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Acute promyelocytic leukemia is characterized by a chromosomal translocation involving the retinoic acid receptor alpha (RARA) gene on chromosome 17. [3] In 95% of cases of APL, the RARA gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (PML) on chromosome 15, a translocation denoted as t(15;17)(q22;q21). [3]
17q12 microdeletion syndrome is an autosomal dominant disorder, where one copy of the relevant mutation is enough to cause the condition. Most cases are de novo, or spontaneous mutations that do not occur in the proband's parents; [10] approximately 75% are de novo, while 25% are inherited. [4]
All subtypes except acute promyelocytic leukemia are usually given induction chemotherapy with cytarabine and an anthracycline such as daunorubicin or idarubicin. [60] 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 ...
The American Cancer Society estimates that in 2014, about 5,980 new cases of chronic myeloid leukemia were diagnosed, and about 810 people died of the disease. This means that a little over 10% of all newly diagnosed leukemia cases will be chronic myeloid leukemia. The average risk of a person getting this disease is 1 in 588.
Acute Promyelocytic Leukemia (APL) is a subtype of Acute Myeloid Leukemia, known for its accumulation of abnormal, course, densely granulated promyelocytes in the bone marrow. [6] The excessive proliferation of promyelocytes, attributing at least 30% of the myeloid cells in the bone marrow, result in a depletion of blood cells, including white ...
Promyelocytic leukemia protein (PML) (also known as MYL, RNF71, PP8675 or TRIM19 [5]) is the protein product of the PML gene. PML protein is a tumor suppressor protein required for the assembly of a number of nuclear structures, called PML-nuclear bodies, which form amongst the chromatin [ 5 ] of the cell nucleus.
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