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
Background: Metastasic deposits from malignancies frequently lodge in the skeleton, including the jaw bones.
Method: A review of the literature was performed in order to provide a coherent overview on the pathogenesis of bone metastasis.
Results: Bone metastasis follows complex molecular interactions that enable tumor cells to detach from the primary site, invade the extracellular matrix, intra-vasate, extra-vasate, and proliferate within bone. They induce local bone changes that could manifest radiologically as either osteolytic or radiodense. In addition to the direct bone changes, malignancies can elaborate mediators that are released in circulation, leading to generalized osteopenia.
Conclusions: The spread of malignant neoplasms to bone is not a random process but rather a cascade of specific molecular events orchestrated through complex interactions between neoplastic cells and their environment.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1111/j.1600-0714.2006.00360.x | DOI Listing |
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