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
Acute myeloid leukemia (AML) is a group of hematological diseases, phenotypic and genetically heterogeneous, characterized by abnormal accumulation of blast cells in the bone marrows and peripheral blood. Its incidence rate is approximately 1.5 per 100,000 in infants younger than 1 year of age and 25 per 100,000 persons in octogenarians. Traditionally, cytogenetic markers are used to stratify patients in three risk categories: favorable, intermediate and unfavorable. However, the forecast stratification and the treatment decision for patients with normal karyotype shows difficulties due to the high clinical heterogeneity. The identification of several genetic mutations additional to classical molecular markers has been useful in identifying new entities. Nowadays, many different mutations and epigenetic aberrations have been implicated in the diagnostic, prognostic and treatment of AML. This review is focused on describing the most important molecular markers with implications for clinical practice.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5767295 | PMC |
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