BACKGROUND: It is believed that Ras mutations drive the proliferation of leukemic cells. The objective of this study was to investigate the association of Ras mutations with childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) with special reference to the presence or absence of mixed-lineage leukemia gene (MLL) rearrangements. METHODS: Bone marrow samples from 313 children with B-precursor ALL and 130 children with de novo AML were studied at diagnosis. Southern blot analysis was used to detect MLL rearrangements, and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis was used to detect common MLL fusion transcripts. Complementary DNA panhandle PCR was used to identify the infrequent or unknown MLL partner genes. DNA PCR or RT-PCR followed by direct sequencing was performed to detect mutations at codons 12, 13, and 61 of the N-Ras and K-Ras genes. RESULTS: Twenty of 313 patients with B-precursor ALL and 17 of 130 patients with de novo AML had MLL rearrangements. N-Ras mutations were detected in 2 of 20 patients with MLL-positive ALL and in 27 of 293 patients with MLL-negative ALL (P = 1.000). N-Ras mutations were detected in 2 of 17 patients with MLL-positive AML and in 14 of 113 patients with MLL-negative AML (P = 1.000). K-Ras mutations were present in 8 of 20 patients with MLL-positive ALL compared with 32 of 293 patients with MLL-negative ALL (P = 0.001). K-Ras mutations were detected in 3 of 17 patients with MLL-positive AML compared with 5 of 113 patients with MLL-negative AML (P = 0.069). CONCLUSIONS: Ras mutations were detected in 20.8% of patients with childhood B-precursor ALL and in 17.7% of patients with childhood AML. MLL-positive B-precursor ALL was associated closely with Ras mutations (50%), especially with K-Ras mutations (40%), whereas MLL-positive AML was not associated with Ras mutations. Copyright 2006 American Cancer Society.
BACKGROUND: It is believed that Ras mutations drive the proliferation of leukemic cells. The objective of this study was to investigate the association of Ras mutations with childhood acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML) with special reference to the presence or absence of mixed-lineage leukemia gene (MLL) rearrangements. METHODS: Bone marrow samples from 313 children with B-precursor ALL and 130 children with de novo AML were studied at diagnosis. Southern blot analysis was used to detect MLL rearrangements, and reverse transcriptase-polymerase chain reaction (RT-PCR) analysis was used to detect common MLL fusion transcripts. Complementary DNA panhandle PCR was used to identify the infrequent or unknown MLL partner genes. DNA PCR or RT-PCR followed by direct sequencing was performed to detect mutations at codons 12, 13, and 61 of the N-Ras and K-Ras genes. RESULTS: Twenty of 313 patients with B-precursor ALL and 17 of 130 patients with de novo AML had MLL rearrangements. N-Ras mutations were detected in 2 of 20 patients with MLL-positive ALL and in 27 of 293 patients with MLL-negative ALL (P = 1.000). N-Ras mutations were detected in 2 of 17 patients with MLL-positive AML and in 14 of 113 patients with MLL-negative AML (P = 1.000). K-Ras mutations were present in 8 of 20 patients with MLL-positive ALL compared with 32 of 293 patients with MLL-negative ALL (P = 0.001). K-Ras mutations were detected in 3 of 17 patients with MLL-positive AML compared with 5 of 113 patients with MLL-negative AML (P = 0.069). CONCLUSIONS: Ras mutations were detected in 20.8% of patients with childhood B-precursor ALL and in 17.7% of patients with childhood AML. MLL-positive B-precursor ALL was associated closely with Ras mutations (50%), especially with K-Ras mutations (40%), whereas MLL-positive AML was not associated with Ras mutations. Copyright 2006 American Cancer Society.
Authors: Nitin Jain; Emily Curran; Neil M Iyengar; Ernesto Diaz-Flores; Rangesh Kunnavakkam; Leslie Popplewell; Mark H Kirschbaum; Theodore Karrison; Harry P Erba; Margaret Green; Xavier Poire; Greg Koval; Kevin Shannon; Poluru L Reddy; Loren Joseph; Ehab L Atallah; Philip Dy; Sachdev P Thomas; Scott E Smith; L Austin Doyle; Walter M Stadler; Richard A Larson; Wendy Stock; Olatoyosi Odenike Journal: Clin Cancer Res Date: 2013-10-31 Impact factor: 12.531
Authors: S Haihua Chu; Evelyn J Song; Jonathan R Chabon; Janna Minehart; Chloe N Matovina; Jessica L Makofske; Elizabeth S Frank; Kenneth Ross; Richard P Koche; Zhaohui Feng; Haiming Xu; Andrei Krivtsov; Andre Nussenzweig; Scott A Armstrong Journal: Blood Adv Date: 2018-10-09
Authors: Henning Fedders; Ameera Alsadeq; Juliane Schmäh; Fotini Vogiatzi; Martin Zimmermann; Anja Möricke; Lennart Lenk; Udo Zur Stadt; Martin A Horstmann; Rob Pieters; Martin Schrappe; Martin Stanulla; Gunnar Cario; Denis M Schewe Journal: Haematologica Date: 2017-08-24 Impact factor: 9.941
Authors: M Braoudaki; M Karpusas; K Katsibardi; Ch Papathanassiou; K Karamolegou; F Tzortzatou-Stathopoulou Journal: Med Oncol Date: 2008-12-16 Impact factor: 3.064
Authors: Alejandro Gutierrez; Takaomi Sanda; Ruta Grebliunaite; Arkaitz Carracedo; Leonardo Salmena; Yebin Ahn; Suzanne Dahlberg; Donna Neuberg; Lisa A Moreau; Stuart S Winter; Richard Larson; Jianhua Zhang; Alexei Protopopov; Lynda Chin; Pier Paolo Pandolfi; Lewis B Silverman; Stephen P Hunger; Stephen E Sallan; A Thomas Look Journal: Blood Date: 2009-05-20 Impact factor: 22.113
Authors: R E Tiedemann; N Gonzalez-Paz; R A Kyle; R Santana-Davila; T Price-Troska; S A Van Wier; W J Chng; R P Ketterling; M A Gertz; K Henderson; P R Greipp; A Dispenzieri; M Q Lacy; S V Rajkumar; P L Bergsagel; A K Stewart; R Fonseca Journal: Leukemia Date: 2008-01-24 Impact factor: 11.528
Authors: Luke B Hesson; Thomas L Dunwell; Wendy N Cooper; Daniel Catchpoole; Anna T Brini; Raffaella Chiaramonte; Mike Griffiths; Andrew D Chalmers; Eamonn R Maher; Farida Latif Journal: Mol Cancer Date: 2009-07-01 Impact factor: 27.401