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: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
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
Tyrosine kinase inhibitor (TKI) has significantly improved the treatment of chronic myeloid leukemia (CML), however the resistance often resulted in treatment failure. Currently, it is known that the survival of CML cells can be affected by regulating autophagy, oxidative stress and mitochondrial metabolism, among which autophagy is an evolution-conserved catabolism process, and closely related to the pathogenesis of CML, thus playing a dual role in regulating the biological characteristics of cells. On the one hand, autophagy can promote the apoptosis of CML cells, and also can induce the drug resistance of CML cells on the other hand. In this review, the effect of autophagy on CML cells was summarzed briefly, so as to provide a useful idea to explore the combination of TKI with the autophagy inhibitor or inducer to overcome the resistance of CML to TKI.
Download full-text PDF |
Source |
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http://dx.doi.org/10.19746/j.cnki.issn.1009-2137.2020.06.049 | DOI Listing |
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