Somatic mutations in PTPN11 in juvenile myelomonocytic leukemia, myelodysplastic syndromes and acute myeloid leukemia

By M. Tartaglia, C. Niemeyer, A. Fragale, Xiaoling Song, J. Buechner, A. Jung, K. Hählen, H. Hasle, J. Licht, B. Gelb. Nature Genetics, 2003

1,030 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/842b6c8d8876089c8d80f1cca748ac6b3d31ef6b

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Citations in the corpus

Germline KRAS mutations cause Noonan syndrome (2006, background): “revealed a novel molecular lesion in JMML cases without RAS or NF1 mutation”
Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. (2005, background): “, 2003), and activating mutations in the SHP-2 phosphatase seen in Noonan’s syndrome and in a subset of juvenile myelomonocytic leukemias disrupt the autoinhibitory SH2 domain/phosphatase domain interface (Tartaglia et al., 2001; Tartaglia et al., 2003).”
Transgenic expression of Helicobacter pylori CagA induces gastrointestinal and hematopoietic neoplasms in mouse (2008, background): “SHP-2 is required for normal development of both myeloid and lymphoid lineage cells (32, 33), and gain-of-function mutations of SHP-2 are associated with childhood leukemias (13, 33, 34).”
Mechanisms of BCR–ABL in the pathogenesis of chronic myelogenous leukaemia (2005, neutral): “DH p185 (1-426) p210 (1-902–927) p230 (1–1,176) Y177 Myr GAG BCR F G 1a 1b”
Oncogenic mechanisms of the Helicobacter pylori CagA protein (2004, neutral): “gov/cancertopics/pdq/treatment/childAML/healthprofessional">acute myelocytic leukaemia (AML”
The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes. (2009, background): “However, except for some patients with t-AML associated with inv(16)(p13.”
Spacing Effect: SHP2 Phosphatase Regulates Resting Intervals Between Learning Trials in Long-Term Memory Induction (2009, positive): “Gain-of-function (GOF)germlinePTPN11mutations causeabout 50% of NS cases (Tartaglia et al., 2001) and somatic mutations with generally stronger GOF effects cause certain childhood leukemias ( Tartaglia et al., 2003 ).”
Protein-tyrosine phosphatases and cancer (2006, background): “Interestingly, somatic mutations of PTPN11 also occur in about one-third of sporadic cases of JMM”
Recurrent somatic alterations of FGFR1 and NTRK2 in pilocytic astrocytoma (2013, neutral): “Both encoded alterations (p.Glu69Lys and p.Glu76Ala) were previously reported in juvenile monomyelocytic leukemia, which is frequently associated with SHP-2 activation 42,43 .”