Diagnosa

tes laboratorium dan studi lain yang digunakan dalam pemeriksaan untuk SEMUA meliputi
berikut ini:

hitung darah lengkap dengan diferensial

studi koagulasi
Pap darah perifer
profil kimia, termasuk dehidrogenase laktat, asam urat, pemeriksaan fungsi hati, dan
BUN / kreatinin
budaya yang sesuai (khususnya, kultur darah) pada pasien dengan demam atau tanda-
tanda lain dari infeksi
Dada x-ray
computed tomography
Multiple-gated scanning akuisisi
elektrokardiografi
Tulang aspirasi sumsum dan biopsi (Definitif untuk mengkonfirmasikan leukemia)
imunohistokimia
arus cytometry
Sitogenetik
polymerase chain reaction
Ekspresi gen profil

Pengelolaan
Pengobatan SEMUA mungkin termasuk yang berikut:

Induksi kemoterapi (misalnya, standar rejimen 4 atau 5-obat, ALL-2, atau hiper-CVAD)
konsolidasi kemoterapi
pemeliharaan kemoterapi
Intrathecal chemotherapy for central nervous system (CNS) prophylaxis
Supportive care (eg, blood products, antibiotics, growth factors)

Pathophysiology
The malignant cells of acute lymphoblastic leukemia (ALL) are lymphoid precursor cells (ie,
lymphoblasts) that are arrested in an early stage of development. This arrest is caused by an
abnormal expression of genes, often as a result of chromosomal translocations. The lymphoblasts
replace the normal marrow elements, resulting in a marked decrease in the production of normal
blood cells. Consequently,anemia, thrombocytopenia, and neutropenia occur to varying degrees.
The lymphoblasts also proliferate in organs other than the marrow, particularly the liver, spleen,
and lymph nodes.

Etiology
Less is known about the etiology of acute lymphoblastic leukemia (ALL) in adults compared
with acute myelogenous leukemia (AML). Most adults with ALL have no identifiable risk
factors.

Although most leukemias occurring after exposure to radiation are AML rather than ALL, an
increased prevalence of ALL was noted in survivors of the Hiroshima atomic bomb but not in
those who survived the Nagasaki atomic bomb.

Rare patients have an antecedent hematologic disorder (AHD) such as myelodysplastic

syndrome (MDS) that evolves to ALL. However, most patients with MDS that evolves to acute
leukemia develop AML rather than ALL. Similarly, a small number of patients receiving
lenalidomide as maintenance therapy for multiple myeloma have developed secondary ALL. [ 1]

Semakin, kasus SEMUA dengan kelainan kromosom Band 11q23 setelah pengobatan dengan
topoisomerase inhibitor II untuk keganasan lain telah dijelaskan. Namun, kebanyakan pasien
yang mengembangkan leukemia akut sekunder setelah kemoterapi untuk kanker lain
mengembangkan AML daripada SEMUA.