This system recognized differences in genetic, immunophenotype, molecular, and morphological features found through cytogenetic and molecular diagnostics tests. : 1531–1535  This subtyping helps determine the prognosis and the most appropriate treatment for each specific case of ALL. The WHO subtypes related to ALL are:
B-lymphoblastic leukemia/lymphoma
Not otherwise specified (NOS)
with recurrent genetic abnormalities
with t(9;22)(q34.1;q11.2);BCR-ABL1
with t(v;11q23.3);KMT2A rearranged
with t(12;21)(p13.2;q22.1); ETV6-RUNX1
with t(5;14)(q31.1;q32.3) IL3-IGH
with t(1;19)(q23;p13.3);TCF3-PBX1
with hyperdiploidy
with hypodiploidy
T-lymphoblastic leukemia/lymphoma
Acute leukemias of ambiguous lineage
Acute undifferentiated leukemia
Mixed phenotype acute leukemia (MPAL) with t(9;22)(q34.1;q11.2); BCR–ABL1
MPAL with t(v;11q23.3); KMT2A rearranged
MPAL, B/myeloid, NOS
MPAL, T/myeloid, NOS

MicroRNA signature
A systematic review of miRNA levels in pediatric B-ALL compared with controls revealed that miR-155 is the most frequently reported upregulated miRNA (followed by miR-146a, miR-181b, miR-222 and miR-708; two citations for miR-16, miR-21, miR-34a, miR-100, miR-128-1, miR-181a, miR-181c, miR-195, miR-210, miR-320a and miR-660), whereas the most frequently reported downregulated miRNA is miR-374a (two citations for miR-27a, miR-30c, miR-196b, miR-223 and miR-494). To date, there is no consensus miRNA signature and this is mainly attributed to different miRNA signatures across ALL subtypes and methodology of conducted studies. Treatment
The aim of treatment is to induce a lasting remission, defined as the absence of detectable cancer cells in the body (usually less than 5% blast cells in the bone marrow). Over the past several decades, there have been strides to increase the efficacy of treatment regimens, resulting in increased survival rates. Possible treatments for acute leukemia include chemotherapy, steroids, radiation therapy, intensive combined treatments (including bone marrow or stem cell transplants), targeted therapy, and/or growth factors.
Treatment of Patau syndrome focuses on the particular physical problems with which each child is born. Many infants have difficulty surviving the first few days or weeks due to severe neurological problems or complex heart defects. Surgery may be necessary to repair heart defects or cleft lip and cleft palate. Physical, occupational, and speech therapy will help individuals with Patau syndrome reach their full developmental potential. Surviving children are described as happy and parents report that they enrich their lives. Prognosis
Approximately 90% of infants with Patau syndrome die within the first year of life. Those children who do survive past 1 year of life are typically severely disabled with intellectual disability, seizures, and psychomotor issues. Children with the mosaic variation are usually affected to a lesser extent. In a retrospective Canadian study of 174 children with trisomy 13, median survival time was 12.5 days. One and ten year survival was 19.8% and 12.9% respectively, including those who underwent aggressive surgical intervention. History
Trisomy 13 was first observed by Thomas Bartholin in 1657, but the chromosomal nature of the disease was ascertained by Dr. Klaus Patau and Dr. Eeva Therman in 1960. The disease is named in Pataus honor.In England and Wales during 2008–09, there were 172 diagnoses of Patau syndrome (trisomy 13), with 91% of diagnoses made prenatally. There were 111 elective abortions, 14 stillbirth/miscarriage/fetal deaths, 30 outcomes unknown, and 17 live births.