Paper Details
- Home
- Paper Details
Vascular Endothelial Growth Factor, Irradiation, and Axitinib Have Diverse Effects on Motility and Proliferation of Glioblastoma Multiforme Cells.
Author: AdamietzIrenäus Anton, BühlerHelmut, KrcekReinhardt, MatschkeVeronika, TheisVerena, TheissCarsten
Original Abstract of the Article :
Glioblastoma multiforme (GBM) is the most common primary brain tumor. It is highly aggressive with an unfavorable prognosis for the patients despite therapies including surgery, irradiation, and chemotherapy. One important characteristic of highly vascularized GBM is the strong expression of vascula...See full text at original site
Dr.Camel's Paper Summary Blogラクダ博士について
ラクダ博士は、Health Journal が論文の内容を分かりやすく解説するために作成した架空のキャラクターです。
難解な医学論文を、専門知識のない方にも理解しやすいように、噛み砕いて説明することを目指しています。
* ラクダ博士による解説は、あくまで論文の要点をまとめたものであり、原論文の完全な代替となるものではありません。詳細な内容については、必ず原論文をご参照ください。
* ラクダ博士は架空のキャラクターであり、実際の医学研究者や医療従事者とは一切関係がありません。
* 解説の内容は Health Journal が独自に解釈・作成したものであり、原論文の著者または出版社の見解を反映するものではありません。
引用元:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572260/
データ提供:米国国立医学図書館(NLM)
Vascular Endothelial Growth Factor, Irradiation, and Axitinib Have Diverse Effects on Motility and Proliferation of Glioblastoma Multiforme Cells
The world of neuro-oncology is a constant struggle against aggressive brain tumors, seeking effective strategies to combat their growth and spread. This study examines the interplay between vascular endothelial growth factor (VEGF), irradiation, and axitinib, a targeted therapy, in the context of glioblastoma multiforme (GBM), a highly malignant brain tumor. Imagine a fierce desert battle, where GBM cells, like invading warriors, rely on a network of blood vessels (VEGF) to sustain their growth. This research investigates how to disrupt this crucial supply line, potentially weakening the GBM cells and giving the body a chance to fight back.
Disrupting the Supply Lines of Glioblastoma Multiforme
The study reveals a fascinating interplay between VEGF, irradiation, and axitinib in GBM cells. While VEGF promotes cell motility and irradiation can accelerate this movement, axitinib effectively inhibits cell motility. Think of VEGF as the vital supply line for GBM cells, providing fuel and resources for their growth and spread. Irradiation, like a strategic bombing campaign, can temporarily disrupt this supply, but axitinib, like a skilled saboteur, permanently disrupts the flow. This research sheds light on the potential of axitinib in targeting VEGF signaling, potentially interrupting the growth and spread of GBM cells.
Fighting Brain Tumors: A Camel's Perspective
As a desert creature, I understand the importance of water for survival. Just as a camel carefully manages its water reserves, GBM cells rely on a network of blood vessels to provide essential resources for their growth. This research highlights the potential of axitinib in disrupting this vital supply line, potentially starving the GBM cells and giving the body a better chance of combating the disease. Think of it as a camel caravan strategically navigating a dry desert landscape, seeking out hidden sources of water while avoiding dangerous traps. This research offers hope for those facing the challenges of brain tumors, providing new weapons in the fight against these aggressive diseases.
Dr. Camel's Conclusion
This study offers valuable insights into the complex interplay between VEGF, irradiation, and axitinib in the context of glioblastoma multiforme. The findings highlight the potential of targeting VEGF signaling, potentially disrupting the growth and spread of this aggressive brain tumor. Just as a camel navigates the desert landscape, seeking out safe and nourishing sources of sustenance, researchers are diligently seeking new strategies to combat brain tumors, offering hope for those facing these challenging diseases.
Date :
- Date Completed n.d.
- Date Revised 2020-10-01
Further Info :
Related Literature
English
This site uses cookies. Visit our privacy policy page or click the link in any footer for more information and to change your preferences.