2020
DOI: 10.1038/s41375-020-0920-z
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The Clinical impact of PTPN11 mutations in adults with acute myeloid leukemia

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Cited by 53 publications
(78 citation statements)
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References 28 publications
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“…Generally, PTPN11 mutations were detected with a frequency of 7%, which is in the range of prevalences (4%-12%) previously reported for AML. 1,25,26,[28][29][30] In line with published data, 26,[28][29][30] mutations predominantly affected the N-terminal SH2 domain of PTPN11, involved in basal inhibition of SHP2, [12][13][14][15] and were found at subclonal levels in most patients. 26 This is consistent with a predominance of RAS signaling gene mutations (eg, FLT3 TKD , NRAS, and KIT) as secondary or subclonal lesions in AML that ether emerge or are lost during clonal disease evolution.…”
Section: Discussionsupporting
confidence: 82%
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“…Generally, PTPN11 mutations were detected with a frequency of 7%, which is in the range of prevalences (4%-12%) previously reported for AML. 1,25,26,[28][29][30] In line with published data, 26,[28][29][30] mutations predominantly affected the N-terminal SH2 domain of PTPN11, involved in basal inhibition of SHP2, [12][13][14][15] and were found at subclonal levels in most patients. 26 This is consistent with a predominance of RAS signaling gene mutations (eg, FLT3 TKD , NRAS, and KIT) as secondary or subclonal lesions in AML that ether emerge or are lost during clonal disease evolution.…”
Section: Discussionsupporting
confidence: 82%
“…1,25,26,[28][29][30] In line with published data, 26,[28][29][30] mutations predominantly affected the N-terminal SH2 domain of PTPN11, involved in basal inhibition of SHP2, [12][13][14][15] and were found at subclonal levels in most patients. 26 This is consistent with a predominance of RAS signaling gene mutations (eg, FLT3 TKD , NRAS, and KIT) as secondary or subclonal lesions in AML that ether emerge or are lost during clonal disease evolution. 1,37,38 The importance of individual PTPN11 variants (eg, E69K, G503A, and E76K), recurrently detected in our cohort, for RAS signaling hyperactivation, leukemic transformation, and chemoresistance in AML, has been summarized recently.…”
Section: Discussionsupporting
confidence: 82%
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“…We found the NEST predicted risk score, age, TP53 mutation, ZRSR2 mutation, TET2 mutation, FLT3-ITD, and U2AF1 mutations were risk factors for a poor prognosis (Figure 8A), as reported by previous studies (6,19,(41)(42)(43)(44). In addition, the result suggested that PTPN11 mutation was a protective factor for CN-AML, which appeared to contrast with previous reports (45). We believe that the low PTPN11 mutation frequency among the BeatAML cohort could explain this discrepancy.…”
Section: Independence Of the Predicted Risk Scorecontrasting
confidence: 47%
“…33,34 GOF mutations in exons 3 and 13 of PTPN11 are the main genetic cause of Noonan syndrome (NS) when germline, 35 or Juvenile myelomonocytic leukemia (JMML) when somatic 36 . In the context of MDS they occur mainly in children, 33,34 but are reported also in cases of acute leukemia 37,38 in adults as well 39,40 . All four mutations in our cohort were previously reported in JMML 41 and MDS patients 33,34 .…”
Section: Discussionmentioning
confidence: 67%