Analysis of class I and II aberrations in Iraqi childhood acute myeloid leukemia using filter paper cards.
The lack of molecular diagnosis in the field of cancer in Iraq has motivated us to perform a genetic analysis of pediatric acute myelogenous leukemia (AML), including class I and II aberrations. Peripheral blood or bone marrow cells were collected from 134 AML children aged ≤15 years. Flinders Technology Associates (FTA) filter paper cards were used to transfer dried blood samples from five Iraqi hospitals to Japan. DNA sequencing was performed to identify class I mutations. Nested RT-PCR was used to detect class II aberrations, except that MLL rearrangement was detected according to long distance inverse-PCR. NPM1 and FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) mutations were analyzed by GeneScan using DNA template. Among 134 Iraqi pediatric AML samples, the most prevalent FAB subtype was M2 (33.6 %) followed by M3 (17.9 %). Class I mutations: 20 (14.9 %), 8 (6.0 %), and 8 (6.0 %) patients had FLT3-ITD, FLT3-TKD, and KIT mutations, respectively. Class II mutations: 24 (17.9 %), 19 (14.2 %), and 9 (6.7 %) children had PML-RARA, RUNX1-RUNX1T1, and CBFB-MYH11 transcripts, respectively. MLL rearrangements were detected in 25 (18.7 %) patients. NPM1 mutation was detected in seven (5.2 %) cases. Collectively, approximately 30 % of AML children were proved to carry favorable prognostic genetic abnormalities, whereas approximately 10 % had high FLT3-ITD allelic burden and needed a special treatment plan including allogeneic hematopoietic stem cell transplantation. Acute promyelocytic leukemia (APL) was frequent among Iraqi pediatric AML. It is likely that molecular diagnosis using FTA cards in underdeveloped countries could guide doctors towards an appropriate treatment strategy.
Department of Pediatrics, Shinshu University School of Medicine, 3-1-1, Asahi, Matsumoto, 390-8621, Nagano, Japan.
Lika'a Fasih Y
LF
Al-Kzayer
Le Thanh N
le TN
Uyen
Mazin Faisal
MF
Al-Jadiry
Salma Abbas
SA
Al-Hadad
Safaa A Faraj
SA
Al-Badri
Hasanein Habeeb
HH
Ghali
Najiha Ahmed
NA
Ameen
Tingting
T
Liu
Kazuyuki
K
Matsuda
Jaafar M H
JM
Abdulkadhim
Tariq Abadi
TA
Al-Shujairi
Zead Ismael I K
ZI
Matti
Janan Ghalib
JG
Hasan
Hussam M Salih
HM
Al-Abdullah
Mouroge H
MH
Al-Ani
Paiman Ali I
PA
Saber
Hisham Maree
HM
Khalil
Toshi
T
Inoshita
Minoru
M
Kamata
Kenichi
K
Koike
Kazuo
K
Sakashita
D000293:Adolescent; D000483:Alleles; D001800:Blood Specimen Collection / Q000295:instrumentation / Q000379:methods; D001853:Bone Marrow / Q000473:pathology; D002648:Child; D002675:Child, Preschool; D002869:Chromosome Aberrations; D004273:DNA, Neoplasm / Q000235:genetics; D005260:Female; D006801:Humans; D007223:Infant; D007493:Iraq; D015470:Leukemia, Myeloid, Acute / Q000097:blood / Q000235:genetics* / Q000473:pathology / Q000628:therapy; D015479:Leukemia, Myelomonocytic, Acute / Q000097:blood / Q000235:genetics / Q000473:pathology / Q000628:therapy; D008297:Male; D009154:Mutation; D000090243:Nucleophosmin; D015514:Oncogene Proteins, Fusion / Q000235:genetics; D009857:Oncogenes; D010209:Paper; D011379:Prognosis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017422:Sequence Analysis, DNA; D013048:Specimen Handling / Q000295:instrumentation / Q000379:methods*; D014178:Translocation, Genetic; D016896:Treatment Outcome
D004273:DNA, Neoplasm; C000716967:NPM1 protein, human; D015514:Oncogene Proteins, Fusion; D000090243:Nucleophosmin