Biography

Bailey博士于2014年9月加入德克萨斯大学医学院Houston，担任胃肠病学，肝病学和营养部内科学系的助理教授。在约翰·霍普金斯大学（Johns Hopkins University）完成博士后奖学金后，她加入了该系。

Dr. Jennifer Bailey earned her B.S. in Molecular Biology from the University of Nebraska-Lincoln in 2002, where she studied the role of algal lipopolysaccharides on the innate immune system in the Laboratory of Professor Ted Pardy. As an undergraduate student she also worked with Professor Bill Tapprich at the University of Nebraska-Omaha, where she studied the RNA structure of viral IRES elements and completed her M.A. in Biochemistry in 2004. While completing her degree, she was accepted as a summer fellow at the National Institutes of Health where she worked in the lab of Dr. Steven Jacobson. She then went on to pursue her Ph.D. in Cancer Research from the Eppley Institute at the University of Nebraska Medical Center in the Laboratory of Professor Tony Hollingsworth. Her dissertation work focused on mechanisms regulating pancreatic cancer progression and metastases. This research effort included the fundamental observation that hedgehog ligands regulate desmoplasia in pancreatic cancer.

完成博士学位后2009年，她移居约翰·霍普金斯大学医学院，继续在胰腺癌中工作。她加入了史蒂文·利奇（Steven Leach）教授的实验室，研究了调节胰腺癌再生和早期肿瘤的机制。值得注意的是，贝利博士在博士后研究期间确定了侵入性胰腺癌中存在的假定癌症干细胞群体，该细胞具有胃肠道“簇”细胞形态，并由DCLK1和乙酰化的α-管ul蛋白标记。她获得了美国国家癌症研究所（National Cancer Institute）的F32个人博士后奖，以资助她的工作，2011年，贝利（Bailey）博士获得了胰腺癌行动网络/AACR领导力奖。

她是美国癌症研究协会的成员，此前她曾在副委员会，美国胃肠道学会和美国科学发展协会任职。beplay苹果手机能用吗

Education

Postdoctoral Fellowship
Johns Hopkins University School of Medicine
Ph.D. Cancer Research
The Eppley Institute, University of Nebraska Medical Center

兴趣范围

beplay苹果手机能用吗研究兴趣

胰腺癌

Research Information

The overall research program in the Bailey Lab is centered on understanding the biology of precancerous and cancerous lesions in the gastrointestinal system, with a focus on the molecular processes that regulate the transition from normal epithelium to cancer. For a number of years, we have employed lineage-tracing techniques to study stem cells and cells of origin in genetically engineered mouse models. In addition, we use these models to understand chronic inflammatory processes that increase the risk for the accumulation of oncogenic mutations in the pancreatic epithelium. There are a number of funded projects in the lab related to these ideas, and our overall goal is to better define therapeutic strategies for the personalized treatment of pancreatic and other GI malignancies.

三个主要思想强调了贝利实验室的工作：1）确定调节上皮再生和转化的遗传，表观遗传学，整体转录组和旁分泌信号事件。2）更好地了解调节细胞可塑性的遗传和表观遗传过程。3）确定调节不同细胞类型如何应对驱动肿瘤进展突变的积累的遗传和表观遗传事件。

我们全面使用遗传小鼠模型，细胞培养和人体组织标本来解决与这些主要目标有关的许多目标假设。我们热情地扩大了德克萨斯医学中心消化疾病中心，埃尔坦消化疾病中心和外科部的转化研究工作和合作。beplay苹果手机能用吗

Current Lab Members:

  • Kishore Polireddy, PhD: Postdoctoral Fellow
  • Kanchan Singh博士：博士后研究员
  • Guanghui Zhu, MD, PhD: Visiting Scientist
  • 尼尔·琼斯：医学生
  • 梅利莎·普鲁斯基（Melissa Pruskibeplay苹果手机能用吗）：高级研究助理

出版物

出版信息

REFERENCES

  • Hendley AM，Wang YJ，Alsina J，Ahmed I，Lafaro KJ，Zhang H，Roy N，Savidge S，Cao Y，Hebrok M，Maitra A，Maitra A，Reynolds AB，Goggins M，Younes M，Iacobuzio-Donahue CA，Leach SD，Leach SD，Leach SD，SD，SD，SD，SD，，，Leach SD，SD，SD，，，LEACH SD，SD，SD，SD，，Younes M，Younes M，Younes M，Younes M，Leachs和Bailey JM。(2016). p120 Catenin suppresses basal epithelial cell extrusion in invasive pancreatic neoplasia.Cancer Research。3月31日。PMID：269844
  • Choi，E，Hendley，AM，Bailey JM，Leach SD，Goldenring Jr。（2015）。在小鼠胃中启动了全癌前化生转化率的启动。胃肠病学。12月8日PMID：26677984
  • Bailey JM*，Hendley AM，Lafaro KJ，Pruski MA，Jones NC，Alsina J，Younes M，Maitra A，McAllister F，Iacobuzio-Donahue CA，Leach SD。（2015）。p53功能获得突变促进胰腺导管细胞的腺癌。Oncogene.Nov 23 *Corresponding author PMID: 26592447
  • Bailey JM*，Hendley AM和Maitra A.（2015）。对胰腺癌可塑性的新见解：癌症细胞通过基本螺旋 - 环螺旋转录因子E47重编程。Pancreas，Jul; 44（5）：683-5。*通讯作者PMID：26061556
  • 亨德利·阿，和Bailey JM。（2015）。Stem Cells and Pancreatic Cancer.Principles of Stem Cell Biology and Cancer: Future Applications and Therapeutics.John Wiley＆Sons，Ltd，英国奇切斯特。
  • Bailey JM, Alsina J,拉希德咱,麦卡利斯特FM,傅等号左边,请耐心ntz R, Zhang H, Pasricha PJ, Bardeesy N, Matsui W, Maitra A, Leach SD. (2014). DCLK1 Marks a Morphologically Distinct Subpopulation of Cells with Stem Cell Properties in Pre-invasive Pancreatic Cancer.Gastroenterology。1月; 146（1）：245-56。PMID：24096005
  • McAllister FM,Bailey JM, Alsina J, Maitra A, Kolls J, Pardoll D, Seers C, and Leach SD. (2014). Oncogenic Kras activates an IL-17+ hematopoietic-to-epithelial signaling axis in preinvasive pancreatic neoplasia.癌细胞。5月; 25（5）：621-637。PMID：24823639
  • Rhim AD, Mirek ET, Aiello NM, Maitra A,Bailey JM, McAllister F, Reichart M, Beatty GL, Rustgi AK, Vonderheide RH, Leach SD, Stanger BZ. (2012). EMT and dissemination precede pancreatic tumor formation.CellJan 20;148(1-2):349-61. PMID: 22265420
  • Bailey JM，Swanson BJ，Hamada T，Eggers JP，Singh PK Caffery TC，Ouellette MM和MA Hollingsworth。（2008）。Sonic刺猬促进胰腺癌中的脱木质。Clin Cancer Res。, Oct 1;14(19):5995-6004. PMID: 18829478
  • Bailey JM，Mohr Am和Ma Hollingsworth。（2009）。Sonic刺猬旁分泌信号传导调节胰腺癌的转移和淋巴管生成。Oncogene。7月27日。PMID：19633682
  • Behrens ME, Grandgenette PM,Bailey JM，Singh PK，Yi CH，Yu F和Ma Hollingsworth。（2010）。反应性肿瘤微环境：MUC1信号传导直接重新编程CTGF的转录。Oncogene。Aug 9. PMID: 20697347
  • Bunt SK，Mohr Am，Bailey JM, Grandgenett PM, and Hollingsworth MA. (2012). Rosiglitazone and Gemcitabine combination therapy reduces immune suppression and modulates T cell populations in pancreatic cancer.癌症免疫免疫。8月5日PMID：22864396
  • Bailey JM, and Leach SD. (2012). Signaling Pathways Mediating Epithelial-Mesenchymal Crosstalk in Pancreatic Cancer: Hedgehog, Notch and TGFβ.胰腺癌和肿瘤微环境。Trivandrum（印度）：Transworld研究网络beplay苹果手机能用吗;第7章PMID：22876389