Tumor hypoxia does not drive differentiation of tumor - associated

نویسندگان

  • Damya Laoui
  • Eva Van Overmeire
  • Giusy Di Conza
  • Chiara Aldeni
  • Jiri Keirsse
  • Yannick Morias
  • Kiavash Movahedi
  • Isabelle Houbracken
  • Elio Schouppe
  • Yvon Elkrim
  • Oussama Karroum
  • Bénédicte Jordan
  • Peter Carmeliet
  • Conny Gysemans
  • Patrick De Baetselier
  • Massimiliano Mazzone
  • Jo A. Van Ginderachter
  • Emmanuel van der Schueren
چکیده

Laboratory of Myeloid Cell Immunology, VIB, Brussels, Belgium Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, VIB, Leuven, Belgium Laboratory of Molecular Oncology and Angiogenesis, Vesalius Research Center, K.U. Leuven, Leuven, Belgium Cell Differentiation Unit, Diabetes Research Centre, Vrije Universiteit Brussel, Brussels, Belgium Biomedical Magnetic Resonance Unit, U.C. Louvain, Brussels, Belgium Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven, Belgium Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, K.U. Leuven, Leuven, Belgium Experimental Medicine and Endocrinology, Department of Experimental Medicine, K.U. Leuven, Leuven, Belgium

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Tumor hypoxia does not drive differentiation of tumor-associated macrophages but rather fine-tunes the M2-like macrophage population.

Tumor-associated macrophages (TAM) are exposed to multiple microenvironmental cues in tumors, which collaborate to endow these cells with protumoral activities. Hypoxia, caused by an imbalance in oxygen supply and demand because of a poorly organized vasculature, is often a prominent feature in solid tumors. However, to what extent tumor hypoxia regulates the TAM phenotype in vivo is unknown. H...

متن کامل

Blockade of Hypoxia: The Impact on Tumor Growth in an Experimental Tumor Model

Background: Tumor microenvironment is an active factor participating in immunoregulation, thereby preventing immunosurveillance and limiting the efficacy of anticancer therapies. Hypoxia as a major characteristic of solid tumors causes the expression of Hypoxia-Inducible Factor-1α (HIF-1α). This is a transcription factor that mediates hypoxic responses of tumor cells and involves in the express...

متن کامل

Hypoxia and tumor-associated macrophages

Tumor-associated macrophages (TAMs) provide a significant contribution to tumor growth and metastasis. We demonstrated the existence of two main TAM subsets, differing in activation state and localization. Of these, M2-like TAMs reside in hypoxic regions of the tumor mass and can be used as targets for hypoxia tracers. This said, hypoxia does not regulate the differentiation of TAMs but finely ...

متن کامل

A Mimic of the Tumor Microenvironment on GPR30 Gene Expression in Breast Cancer

Introduction: The G-protein coupled receptor 30 (GPR30) gene is a member of the G-protein coupled receptor (GPCR) family; involved in breast, endometrial, and ovarian cancers. Many GPCR receptors that are implicated in several types of human cancers are correlated with increased cell proliferation and tumor progression; especially GPR30 gene. Methods: The breast cancer MCF-7 and MDA-MB-231 cel...

متن کامل

Role of Cyclooxygenese-2 (COX-2) Expression in Breast Cancer Differentiation and Its Relationship with Hormone Receptors Status

Background and Objectives: Cyclooxygenese-2 (COX-2) expression in breast cancer and its correlation with tumor prognosis is unclear. We investigated the incidence of COX-2 expression in patients and assessed interactions between COX-2 and clinical features of cancer and expression of HER2/neu, estrogen receptor (ER), and progesterone receptor (PR). Methods: COX-2 expression was investigated by...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2013