for this type of aml (with previous history of mds or mpd that has gone unnoticed in the past, but the cytogenetics is still suggestive of mds/mpd history); or who have aml with morphologic features of myelodysplasia (dysplastic changes in multiple cell lines). people who have previously received chemotherapy or radiation treatment for a non-mds/mpd disease, and people who have genetic markers associated with aml with recurrent genetic abnormalities, are excluded from this category. this category of aml occurs most often in elderly people and often has a worse prognosis. cytogenetic markers for aml with myelodysplasia-related changes include: complex karyotype (meaning more than three chromosomal abnormalities) unbalanced abnormalities deletions or loss of chromosome 7 – deletions or translocations in chromosome 5 – unbalanced chromosomal aberrations in chromosome 17 – deletions or loss of chromosome 13 – deletions of chromosome 11 – unbalanced chromosomal aberrations in chromosome 12 – aberrations in chromosome x – balanced abnormalities translocations between chromosome 11 and 16 – translocations between chromosome 3 and 21 – translocations between chromosome 1 and 3 – translocations between chromosome 2 and 11 – translocations between chromosome 5 and 12 – translocations between chromosome 5 and 7 – translocations between chromosome 5 and 17 – translocations between chromosome 5 and 10 – translocations between chromosome 3 and 5 – m9895/3 therapy-related myeloid neoplasms this category includes people who have had prior chemotherapy and/or radiation and subsequently develop aml or mds. these leukemias may be characterized by specific chromosomal abnormalities, and often carry a worse prognosis. m9920/3 myeloid sarcoma this category includes myeloid sarcoma. myeloid proliferations related to down syndrome this category includes "transient abnormal myelopoiesis" and "myeloid leukemia associated with down syndrome". in young children, myeloid leukemia associated with down syndrome has a much better prognosis than other types of childhood aml. the prognosis in older children is similar to conventional aml. aml not otherwise categorized includes subtypes of aml that do not fall into the above categories: aml with minimal differentiation aml without maturation aml with maturation acute myelomonocytic leukemia acute monoblastic and monocytic leukemia pure erythroid leukemia acute megakaryoblastic leukemia acute basophilic leukemia acute panmyelosis with myelofibrosis m9861/3 relative incidence of acute myeloid leukemia subtypes by genetic changes. acute leukemias of ambiguous lineage (also known as mixed phenotype or biphenotypic acute leukemia) occur when the leukemic cells can not be classified as either myeloid or lymphoid cells, or where both types of cells are present. french-american-british the french-american-british (fab) classification system provides terminology that is still sometimes used, and it remains a valuable diagnostic tool in areas without access to genetic testing, this system has largely become obsolete in favor of the who classification, which correlates more strongly with treatment outcomes. the fab system divides aml into eight subtypes, m0 through to m7, based on the type of cell from which the leukemia developed and its degree of maturity. aml of types m0 to m2 may be called acute myeloblastic leukemia. classification is done by examining the appearance of the malignant cells with light microscopy and/or by using cytogenetics to characterize any underlying chromosomal abnormalities. the subtypes have varying prognoses and responses to therapy. six fab subtypes (m1 through to m6) were initially proposed in 1976, although later revisions added m7 in 1985 and m0 in 1987. type name cytogenetics percentage of adults with aml immunophenotype cd14 cd15 cd33 hla-dr other m0 acute myeloblastic leukemia, minimally differentiated 5% − − + + mpo − m1 acute myeloblastic leukemia, without maturation 15% − − + + mpo + m2 acute myeloblastic leukemia, with granulocytic maturation t(8;21)(q22;q22), t(6;9) 25% − + + + m3 promyelocytic, or acute promyelocytic leukemia (apl) t(15;17) 10% − + + − m4 acute myelomonocytic leukemia inv(16)(p13q22), del(16q) 20% <45% + + + m4eo myelomonocytic together with bone marrow eosinophilia inv(16), t(16;16) 5% +/− + + cd2+ m5 acute monoblastic leukemia (m5a) or acute monocytic leukemia (m5b) del (11q), t(9;11), t(11;19) 10% >55% + + + m6 acute erythroid leukemias, including erythroleukemia (m6a) and very rare pure erythroid leukemia (m6b) 5% − +/− +/− +/− glycophorin + m7 acute megakaryoblastic leukemia t(1;22) 5% − − + +/− cd41/cd61+ the morphologic subtypes of aml also include rare types not included in the fab system, such as acute basophilic leukemia, which was proposed as a ninth subtype, m8, in 1999. treatment first-line treatment of aml consists primarily of chemotherapy, and is divided into two phases: induction and consolidation. the goal of induction therapy is to achieve a complete remission by reducing the number of leukemic cells to an undetectable level; the goal of consolidation therapy is to eliminate any residual undetectable disease and achieve a cure. hematopoietic stem cell transplantation is usually considered if induction chemotherapy fails or after a person relapses, although transplantation is also sometimes used as front-line therapy for people with high-risk disease. efforts to use tyrosine kinase inhibitors in aml continue. induction main article: induction chemotherapy the goal of the induction phase is to reach a complete remission. complete remission does not mean the disease has been cured; rather, it signifies no disease can be detected with available diagnostic methods. all subtypes except acute promyelocytic leukemia are usually given induction chemotherapy with cytarabine and an anthracycline such as daunorubicin or idarubicin. this induction chemotherapy regimen is known as "7+3" (or "3+7"), because the cytarabine is given as a continuous iv infusion for seven consecutive days while the anthracycline is given for three consecutive days as an iv push. response to this treatment varies with age, with people aged less than 60 years having better remission rates between 60% and 80%, while older people having lower remission rates between 33% and 60%. because of the toxic effects of therapy and a greater chance of aml resistance to this induction therapy, different treatment, such as that in clinical trials might be offered to people 60–65 years or older. acute promyelocytic leukemia is treated with all-trans-retinoic acid (atra) and either arsenic trioxide (ato) monotherapy or an anthracycline. a syndrome similar to disseminated intravascular coagulation can develop during the initial few days of treatment or at the time the leukemia is diagnosed, and treatment can be complicated by a differentiation syndrome characterised by fever, fluid overload and low oxygen levels. acute promyelocytic leukemia is considered curable. there is insufficient evidence to determine if prescribing atra in addition to chemotherapy to adults who have other subtypes of acute myeloid leukaemia is helpful. consolidation even after complete remission is achieved, leukemic cells likely remain in numbers too small to be detected with current diagnostic techniques. if no consolidation therapy or further postremission is given, almost all people with aml will eventually relapse. the specific type of postremission therapy is individualized based on a person's prognostic factors (see above) and general health. for good-prognosis leukemias (i.e. inv(16), t(8;21), and t(15;17)), people will typically undergo an additional three to five courses of intensive chemotherapy, known as consolidation chemotherapy. this generally involves cytarabine, with the doses administered being higher in younger patients, who are less likely to develop toxicity related to this treatment. stem cell transplantation stem cell transplantation from a donor, called allogenic stem cell transplantation, is usually pursued if the prognosis is not considered favourable, a person can tolerate a transplant and has a suitable donor. the basis of allogenic stem cell transplantation is on a graft versus leukemia effect whereby graft cells stimulate an immune response against leukemia cells. unfortunately this is accompanied by immune responses against other host organs, called a graft versus host disease. supportive treatment support is necessary throughout treatment because of problems associated with aml and also arising from treatment. blood transfusions, including of red blood cells and platelets, are necessary to maintain health levels, preventing complications of anemia (from low red blood cells) and bleeding (from low platelets). aml leads to an increased risk of infections, particularly drug-resistant strains of bacteria and fungi. antibiotics and antifungals can be used both to treat and to prevent these infections, particularly quinolones. adding aerobic physical exercises to the standard of care may result in little to no difference in the mortality, in the quality of life and in the physical functioning. these exercises may result in a slight reduction in depression. furthermore, aerobic physical exercises probably reduce fatigue. recent research into the role that epigenetic regulators play in hematopoietic malignancies has yielded new insights in the development of targeted epigenetic therapies as a supportive treatment for aml. the fda has approved certain epigenetic modifying drugs like ivosidenib and enasidenib, which are used in patients that can no longer receive intensive induction chemotherapy; specifically, they are involved in the therapy of idh1 and idh2 mutations. further research must be done to prove the efficacy of epigenetic treatments, but the development of new epigenetic therapies along with immunotherapies holds potential in the future treatment of aml. in pregnancy aml is rare in pregnancy, affecting about 1 in 75,000 to 100,000 pregnant women. it is diagnosed and treated similarly to aml in non pregnancy, with a recommendation that it is treated urgently. however, treatment has significant implications for the pregnancy. first trimester pregnancy is considered unlikely to be viable; pregnancy during weeks 24 – 36 requires consideration of the benefits of chemotherapy to the mother against the risks to the foetus; and there is a recommendation to consider delaying chemotherapy in very late pregnancy (> 36 weeks). some elements of supportive care, such as which antibiotics to prevent or treat infections, also change in pregnancy. medication olutasidenib (rezlidhia) was approved for medical use in the united states in december 2022. prognosis expected survival upon diagnosis of acute myeloid leukemia in the united states chromosomal translocation (9;11), associated with aml multiple factors influence prognosis in aml, including the presence of specific mutations, and a person with aml's age. in the united states between 2011 and 2016, the median survival of a person with aml was 8.5 months, with the 5 year survival being 24%. this declines with age, with the poorer prognosis being associated with an age greater than 65 years, and the poorest prognosis seen in those aged 75–84. as of 2001, cure rates in clinical trials have ranged from 20 to 45%; although clinical trials often include only younger people and those able to tolerate aggressive therapies. the overall cure rate for all people with aml (including the elderly and those unable to tolerate aggressive therapy) is likely lower. cure rates for apl can be as high as 98%. subtypes secondary aml has a worse prognosis, as does treatment-related aml arising after chemotherapy for another previous malignancy. both of these entities are associated with a high rate of unfavorable genetic mutations. cytogenetics different genetic mutations are associated with a difference in outcomes. certain cytogenetic abnormalities are associated with very good outcomes (for example, the (15;17) translocation in apl). about half of people with aml have "normal" cytogenetics; they fall into an intermediate risk group. a number of other cytogenetic abnormalities are known to associate with a poor prognosis and a high risk of relapse after treatment. a large number of molecular alterations are under study for their prognostic impact in aml. however, only flt3-itd, npm1, cebpa and c-kit are currently included in validated international risk stratification schema. these are expected to increase rapidly in the near future. flt3 internal tandem duplications (itds) have been shown to confer a poorer prognosis in aml with normal cytogenetics. several flt3 inhibitors have undergone clinical trials, with mixed results. two other mutations – npm1 and biallelic cebpa are associated with improved outcomes, especially in people with normal cytogenetics and are used in current risk stratification algorithms. researchers are investigating the clinical significance of c-kit mutations in aml. these are prevalent, and potentially clinically relevant because of the availability of tyrosine kinase inhibitors, such as imatinib and sunitinib that can block the activity of c-kit pharmacologically. it is expected that additional markers (e.g., runx1, asxl1, and tp53) that have consistently been associated with an inferior outcome will soon be included in these recommendations. the prognostic importance of other mutated genes (e.g., dnmt3a, idh1, idh2) is less clear. other prognostic factors elevated lactate dehydrogenase level were also associated with poorer outcomes. use of tobacco is associated with a person having a poorer prognosis, and people