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简介：在肿瘤开始的癌症干细胞(CSC)的重要性坚定地在白血病被建立了并且最近为许多稳固的肿瘤报导了。然而，特别地关于转移，在多级式的癌症前进的CSC的角色有不定义beenwell。癌症转移要求在远机关播种和specializedCSCs的成功的殖民。正常干细胞和CSC的生物学分享显著类似并且当适用于癌症的学习时，可以有重要含意转移。而且，重叠分子和小径的集合最近被识别了调整干细胞移植和癌症转移。这些分子组成两个都为移植CSC由主要肿瘤和养育的机关微型环境的形成便于转移前壁龛的开始的细胞的相互作用的一个复杂网络。在这评论，我们在这个动态领域里调查了最近的进展并且建议CSC在tumorigenesis和转移在假定一个中央角色的癌症前进的一个统一模型。更好作为变形串联的一个基本部件理解ofCSCs将对变形癌症导致新奇治疗学的策略。

简介：AbstractPlacentation and tumorigenesis have many common features. Human placentation builds a maternal-fetal connection, circumvents maternal immune rejection of the fetus, and utilizes mechanisms that support tumorigenesis, such as proliferation, invasion, angiogenesis, and immune tolerance. Trophoblasts of the human placenta mimic the behavior of malignant cells, proliferating and invading the uterine decidua until reaching the myometrium and remodeling the spiral arteries that establish a new vascular system and escape the maternal immune response. These processes are under precise temporal and spatial regulation, and their dysregulation is associated with different pregnancy syndromes, including preeclampsia (PE), a pregnancy syndrome that is the leading cause of maternal and perinatal mortality and morbidity. At present, the precise mechanisms underlying the development of PE remain unclear. Here, we summarize and dissect the features between physiological placentation and pathological tumorigenesis to explore the pathogenesis of PE - which we believe to be the result of insufficient placentation, compared to the overaggression of tumorigenesis - to provide novel strategies to prevent and treat PE.

简介：Wnt/尾-catenin调整与肿瘤有关的细胞的功能开始和前进，房间增长，区别，幸存，和粘附。尾-Catenin独立的Wnt小径被建议了调整房间极性和移植，包括转移。在这评论，我们在肿瘤前进讨论catenin依赖的尾-和独立人士发信号小径的可能的角色，与他们Rho家庭GTPases，改变的细胞骨架，和与房间房间粘附和cilia/ciliogenesis的关系的规定上的一个重音。

简介：在源于mitochondrial机能障碍的氧化phosphorylation的改变长被假设了涉及tumorigenesis。线粒体最近被显示了在调整规划房间死亡和房间增长起一个重要作用。而且，mitochondrialDNA(mtDNA)变化在各种各样的癌症房间被发现了。然而，在tumorigenesis的这些mtDNA变化的角色仍然保持大部分未知。这评论集中于基本mitochondrial遗传，mtDNA变化和与癌症联系的结果的mitochondrial机能障碍。潜在的分子的机制，调停从mtDNA变化的致病和到tumorigenesis的mitochondrial机能障碍也被讨论。

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简介：人的间充质的干细胞(hMSCs)装家到肿瘤地点并且禁止肿瘤细胞的生长。很少对内在的分子的机制被知道连接hMSCs到肿瘤房间的指向的抑制。在这研究，我们从hMSCs用一个动物移植模型，一个合作文化系统和调节媒介在二根人的hepatoma房间线(H7402和HepG2)上调查了hMSCs的效果。当SCID老鼠与H7402细胞和Z3hMSCs的一个相等的数字被注射时，动物移植研究证明肿瘤形成的潜伏的时间被延长并且肿瘤尺寸更小。当co有教养时与Z3房间，H7402细胞增殖减少了，增加的apoptosis，和Bcl-2的表示，c-Myc，原子抗原(PCNA)和survivin低是的增殖的房间调整了。在有调节媒介的处理源于Z3hMSC文化以后，H4702房间出现了减少的形成殖民地的能力和减少的增长。Immunoblot分析证明beta-catenin，Bcl-2，c-Myc，PCNA和survivin表示是在H7402和HepG2房间调整的down。总起来说，我们的调查结果证明hMSCs禁止H7402和HepG2人的肝癌症房间线的恶意的显型，它包括增长，形成殖民地的能力和oncogene表示试管内和体内。而且，我们的研究提供表明小径的Wnt可以在调停hMSC的指向和肿瘤房间抑制有一个角色的证据。

简介：瞄准：Disabled-2(DAB2)是在卵巢的癌症识别否定地影响生长因素和块地岬活动的致有丝分裂信号转导变异的候选人tumor-suppressor基因。在最近的研究，我们用cDNA在ESCC观察了DAB2抄本的下面规定微数组。在现在的学习，我们试图在食道的肿瘤发生决定DAB2蛋白质的损失的临床的意义，假设那个DAB2倡导者调停hypermethylation的基因silencing可以说明蛋白质的损失。方法：DAB2表示被免疫组织化学在50主要食道的有鳞的房间分析癌(ESCC)，30不同增生，15发育异常和10非恶意的食道的纸巾。决定倡导者hypermethylation是否在ESCC贡献DAB2表示的损失，DAB2倡导者的甲基化地位用methylation特定的PCR在DAB2免疫否定的肿瘤被分析。结果：DAB2蛋白质的损失在5/30(17%)被观察增生，10/15(67%)发育异常和34/50(68%)ESCC。DAB2蛋白质的重要损失从食道的正常粘膜被观察到增生，发育异常和侵略癌症(P(趋势)<0.001)。DAB2的倡导者hypermethylation在10中的2个被观察(20%)DAB2免疫否定的ESCC。结论：DAB2蛋白质表示的损失发生在食道的癌症的开发的早pre肿瘤的阶段并且在致瘤的小径下面被支撑。在ESCC的很少发生的DAB2倡导者甲基化建议渐成说基因silencing仅仅是在ESCC引起DAB2表示的损失的机制之一。

简介：CREB有约束力的蛋白质(CBP)和它的相当或相同事物p300是涉及细胞的活动的一个宽数组的各种各样的顺序特定的抄写因素的transcriptionalco使活跃之物，例如脱氧核糖核酸修理，房间生长，区别和apoptosis。Severalstudies建议了CBP和p300可能被看作瘤压制ors，与他们是的突出的角色响应各种各样的刺激的不同基因表示模式的跨coupling。他们主要经由乙酰化施加行动嘘和另外的规章的蛋白质(例如p53)。在CBP/p300功能的主要悖论是他们似乎能够贡献各种各样的反对细胞的进程。呼吸上皮tumorigenesis代表一个范围的多步累积的一个复杂过程基因并且epigenetic错误。通过激活和压抑的建筑群的交替的形成的Transcriptionmodulation是这些精神错乱的最终的收敛点，并且CBP/p300在这相互影响代表关键参加者。因此，他们的分子的行动和相互作用的照明能在呼吸上皮carcinogenesis为药理学干预揭示新潜在的目标。

简介：AbstractThe LIM domain only 1 (LMO1) gene belongs to the LMO family of genes that encodes a group of transcriptional cofactors. This group of transcriptional cofactors regulates gene transcription by acting as a key "connector" or "scaffold" in transcription complexes. All LMOs, including LMO1, are important players in the process of tumorigenesis. Unique biological features of LMO1 distinct from other LMO members, such as its tissue-specific expression patterns, interacting proteins, and transcriptional targets, have been increasingly recognized. Studies indicated that LMO1 plays a critical oncogenic role in various types of cancers, including T-cell acute lymphoblastic leukemia, neuroblastoma, gastric cancer, lung cancer, and prostate cancer. The molecular mechanisms underlying such functions of LMO1 have also been investigated, but they are currently far from being fully elucidated. Here, we focus on reviewing the current findings on the role of LMO1 in tumorigenesis, the mechanisms of its oncogenic action, and the mechanisms that drive its aberrant activation in cancers. We also briefly review its roles in the development process and non-cancer diseases. Finally, we discuss the remaining questions and future investigations required for promoting the translation of laboratory findings to clinical applications, including cancer diagnosis and treatment.

简介：Objective:Polycystickidneydisease(PKD)isthemajorcauseofkidneyfailureandmortalityinhumans.Ithasalwaysbeensuspectedthatthedevelopmentofcystickidneydiseasesharesfeatureswithtumorigenesis,althoughtheevidenceisunclear.Methods:Wecrossedp53mutantmice(p53N236S,p53S)withWernersyndromemiceandanalyzedthepathologicalphenotypes.TheRNA-seq,ssGSEAanalysis,andreal-timePCRwereperformedtodissectthegenesignaturesinvolvedinthedevelopmentofdiseasephenotypes.Results:Wefoundenlargedkidneyswithfluid-filledcystsinoffspringmicewithagenotypeofG3mTerc-/-WRN-/-p53S/S(G3TM).PathologyanalysisconfirmedtheoccurrenceofPKD,anditwashighlycorrelatedwiththeincidenceoftumorigenesis.RNA-seqdatarevealedthegenesignaturesinvolvedinPKDdevelopment,anddemonstratedthatPKDandtumorigenesissharedcommonpathways,includingcomplementpathways,lipidmetabolism,mitochondriaenergyhomeostasisandothers.Interestingly,thisG3TMPKDandtheclassicalPKD1/2deficientPKDsharedcommonpathways,possiblybecausethemutantp53ScouldregulatetheexpressionlevelsofPKD1/2,Pkhd1,andHnf1b.Conclusions:WeestablishedadualmousemodelforPKDandtumorigenesisderivedfromabnormalcellularproliferationandtelomeredysfunction.TheinnovativepointofourstudyistoreportPKDoccurringinconjunctionwithtumorigenesis.ThegenesignaturesrevealedmightshednewlightonthepathogenesisofPKD,andprovidenewmolecularbiomarkersforclinicaldiagnosisandprognosis.