Utility of Tissue Similarity Maps Based on Relative Cerebral Blood Volume for Grading Gliomas as Validated by Histological Results

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Nidogen 1 regulates proliferation and migration/invasion in murine claudin-low mammary tumor cells

Nidogen 1 (NID1) is a glycoprotein found in basement membranes involved in cross-linking collagen IV and laminin. The role of NID in breast cancer has only been evaluated in a small number of studies and the findings of these studies have been inconsistent. Our previous work revealed that highly tumorigenic murine mammary tumor cells express high levels of Nid1 while weakly tumorigenic mammary tumor cells express low levels of Nid1. To investigate Nid1, two stable knockdown lines were created, and Nid1 knockdown was confirmed at both the mRNA and protein level. Nid1 knockdown significantly reduced cell proliferation and migration/invasion and these reductions in proliferation and migration/invasion could be rescued by conditioned media containing NID1 protein. The reduced migration/invasion observed in the Nid1 knockdown cells was not associated with significant alterations in the epithelial gene Cdh1 or the mesenchymal genes Snai1, Snai2, Twist1, Twist2, Zeb1 and Zeb2. Therefore, suppression of Nid1 expression reduces proliferation and migration/invasion in claudin-low murine mammary tumor cells.     

Hiperplasia endotelial papilar intravascular (tumor Masson) de localización ginecológica

Intravascular papillary endothelial hyperplasia or Masson's tumour is a non-neoplastic vascular lesion of reactive character. It is a rare diagnosis, clinically non-specific and with diverse locations. It is essential to take it into consideration and make a differential diagnosis with malignant vascular tumours such as angiosarcoma. Pathological study is fundamental for diagnosis. Treatment consists of complete resection of the tumour, including sufficiently wide margins to avoid recurrence.The case reported is an exceptional event, because of the pelvic location of the Masson's tumour that was diagnosed as part of the surgical staging of an ovarian cancer.     

热疗对肿瘤免疫微环境中免疫细胞及免疫相关细胞因子的影响

随着对肿瘤热疗和肿瘤免疫微环境(TIME)的深入研究,近年来热疗对TIME的作用越来越受到学者们的重视。本文就目前国内外研究进展,对热疗与TIME中几类主要免疫细胞和免疫相关细胞因子的影响及作用机制作一综述。全面而透彻的了解热疗对TIME的调控作用,有助于为肿瘤治疗提供新的思路和方法。     

Suppression of PRDX4 inhibits cell proliferation and invasion of ectopic endometrial stromal cells in endometriosis

Abstract

Oxidative stress (OS) has been proposed to play a role in the development of EMs. Peroxiredoxins are a family of antioxidant proteins that exhibit peroxidase activity in a thioredoxin-dependent manner, protecting cells against OS. The Western blotting results showed that the relative expression of PRDX4 was significantly increased in ectopic endometria compared with the normal endometria of EMs-free (p?<?.05). The H₂O₂ concentration was also significantly higher in the ectopic endometrium. PRDX4 siRNA was transfected into primary ectopic endometrial stromal cells (EESCs). The viability of the transfected EESCs was measured by CCK-8 assay, and the results showed significantly decreased cell viability. Furthermore, the apoptosis rate and ROS generation in flow cytometry assays were significantly increased after the knockdown of PRDX4 expression (p?<?.05). Scratch assays and transwell assays revealed that decreased expression of PRDX4 mediated by siRNA inhibited EESC migration and invasion. In conclusion, these findings indicate the potential role of PRDX4 in the development of EMs and PRDX4 as a possible therapeutic target for EMs treatment.     

吉西他滨联合西妥昔单抗对三阴乳腺癌细胞转移相关基质金属蛋白酶-9(MMP-9)活性的影响

目的：探讨吉西他滨联合西妥昔单抗对三阴乳腺癌细胞增殖、迁移、侵袭的影响，并对可能的机制进行初步的探究。方法：将实验分为西妥昔单抗组（150 μg · mL^-1）、吉西他滨联合用药组（西妥昔单抗150 μg · mL^-1，吉西他滨2.8 μg·mL^-1）。通过MTT、Transwell实验检测联合用药对MDA-MB-231细胞增殖、迁移、侵袭能力的影响，Western blotting实验检测合用药对MDA-MB-231细胞MMP-9、TIMP-1、p-IkB、NF-kB-p65表达水平的影响。结果：吉西他滨联合西妥昔单抗作用MDA-MB-231细胞后，其生长被不同程度的抑制，抑制率随吉西他滨浓度的增加而增高（P<0.05）；联合用药组MDA-MB-231细胞迁移、侵袭数目明显减少（P<0.05），同时MMP-9、p-IkB、NF-kB-p65的表达含量降低，TIMP-1表达含量增加。结论：吉西他滨联合西妥昔单抗对三阴乳腺癌细胞增殖、侵袭、迁移具有抑制作用，并明显抑制MMP-9的表达，其机制可能是通过抑制NF-kB通路实现。     

A Novel Nomogram to Identify Candidates for Extended Pelvic Lymph Node Dissection Among Patients with Clinically Localized Prostate Cancer Diagnosed with Magnetic Resonance Imaging-targeted and Systematic Biopsies

Background

Available models for predicting lymph node invasion (LNI) in prostate cancer (PCa) patients undergoing radical prostatectomy (RP) might not be applicable to men diagnosed via magnetic resonance imaging (MRI)-targeted biopsies.

ELAM-1在鼻咽癌裸鼠移植瘤中的表达及其与转移的关系

目的 建立裸鼠鼻咽癌转移模型并探讨 E-选择素（ELAM-1）与鼻咽癌转移的相关性。方法 将鼻咽癌5-8F细胞悬液注射于裸鼠左后肢爪垫，观察裸鼠状态、成瘤情况并测量裸鼠体重及移植瘤长短径；采用连续病理切片苏木精-伊红染色观察移植瘤及转移情况，将16只人鼻咽癌荷瘤裸鼠分为转移组和非转移组；采用免疫组织化学法检测两组移植瘤组织中ELAM-1的表达。 结果 16只裸鼠均成瘤，成瘤率为100.0%，其中10只裸鼠出现转移瘤，转移率为62.5%。建模前，两组裸鼠体重差异无统计学意义［（13.83±0.56）g vs （14.62±0.30） g，t=1.026，P=0.071］。建模后4~7周，裸鼠瘤体体积呈指数增长，且转移组移植瘤增长速度较非转移组快，非转移组裸鼠瘤体体积小于转移组［（198.91 ± 163.29） mm³ vs （268.76 ±174.31） mm³，t=4.376，P=0.005］。ELAM-1在鼻咽癌裸鼠移植瘤、淋巴结转移灶及远处转移灶中的表达均为阳性，主要表达于细胞膜。转移组移植瘤光密度值高于非转移组（0.4497±0.0705 vs 0.0435±0.0082，t=4.388，P＝0.001）。结论 本研究成功构建稳定性好、转移率高的鼻咽癌裸鼠移植瘤转移模型，且ELAM-1在裸鼠移植瘤中高表达，可促进鼻咽癌裸鼠移植瘤生长和转移。     

外科治疗ⅢA期N2非小细胞肺癌的预后分析及临床意义

目的 探讨影响ⅢA期N2非小细胞肺癌（NSCLC）预后的因素，并分析经手术治疗不同亚组病人的生存率差异。方法 分析1997年1月至2000年1月146例手术治疗的ⅢA期N2 NSCLC病人的可能影响预后因素：病理类型、肿瘤位置、肿瘤大小、手术方式、临床N2情况，N2转移组数及个数、术后辅助治疗等，并用Kaplan-Meier曲线及Logr ank检验生存率差异，Cox单因素、多因素分析各因素对生存率的影响。结果 ⅢA期N2 NSCLC病人的3年和5年生存率分别为19．86％和14．56％。单因素分析示肿瘤位置、临床N2情况、N2转移组数及个数是影响生存率的因素；多因素分析示肿瘤大小、临床N2情况，N2转移组数和肿瘤位置影响预后。右肺下叶肿瘤单组或单个N2转移，预后最好。结论 纵隔N2转移淋巴结的大小、个数和组数是影响术后生存率主要因素。手术前未发现N2转移（mN2），有1组N2转移（N2h），N2转移数少于4个者手术治疗效果好。右肺下叶肿瘤发生单组N2淋巴结转移预后好。