専攻分野
出典: フリー百科事典『ウィキペディア（Wikipedia）』 (2021/10/07 04:48 UTC 版)
「ヨハン・ヴォルフガング・ゲーテ大学フランクフルト・アム・マイン」の記事における「専攻分野」の解説
フランクフルト大学では以下の16の専攻分野 (Fachbreich, FB) を開講している。 FB 01: 法学 FB 02: 経済学 FB 03: 社会学 FB 04: 教育学 FB 05: 心理学・体育学 FB 06: 福音主義神学 FB 07: カトリック神学 FB 08: 哲学・歴史学 FB 09: 言語学・文化学 FB 10: 文献学 FB 11: 地学／地理学 FB 12: 情報科学・数学 FB 13: 物理学 FB 14: 生化学・化学・薬学 FB 15: 生物学 FB 16: 医学
※この「専攻分野」の解説は、「ヨハン・ヴォルフガング・ゲーテ大学フランクフルト・アム・マイン」の解説の一部です。
「専攻分野」を含む「ヨハン・ヴォルフガング・ゲーテ大学フランクフルト・アム・マイン」の記事については、「ヨハン・ヴォルフガング・ゲーテ大学フランクフルト・アム・マイン」の概要を参照ください。
専攻分野
出典: フリー百科事典『ウィキペディア（Wikipedia）』 (2022/06/29 06:06 UTC 版)
日本における大学通信教育が行われている学問領域は、郵便による通信添削により学修成果の評価が可能である「教養学」・「経済学・経営学・商学」・「法学」・「文学」・「教育学（主に教員養成）」・「臨床心理学」等の人文科学系・社会科学系、及び「芸術学」系が中心になっていた。 現在ではインターネットの普及等による通信技術の進歩、大学等設置基準の緩和、各大学のカリキュラム編成の工夫等により、旧来の郵便による通信では学修成果を評価することが困難であった学問領域についても適正な学修評価が可能となった事により大学通信教育による学問領域は拡大し、「情報科学」・「建築学」・「自然科学」・「環境学」・「栄養学」・「社会福祉学」その他多様な学問領域が学べるようになっている。
※この「専攻分野」の解説は、「大学通信教育」の解説の一部です。
「専攻分野」を含む「大学通信教育」の記事については、「大学通信教育」の概要を参照ください。
専攻分野
出典: フリー百科事典『ウィキペディア（Wikipedia）』 (2021/09/12 06:41 UTC 版)
癌転移 婦人科癌; endometrial carcinoma; cervical cancer; ovarian cancer microRNA EMT: epithelial to mesenchymal transition (EMT) Twist1 gene, a critical EMT inducer in endometrial cancer en:Cervical_cancer cervical cancer p53: TP53, tumor suppressor in human tumors endometrial cancer ovarian cancer miR-194 is a tumor suppressor in endometrial cancer Prognostic significance of miR-194 in endometrial cancer miR-130b in endometrial cancer miR-101 is key tumor suppressor in both type I and type II endometrial cancer IQGAP1 is novel oncogene in endometrial cancer and ovarian cancer miR-106b acts as tumor suppressor in aggressive in endometrial cancer KLF17 gene induces EMT in endometrial cancer miR-31 functions as an oncogene by suppressing Hippo tumor suppressor pathway in endometrial cancer MiR-137 and miR-34a directly target Snail and inhibit EMT, invasion and sphere-forming ability of ovarian cancer cells. 35, Article number: 132 (2016) iASPP and p53 in human tumors miRNA-mediated PI3K/AKT signaling in endometrial cancer miRNA-124 directly targets and inhibits IQGAP1 expression in endometrial cancer EZH2 induces Twist expression by repressing miR-361 expression in aggressive type II endometrial cancer CRISPR/Cas9 vector mediated miR-21 gene editing inhibits the epithelial to mesenchymal transition in ovarian cancer cells lentiviral CRISPR/Cas9-mediated disruption of miR-21 inhibits EMT in ovarian cancer cells miR-124 binds to and suppresses oncogene iASPP expression in cervical cancer iASPP induces EMT and cisplatin resistance through miR-20a-FBXL5/BTG3 signaling in cervical cancer p53 gain of function mutations promote endometrial cancer progression and metastasis EZH2, MCL-1 and FOS gene are important oncogenes and EMT inducers in endometrial cancer CRISPR/Cas9 and and genome editing ZEB1 acts as a novel EMT inducer in endometrial cancer BMI-1 gene functions as a important EMT inducer in endometrial cancer cells Musashi-2 (MSI-2) has a crucial role in promoting cervical cancer metastasis PD-L1 is a critical oncogenic factor in cervical cancer progression, and miR-140/142/340/383 regulate the expression of PD-L1 in cervical cancer Exploring lncRNA-Mediated Regulatory Networks in Endometrial Cancer Long noncoding RNA NEAT1 drives aggressive endometrial cancer progression via miR-361-regulated networks involving STAT3 and tumor microenvironment-related genes B7H3 As a Promoter of Metastasis and Promising Therapeutic Target miR-203 inhibits ovarian tumor metastasis by targeting BIRC5 and attenuating the TGFβ pathway KLF4 expression enhances the efficacy of chemotherapy drugs in ovarian cancer cells Lentiviral vector mediated-ASAP1 expression promotes epithelial to mesenchymal transition in ovarian cancer cells miR-34a, miR-424 and miR-513 inhibit MMSET expression to repress endometrial cancer cell invasion and sphere formation Molecular-targeted therapies and precision medicine for endometrial cancer Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 editing inhibits epithelial to mesenchymal transition in ovarian cancer cells The Expression, Functions and Mechanisms of Circular RNAs in Gynecological Cancers Ovarian Primary and Metastatic Tumors Suppressed by Survivin Knockout or a Novel Survivin Inhibitor Yue, Junming and Du, Ziyun and Zhou, Fu-Ming and Dong, Peixin and Pfeffer, Lawrence M「Applications of CRSIPR/Cas9 in Cancer Research」『Cancer Medicine & Anti Cancer Drugs』第1巻第1号、OMICS International、2016年3月、 1000103頁、 NAID 120005752854。 LncRNA NEAT1-mediated miR-361 downregulation contributes to EMT of cervical cancer cells via increasing HSP90 expression: Epithelial-mesenchymal transition (EMT) is a key process contributing to cervical cancer (CC) metastasis, and microRNAs (miRNAs) modulate the expression of genes implicated in EMT. However, the accurate role of miR-361 in CC-associated EMT and the mechanisms underlying its function in CC remains largely unknown. The functional roles of miR-361 in CC cells were explored by a series of cell functional assays. Luciferase reporter assays were used to demonstrate the potential interaction between miR-361, HSP90, and long non-coding RNA (lncRNA) NEAT1. We detected a reduction of miR-361 expression in CC tissues compared with normal tissues, and miR-361 overexpression inhibited invasion and EMT phenotypes of CC cells by directly targeting a key EMT activator HSP90. Additionally, we detected significantly higher levels of HSP90 in CC tissues compared with normal tissues, and high expression of HSP90 predicted a poorer prognosis. We further identified NEAT1 as a significantly upregulated lncRNA in CC tissues and high expression of NEAT1 was associated with worse survival in CC patients. NEAT1 directly repressed miR-361 expression and played an oncogenic role in CC cell invasion and sphere formation. Conclusions: These results demonstrated that miR-361 directly targets HSP90 to inhibit the invasion and EMT features, and NEAT1 functions as an oncogenic lncRNA that suppresses miR-361 expression and induces EMT and sphere formation in CC cells, thus providing critical insights into the molecular pathways operating in this malignancy. MicroRNA-361: A Multifaceted Player Regulating Tumor Aggressiveness and Tumor Microenvironment Formation PD-L1 Is a Tumor Suppressor in Aggressive Endometrial Cancer Cells and Its Expression Is Regulated by miR-216a and lncRNA MEG3 Background: Poorly differentiated endometrioid adenocarcinoma and serous adenocarcinoma represent an aggressive subtype of endometrial cancer (EC). Programmed death-ligand-1 (PD-L1) was known to exhibit a tumor cell-intrinsic function in mediating immune-independent tumor progression. However, the functional relevance of tumor cell-intrinsic PD-L1 expression in aggressive EC cells and the mechanisms regulating its expression remain unknown. Methods: PD-L1 expression in 65 EC tissues and 18 normal endometrium samples was analyzed using immunohistochemical staining. The effects of PD-L1 on aggressive EC cell growth, migration and invasion were investigated by cell functional assays. Luciferase reporter assays were used to reveal the microRNA-216a (miR-216a)-dependent mechanism modulating the expression of PD-L1. Results: Positive PD-L1 expression was identified in 84% of benign cases but only in 12% of the EC samples, and the staining levels of PD-L1 in EC tissues were significantly lower than those in the normal tissues. Higher PD-L1 expression predicts favorable survival in EC. Ectopic expression of PD-L1 in aggressive EC cells results in decreased cell proliferation and the loss of mesenchymal phenotypes. Mechanistically, PD-L1 exerts the anti-tumor effects by downregulating MCL-1 expression. We found that PD-L1 levels in aggressive EC cells are regulated by miR-216a, which directly targets PD-L1. We further identified a mechanism whereby the long non-coding RNA MEG3 represses the expression of miR-216a, thereby leading to increased PD-L1 expression and significant inhibition of cell migration and invasion. Conclusion: These results reveal an unappreciated tumor cell-intrinsic role for PD-L1 as a tumor suppressor in aggressive EC cells, and identify MEG3 and miR-216a as upstream regulators of PD-L1.
※この「専攻分野」の解説は、「董培新」の解説の一部です。
「専攻分野」を含む「董培新」の記事については、「董培新」の概要を参照ください。
専攻分野
出典: フリー百科事典『ウィキペディア（Wikipedia）』 (2021/03/04 06:54 UTC 版)
「サウスイースト・ミズーリ州立大学」の記事における「専攻分野」の解説
会計学、システム管理マネージメント学、経営学、経済学、起業・小規模経営学、財務学、インターナショナルビジネス学、物理管理学、情報システム経営学、マーケティング学、組織管理学、幼児教育学、初等教育学、特殊教育学、中等教育学、宇宙空間学、コミュニケーション障害学、犯罪心理学、犯罪学、健康管理学、人間環境学、看護学、体育学、レクリエーション学、社会福祉学、人類学、英語学、一般教養学、国際学、マスコミュニケーション学、倫理学、政治学、心理学、宗教学、演劇学、女性学、生物学、機械物理学、環境科学、地球科学、数学、環境土壌学、物理学、農学、建築学、電子工学、グラフィックコミュニケーション工学、産業工学、土壌学など他多数。
※この「専攻分野」の解説は、「サウスイースト・ミズーリ州立大学」の解説の一部です。
「専攻分野」を含む「サウスイースト・ミズーリ州立大学」の記事については、「サウスイースト・ミズーリ州立大学」の概要を参照ください。
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