Acute Myeloid Leukemia Should Be Consideredas either inherited or Acquired Disease based onExpressed Biomarkers

Background: Acute myeloid leukemia (AML) is a type of malignantneoplasm in blood line in which abnormal myeloid cellsgrow rapidly and cause malignancy. In this review, we reportedwhether AML can be considered as inherited disease and investigatedall data from ۳۶ studies.Materials and Methods: Comparison of data was done by statisticalanalysis.Results: Advances in identification of cytogenetic abnormalitiesand mutations have provided novel insights into the pathogenesisof AML and novel insight in diagnostic and therapeuticstrategies have been introduced based on specific biomarkers.Cell surface biomarkers including CD۳۳ and CD۱۲۳ (up to ۸۰%of patients) are being considered as therapeutic targets as well assome others like CD۴۴ which are significantly increase in caseof AML (~۸۰%), however, they wouldn't be indicative for typeof mutations, thus, more biomarkers must be detected such asRas (controlling proliferation/differentiation and being frequentin AML), TET (epigenetic regulation), FLT۳ (controlling cellularprocesses including growth, proliferation, and survival ofcells), IDH۱/۲ (Isocitrate dehydrogenase ۱/۲) and KIT (CD۱۱۷;controlling cell growth, proliferation, survival, and migration)etc., to exactly find out the type of mutations which have causedthe disease. In the other hand, there are some others includingC/EBPAα and RUNX۱ can be associated with germline mutationswhich are present at birth and cause malignancy so calledinherited AML. C/EBPAα arrests cell proliferation and if getsmutant, the proliferation won't be controlled, thus malignancyoccurs. Mutant Runx۱ has also been demonstrated to be reasonfor malignancy as well as drug resistance.Conclusion: According to our study, we can conclude that,based on statistical data, significant percent of AML patients(~۱۵%) are as inherited-AML. So more genetical investigationsare needed to be performed in AML cases.

کلیدواژه ها:

Inherited AML ، Biomarkers ، Mutations ، C/EBPAα ، Runx۱