Bone marrow: myeloblasts with Auer rods seen in<unk>  A complete blood count, which is a blood test, is one of the initial steps in the diagnosis of<unk> . It may reveal both an excess of white blood cells (leukocytosis) or a decrease (leukopenia), and a low red blood cell count (anemia) and low platelets (thrombocytopenia) can also be commonly seen. A blood film may show<unk>  blast cells. Inclusions within the cells called Auer rods, when seen, make the diagnosis highly likely. A definitive diagnosis requires a bone marrow aspiration and biopsy. Bone marrow is examined under light microscopy, as well as flow cytometry, to diagnose the presence of<unk> , to differentiate<unk>  from other types of<unk>  (e.g. acute lymphoblastic<unk> , and to provide information about how mature or immature the affected cells are that can assist in classifying the subtype of disease. A sample of marrow or blood is typically also tested for chromosomal abnormalities by routine cytogenetics or fluorescent in situ hybridization. Genetic studies may also be performed to look for specific mutations in genes such as FLT3, nucleophosmin, and KIT, which may influence the outcome of the disease. Cytochemical stains on blood and bone marrow smears are helpful in the distinction of<unk>  from ALL, and in subclassification of<unk> . The combination of a myeloperoxidase or Sudan black stain and a nonspecific esterase stain will provide the desired information in most cases. The myeloperoxidase or Sudan black reactions are most useful in establishing the identity of<unk>  and distinguishing it from ALL. The nonspecific esterase stain is used to identify a monocytic component in<unk> s and to distinguish a poorly differentiated monoblastic<unk>  from ALL. The standard classification scheme for<unk>  is the World Health Organization (WHO) system. According to the WHO criteria, the diagnosis of<unk>  is established by demonstrating involvement of more than 20% of the blood and/or bone marrow by<unk>  myeloblasts, except in three forms of<unk>  with recurrent genetic abnormalities: t(8;21), inv(16) or t(16;16), and acute promyelocytic<unk>  with PML-RARA, in which the presence of the genetic abnormality is diagnostic irrespective of blast percent.<unk>  sarcoma is also considered a subtype of<unk>  independently of the blast count. The older French-American-British (FAB) classification, which is no longer widely used, is a bit more stringent, requiring a blast percentage of at least 30% in bone marrow or peripheral blood for the diagnosis of<unk> . Because acute promyelocytic<unk>  has the highest curability and requires a unique form of treatment, it is important to quickly establish or exclude the diagnosis of this subtype of<unk> . Fluorescent in situ hybridization performed on blood or bone marrow is often used for this purpose, as it readily identifies the chromosomal translocation t(15;17)(q22;q12); that characterizes APL. There is also a need to molecularly detect the presence of PML/RARA fusion protein, which is an oncogenic product of that translocation. World Health Organization The WHO classification of<unk>  attempts to be more clinically useful and to produce more meaningful prognostic information than the FAB criteria. Each of the WHO categories contains numerous descriptive subcategories of interest to the hematopathologist and oncologist; however, most of the clinically significant information in the WHO schema is communicated via categorization into one of the subtypes listed below. The revised fourth edition of the WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues was released in 2016. This classification, which is based on a combination of genetic and immunophenotypic markers and morphology, defines the subtypes of<unk>  and related neoplasms as: Name Description ICD-O<unk>  with recurrent genetic abnormalities Includes: *<unk>  with translocations between chromosome 8 and 21 – t(8;21)(q22;q22.1); RUNX1-RUNX1T1; (ICD-O 9896/3); *<unk>  with inversions in chromosome 16 – inv(16)(p13.1q22) or internal translocations in it – t(16;16)(p13.1;q22); CBFB-MYH11; (ICD-O 9871/3); * Acute promyelocytic<unk>  with PML-RARA; (ICD-O 9866/3); *<unk>  with translocations between chromosome 9 and 11 – t(9;11)(p21.3;q23.3); KMT2A-MLLT3; *<unk>  with translocations between chromosome 6 and 9 – t(6;9)(p23;q34.1); DEK-NUP214; *<unk>  with inversions in chromosome 3 – inv(3)(q21.3q26.2) or internal translocations in it – t(3;3)(q21.3;q26.2); GATA2, MECOM * Megakaryoblastic<unk>  with translocations between chromosome 1 and 22 – t(1;22)(p13.3;q13.1); RBM15-MKL1; *<unk>  with mutated NPM1 *<unk>  with biallelic mutations of CEBPA *Provisional:<unk>  with BCR-ABL1 and<unk>  with mutated RUNX1 Multiple<unk>  with<unk> ysplasia-related changes This category includes people who have had a prior documented<unk> ysplastic syndrome (MDS) or myeloproliferative disease (MPD) that then has transformed into<unk> ; who have cytogenetic abnormalities characteristic for this type of<unk>  (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<unk>  with morphologic features of<unk> ysplasia (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<unk>  with recurrent genetic abnormalities, are excluded from this category. This category of<unk>  occurs most often in elderly people and often has a worse prognosis. Cytogenetic markers for<unk>  with<unk> ysplasia-related changes include: * Complex karyotype (meaning more than three chromosomal abnormalities) * Unbalanced abnormalities * Deletions or loss of chromosome 7 – del(7q)/-7; * Deletions or translocations in chromosome 5 – del(5q)/t(5q); * Unbalanced chromosomal aberrations in chromosome 17 – i(17q)/t(17p); * Deletions or loss of chromosome 13 – del(13q)/-13; * Deletions of chromosome 11 – del(11q); * Unbalanced chromosomal aberrations in chromosome 12 – del(12p)/t(12p); * Aberrations in chromosome X – idic(X)(q13); * Balanced abnormalities * Translocations between chromosome 11 and 16 – t(11;16)(q23.3;q13.3); * Translocations between chromosome 3 and 21 – t(3;21)(q26.2;q22.1); * Translocations between chromosome 1 and 3 – t(1;3)(p36.3;q21.2); * Translocations between chromosome 2 and 11 – t(2;11)(p21;q23.3); * Translocations between chromosome 5 and 12 – t(5;12)(q32;p13.2); * Translocations between chromosome 5 and 7 – t(5;7)(q32;q11.2); * Translocations between chromosome 5 and 17 – t(5;17)(q32;p13.2); * Translocations between chromosome 5 and 10 – t(5;10)(q32;q21); * Translocations between chromosome 3 and 5 – t(3;5)(q25.3;q35.1); Therapy-related<unk>  neoplasms This category includes people who have had prior chemotherapy and/or radiation and subsequently develop<unk>  or MDS. These<unk> s may be characterized by specific chromosomal abnormalities, and often carry a worse prognosis.<unk>  sarcoma This category includes<unk>  sarcoma.<unk>  proliferations related to Down syndrome This category includes "transient abnormal myelopoiesis" and<unk><unk>  associated with Down syndrome". In young children,<unk><unk>  associated with Down syndrome has a much better prognosis than other types of childhood<unk> . The prognosis in older children is similar to conventional<unk> .<unk>  not otherwise categorized Includes subtypes of<unk>  that do not fall into the above categories: *<unk>  with minimal differentiation *<unk>  without maturation *<unk>  with maturation * Acute myelomonocytic<unk>  * Acute monoblastic and monocytic<unk>  * Pure erythroid<unk>  * Acute megakaryoblastic<unk>  * Acute basophilic<unk>  * Acute panmyelosis with myelofibrosis Relative incidence of<unk>  subtypes by genetic changes. Acute<unk> s of ambiguous lineage (also known as mixed phenotype or biphenotypic acute<unk>  occur when the<unk>  cells can not be classified as either<unk>  or lymphoid cells, or where both types of cells are present. French-American-British The French-American-British (FAB) classification system divides<unk>  into eight subtypes, M0 through to M7, based on the type of cell from which the<unk>  developed and its degree of maturity.<unk>  of types M0 to<unk>  may be called acute myeloblastic<unk> . 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. While the terminology of the FAB system 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. 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<unk>  Immunophenotype CD14 CD15 CD33 HLA-DR Other M0 acute myeloblastic<unk> , minimally differentiated 5% − − + + MPO − M1 acute myeloblastic<unk> , without maturation 15% − − + + MPO +<unk>  acute myeloblastic<unk> , with granulocytic maturation t(8;21)(q22;q22), t(6;9) 25% − + + + M3 promyelocytic, or acute promyelocytic<unk>  (APL) t(15;17) 10% − + + − M4 acute myelomonocytic<unk>  inv(16)(p13q22), del(16q) 20% 55% + + + M6 acute erythroid<unk> s, including erythroleukemia (M6a) and very rare pure erythroid<unk>  (M6b) 5% − +/− +/− +/− Glycophorin + M7 acute megakaryoblastic<unk>  t(1;22) 5% − − + +/− CD41/CD61+ The morphologic subtypes of<unk>  also include rare types not included in the FAB system, such as acute basophilic<unk> , which was proposed as a ninth subtype, M8, in 1999.
Acute myeloid leukemia
Acute lymphoblastic leukemia
Myeloid leukemia
Lymphoid leukemia
Prolymphocytic leukemia
Acute monocytic leukemia
Leukemoid reaction
T-cell leukemia