Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Angiogenesis is a hallmark of glioblastoma (GBM) and remains an important therapeutic target in its treatment, especially for recurrent GBM. GBMs are characterized by the release of vascular endothelial growth factor (VEGF), an important regulator and promoter of angiogenesis. Therefore, antiangiogenic therapies (AATs) targeting VEGF or VEGF receptors (VEGFRs) were designed and thought to be an effective tool for controlling the growth of GBM. However, recent results of different clinical trials using humanized monoclonal antibodies against VEGF (bevacizumab), as well as tyrosine kinase inhibitors (TKIs) that target different VEGFRs alone or in combination with other therapeutic agents demonstrated mixed results, with the majority of reports indicating that GBM developed resistance against antiangiogenic treatments.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7486014 | PMC |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!