6±27.0) μm, respectively] than those in control groups [(63.6±4.2) and (458.3±22.3) μm, respectively]. Moreover, Western blots showed a significant overexpression of miR-324-5p inhibited epithelial-mesenchymal transition (EMT). According to the data from miRNA target genes prediction and the functional analysis we found KLF3, MGAT3, PBX1 and ZNRF2 were considered as the potential downstream target genes of miR-324-5p.Conclusions:Our results indicated that miR-324-5p is lowly expressed and acts as the tumor suppressor gene in pancreatic cancer, and low level of miR-324-5p is correlated to a higher rate of nerve invasion and poor prognosis. In human pancreatic cancer cell, miR-324-5p may regulate EMT by directly inhibiting target genes such as KLF3, MGAT3, PBX1, ZNRF2, which in turn suppresses cancer cell proliferation and migration.
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The incidence of pancreatic cancer (PC) has continuously shown an upward trend all over the world. It remains one of the most challenging malignant tumors in clinical practice and is characterized by difficult diagnosis in early stages, low surgical resection rate and poor prognosis. Due to its significant genetic heterogeneity, there are notable individual differences in disease progression, clinical efficacy, sensitivity to chemoradiotherapy, and prognosis among PC patients. In-depth study is needed to reveal the molecular biological characteristics of different PC subtypes and their correlation with clinical manifestations and chemoradiotherapy sensitivity, which could contribute to develop corresponding targeted therapeutic strategies.It is not only the fundamental basis for the innovation of PC morphological classification to molecular subtyping, but also a prerequisite for achieving a shift in treatment mode from "standard therapeutic strategy for different diseases" to "treat the same disease with different strategies" .This article reviews several hot issues on the comprehensive diagnosis and treatment of PC in the era of targeted therapy and prospects its future development.
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Rational molecular subtyping of pancreatic cancer based on genome,transcriptome,proteomics and metabolomics data,in combination with systematic biological analysis,have greatly enriched the traditional histopathological typing methods based on morphology.The introduction of molecular subtyping reflects the progress in deep understanding of the essence of tumorigenesis of pancreatic cancer,providing a necessary foundation for the development of molecular targeted therapy and implementation of precision medicine.Therefore,molecular subtyping of pancreatic cancer has broad application prospects.The current article reviews the current research status and recent progress of molecular subtyping of pancreatic cancer,and discusses the clinical significance of different subtyping methods.
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Transforming growth factor-β (TGF-β) members are key cytokines that control embryogenesis and tissue homeostasis via transmembrane TGF-β type II (TβR II) and type I (TβRI) and serine/threonine kinases receptors. Aberrant activation of TGF-β signaling leads to diseases, including cancer. In advanced cancer, the TGF-β/SMAD pathway can act as an oncogenic factor driving tumor cell invasion and metastasis, and thus is considered to be a therapeutic target. The activity of TGF-β/SMAD pathway is known to be regulated by ubiquitination at multiple levels. As ubiquitination is reversible, emerging studies have uncovered key roles for ubiquitin-removals on TGF-β signaling components by deubiquitinating enzymes (DUBs). In this paper, we summarize the latest findings on the DUBs that control the activity of the TGF-β signaling pathway. The regulatory roles of these DUBs as a driving force for cancer progression as well as their underlying working mechanisms are also discussed.