【敬邀參加】2022.3.15 (二)12:00-13:00 美商默沙東藥廠全球臨床試驗執行處總監專題演講-臨床試驗工作剖析
|Chromatin remodeling genes in gynecologic cancer progression and therapy|
|施益民 教授 Ie-Ming Shih, M.D., Ph.D.
Richard W. TeLinde Distinguished Professor
Director, TeLinde Gynecologic Disease Program
Co-Director, Women’s Malignancies Program
February 22, 2022, 10:00-12:00
4F Hall, Comprehensive Medical Building (Front Building)
ARID1A has emerged as a tumor suppressor gene, which is mutated in a broad spectrum of cancers, especially in those gynecologic cancers arising from ectopic or eutopic endometrium including ovarian clear cell, ovarian endometrioid and uterine endometrioid carcinomas. As a subunit of SWI/SNF chromatin remodeler, ARID1A facilitates target-specific binding of SWI/SNF complexes to chromatin, thereby altering the accessibility of chromatin to a variety of nuclear factors. In human cancer, ARID1A possesses not only features of a gatekeeper, regulating cell cycle progression, but also features of a caretaker, preventing genomic instability through DNA damage repair. Moreover, an increasing body of evidence suggests that ARID1A containing SWI/SNF complexes play a pivotal role in transcriptional regulation of genes involving in several cancer-associated signaling pathways. In this seminar, we will discuss the mechanisms underlying how ARID1A mutations cause cancer progression and the clinical implications of synthetic lethality in developing ARID1A mutation-based therapeutics.
請登入「人才發展系統」https://ehrd.tmu.edu.tw/eHRD/eHRDOrg → (左上方) 查詢與申請→ 課程「醫科所【拇山生物醫學研究講座】– 111/02/22 演講者：施益民 教授 (Johns Hopkins University School of Medicine)」(「關鍵字」可以搜尋：拇山 ) →教室→確認
敬邀參加【單細胞基因體核心實驗室系列研討會】-自動化微流體分子標記基因庫建構系統 10X Chromium Controller系列課程: 空間基因表達技術 (Visium)
|2021.11.23 (二) 10:00-11:00|
題 目：CCRL2 is prostate cancer cell stemness mediator that regulates the organ-specific cancer metastasis
講 者：宋賢穎 副教授
日 期：2021 年 8 月 16日
講 題：CRISPR engineered human brown like adipocytes ameliorate metabolic dysregulation in mice
時 間：109年12月16日(W3) 13:00~15:00
地 點：大安校區 B2 B203會議室
Speaker: Chih-Hao Wang (Assistant Professor)
Date ：2020-12-16 (Wednesday)
Venue: B203, B2F, Daan campus
CRISPR-engineered human brown-like adipocytes ameliorate metabolic dysregulation in mice
Brown and white fats play crucial roles in systemic energy homeostasis. Brown fat is specific for energy dissipation and has multilocular lipid droplets, while white fat is the main site for storing excess fuel containing unilocular lipid droplets. The activity and amount of brown fat are inversely correlated with body mass index in mammals, making brown fat an appealing target for anti-obesity therapies. Aiming for transforming white fat to brown fat may hold great potential in preventing or treating obesity and obesity-related metabolic disorders, since white fat is more easily reachable and manipulatable considering its abundance and location. Uncoupling protein 1 (UCP1) is uniquely expressed in brown adipocytes and facilitates fuel utilization and energy expenditure. Here, we utilized the CRISPR/Cas9 synergistic activation mediator and specific gRNAs to boost endogenous UCP1 expression in human white adipocytes. The CRISPR/Cas9 engineered human brown fat-like (HUMBLE) cells had acquired human brown fat features when comparing bona fide human brown adipocytes derived from the same individual. Obese mice that received HUMBLE cell transplants showed lower body weight, a sustained improvement in glucose tolerance and insulin sensitivity, as well as increased energy expenditure. Mechanistically, increased arginine/nitric oxide (NO) metabolism in HUMBLE adipocytes promoted the production of NO that was carried by S-nitrosothiols and nitrite in red blood cells to activate endogenous brown fat and improved glucose homeostasis in recipient animals. Taken together, these data demonstrate the utility of using CRISPR/Cas9 technology to engineer human white adipocytes to display brown fat-like phenotypes and may open up cell-based therapeutic opportunities to combat obesity and diabetes.
Speaker: Prof. Kang-Yun Lee
Date ：2020-12-9 (Wednesday)
Venue: B203, B2F, Daan campus
Epigenetic regulation of inflammation in airway disease
From aberrant inflammation to repair and regeneration
– An Evolutionary Perspective on COPD
COPD has great impact on human health, which is the fourth leading cause of death worldwide. It is believed that chronic inflammation is central to the pathogenesis of the disease, causing progressive and irreversible airflow limitation. The inflammation in the airways and the lung is chronic, amplified and self-perpetuated with poor response to glucocorticoids. Although large efforts have been made to develop anti-inflammatory medications, particularly kinases inhibitors, none of them has promising results. Other directions including the epigenetic, anti-oxidant, specific immune abnormality (e.g. Th-17, Tc1, ILC1…) are still struggling. In addition to inflammation, other pathogenetic mechanisms might also have implication, in particular repair and regeneration. We currently focus on air pollution-induced emphysema and has identified novel players in the pathogenesis of the disease, such as Inter-alpha-trypsin inhibitor heavy chain H4 (ITIH4). In this talk, the evolution of the concept of COPD pathogenesis will be reviewed, which will point to a new direction of treatment of COPD.
，提供影片連結如下。歡迎踴躍觀看！English Version : https://www.youtube.com/ watch?v=IqLpyTC7fbM&feature= youtu.be