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Alterations in the RAS pathway have been implicated in the pathogenesis of various hematological malignancies
.
However, their clinical relevance in pediatric acute myeloid leukemia
leukemia
Figure 1.
Molecular and cytogenetic abnormalities in 80 pediatric acute myeloid leukemia patients with altered RAS pathway
.
Each column shows the pattern of cytogenetic abnormalities and clinical status for a single sample
Figure 1.
Figure 2.
Genetic map depicting RAS pathway mutations in pediatric acute myeloid leukemia patients
.
(A)NF1 mutation (NCBI reference sequence; NM_000267); (B)PTPN11 mutation (NCBI reference sequence; NM_002834); (C)CBL mutation (NCBI reference sequence; NM_005188); (D)NRAS mutation (NCBI reference sequence; NM_002524) ); (E)KRAS mutation (NCBI reference sequence; NM_004985)
Figure 2.
Table.
Univariate and multivariate Cox regression analysis of overall survival and event-free survival
Univariate and multivariate Cox regression analysis table for overall survival and event-free survival.
Table.
Univariate and multivariate Cox regression analysis table for overall survival and event-free survival.
Univariate and multivariate Cox regression analysis foroverall survival and event-free survival Variable and multivariate Cox regression analysis
NF1 alterations were frequently detected in patients with complex karyotypes (P = 0.
031) and were found to be an independent predictor of poor overall survival (OS) in multivariate analysis (P = 0.
007)
.
At least 4 of 7 patients with NF1 alterations had biallelic inactivation
stem cell
In conclusion, NF1 alterations may be a poor prognostic factor, whereas NRAS mutation is a favorable prognostic factor in pediatric
AML patients .
Pediatric AML patients with PTPN11 mutations may exhibit a greater propensity for relapse and induction failure
child
Original source:
Kaburagi T, Yamato G, Shiba N, Yoshida K, Hara Y, Tabuchi K, Shiraishi Y, Ohki K, Sotomatsu M, Arakawa H, Matsuo H, Shimada A, Taki T, Kiyokawa N, Tomizawa D, Horibe K, Miyano S , Taga T, Adachi S, Ogawa S, Hayashi Y.leave a message here