Discussion: Chromosomal Abnormalities
NOW FOR AN ORIGINAL PAPER ASSIGNMENT:Discussion: Chromosomal Abnormalities
Cytogenetics
Non-random chromosomal abnormalities (e.g., deletions, translocations) are identified in approximately 52% of all adult primary AML patients and have long been recognized as the genetic events that cause and promote this disease [8]. Certain cytogenetic abnormalities, including the t(8;21)(q22;q22), t(15;17)(q22;q12) and inv(16)(p13.1;q22) are associated with longer remission and survival, while alterations of chromosomes 5, 7,
complex karyotype (described as >3 chromosomal abnormalities) and 11q23 are associated with poor response to therapy and shorter overall survival [1]. In contrast, about 40%–50% of all AML cases are cytogenetically normal (CN-AML) when assessed using conventional banding analysis [9]. Although, this group has an intermediate risk of relapse, a substantial heterogeneity is found in this population in terms of clinical outcome. Molecular screening of this AML category is critical for prognostic categorization and treatment strategy.
Molecular Abnormalities
During the last decade, several studies have shown that the presence or absence of specific gene mutations and/or changes in gene expression can further classify AML cases and have an effect on the patients’ prognosis [7,10,11]. As stated above, this is particularly relevant for patients with CN-AML. With the advent of next generation sequencing, the genetic landscape of CN-AML has been more defined with each case having an average of 13 mutations, eight of which are random “passenger” mutations and five of which are recurrent “driver” mutations [10]. Key molecular abnormalities have been identified and are now used to predict outcome and help guide treatment for AML patients. In the next sections we will describe the most relevant AML mutations discussed in relative order of frequency.
Nucleophosmin 1 (NPM1) Mutations
Nucleophosmin 1 (NPM1) mutations are the most frequent mutation in AML, occurring in 25%–30% of AML patients, with female predominance [12,13]. NPM1 mutations result in the aberrant expression of the NPM1 protein in the cytoplasm rather than the nucleus, stimulating myeloid proliferation and leukemia development [13,14,15].
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