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
Colorectal adenocarcinomas were long thought to be an homogeneous entity, in which traditional adenomas of the colon were the best-recognized and most common precursor lesions. Current morphological and molecular data suggest an alternative pathway of colorectal carcinogenesis involving "serrated neoplasia". This pathway seems to be responsible for approximately 10% to 15% of sporadic colorectal adenocarcinomas. These serrated lesions, that may progress to cancer, show relatively distinct histopathological molecular and epigenetic features not commonly seen in traditional adenomas. Key characteristics of the serrated neoplasia pathway include BRAF gene mutations, excess CpG island methylation, and subsequent microsatellite instability. A major challenge for pathologists is to identify these new potential precursor lesions, in order to enable early diagnosis and treatment.
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