M L Loh
Affiliation: University of California
- TEL/AML1-positive pediatric leukemia: prognostic significance and therapeutic approachesMignon L Loh
Department of Pediatric Hematology Oncology, University of California San Francisco, San Francisco, California 94143 0519, USA
Curr Opin Hematol 9:345-52. 2002..Incorporating knowledge of this gene rearrangement into treatment decisions serves as a paradigm for translating molecular discoveries into clinically meaningful data to direct patient care and improve outcome...
- Childhood myelodysplastic syndrome: focus on the approach to diagnosis and treatment of juvenile myelomonocytic leukemiaMignon L Loh
Department of Pediatrics and the Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94143, USA
Hematology Am Soc Hematol Educ Program 2010:357-62. 2010..This review is focused on the genetic abnormalities that occur in JMML, with particular attention to germ-line predisposition syndromes associated with the disorder. Current approaches to therapy are also discussed...
- PTPN11 mutations in pediatric patients with acute myeloid leukemia: results from the Children's Cancer GroupM L Loh
Department of Pediatrics, University of California, San Francisco, CA 94143, USA
Leukemia 18:1831-4. 2004..There was no difference in clinical outcome for patients with and without PTPN11 mutations. These characteristics identify a subset of pediatric AML with PTPN11 mutations that share clinical and biologic features with JMML...
- Mutations in PTPN11 implicate the SHP-2 phosphatase in leukemogenesisMignon L Loh
Department of Pediatrics, University of California, Rm HSE 302 Box 0519, San Francisco, CA 94143, USA
Blood 103:2325-31. 2004..We conclude that SHP-2 is an important cellular PTPase that is mutated in myeloid malignancies. Further investigation is required to clarify how these mutant proteins interact with Ras and other effectors to deregulate myeloid growth...
- Treatment of infantile fibrosarcoma with chemotherapy and surgery: results from the Dana-Farber Cancer Institute and Children's Hospital, BostonMignon L Loh
Department of Pediatric Hematology Oncology, University of California San Francisco, San Francisco, CA 94143 0519, USA
J Pediatr Hematol Oncol 24:722-6. 2002..To retrospectively evaluate the treatment and outcome of patients diagnosed with infantile fibrosarcoma at the Dana-Farber Cancer Institute and Children's Hospital, Boston...
- Mutations in CBL occur frequently in juvenile myelomonocytic leukemiaMignon L Loh
Department of Pediatrics and the Comprehensive Cancer Center, University of California, San Francisco, California, USA
Blood 114:1859-63. 2009..Moreover, the exclusivity of CBL mutations with respect to other Ras pathway-associated mutations indicates that CBL may have a role in deregulating this key pathway in JMML...
- Prospective analysis of TEL/AML1-positive patients treated on Dana-Farber Cancer Institute Consortium Protocol 95-01Mignon L Loh
Department of Pediatrics, Comprehensive Cancer Center, University of California, San Francisco, CA 94143, USA
Blood 107:4508-13. 2006..However, factors such as age at diagnosis and presenting leukocyte count should be taken into consideration when treating this group of patients...
- The mutational spectrum of PTPN11 in juvenile myelomonocytic leukemia and Noonan syndrome/myeloproliferative diseaseChristian P Kratz
University of California, Room HSE 302 Box 0519, San Francisco, CA 94143, USA
Blood 106:2183-5. 2005..This supports the need to characterize the spectrum of hematologic abnormalities in individuals with NS and to better define the impact of the PTPN11 lesion on the disease course in patients with NS/MPD and JMML...
- Functional analysis of leukemia-associated PTPN11 mutations in primary hematopoietic cellsSuzanne Schubbert
Department of Pediatrics, University of California at San Francisco, 513 Parnassus Ave, HSE 302, San Francisco, CA 94143, USA
Blood 106:311-7. 2005..Mutant SHP-2 proteins induce aberrant growth in multiple hematopoietic compartments, which supports a primary role of hyperactive Ras in the pathogenesis of JMML...
- Activating mutations of the noonan syndrome-associated SHP2/PTPN11 gene in human solid tumors and adult acute myelogenous leukemiaMohamed Bentires-Alj
Cancer Biology Program, Department of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA
Cancer Res 64:8816-20. 2004..Our data demonstrate that mutations in PTPN11 occur at low frequency in several human cancers, especially neuroblastoma and AML, and suggest that Shp2 may be a novel target for antineoplastic therapy...
- Acquired PTPN11 mutations occur rarely in adult patients with myelodysplastic syndromes and chronic myelomonocytic leukemiaMignon L Loh
Department of Pediatrics, University of California, San Francisco, CA, USA
Leuk Res 29:459-62. 2005..Here, we investigated contribution of PTPN11 mutations to adult MDS and CMML pathogenesis. Our results indicate that PTPN11 lesions might play a role in adult MDS/CMML pathogenesis but do not represent a major molecular event...
- SHP-2 and myeloid malignanciesMarco Tartaglia
Dipartimento di Biologia Cellulare e Neuroscienze, Istituto Superiore di Sanita, Rome, Italy
Curr Opin Hematol 11:44-50. 2004..Specifically, we discuss the role of inherited and somatic mutations that result in SHP-2 gain-of-function in human disease, including myeloid malignancies...
- Favorable outcome for adolescents with acute lymphoblastic leukemia treated on Dana-Farber Cancer Institute Acute Lymphoblastic Leukemia Consortium ProtocolsElly Barry
Department of Pediatric Oncology, Dana Farber Cancer Institute, Boston, MA 02115, USA
J Clin Oncol 25:813-9. 2007..We report the outcome of adolescents treated on Dana-Farber Cancer Institute (DFCI; Boston, MA) ALL Consortium Protocols conducted between 1991 and 2000...
- Inherited predispositions and hyperactive Ras in myeloid leukemogenesisJennifer O Lauchle
Department of Pediatrics and Comprehensive Cancer Center, University of California, San Francisco, California 94143, USA
Pediatr Blood Cancer 46:579-85. 2006..These strains model human disease features and provide an opportunity to investigate novel therapeutic strategies that may ultimately cure JMML and other myeloid malignancies characterized by hyperactive Ras...
- Cytogenetics of Hispanic and White children with acute lymphoblastic leukemia in CaliforniaMelinda C Aldrich
University of California Berkeley, 2150 Shattuck Avenue, Suite 500, Berkeley, CA 94720 7380, USA
Cancer Epidemiol Biomarkers Prev 15:578-81. 2006..The mechanistic basis for this 2-fold variation in frequency of TEL-AML1 may be due to ethnic-specific risk factors or genetics and should be explored further...
- Risk- and response-based classification of childhood B-precursor acute lymphoblastic leukemia: a combined analysis of prognostic markers from the Pediatric Oncology Group (POG) and Children's Cancer Group (CCG)Kirk R Schultz
Children s Oncology Group, Department of Pediatrics, BC Children s Hospital, University of British Columbia, Vancouver, Canada
Blood 109:926-35. 2007....
- The JAK2V617F activating mutation occurs in chronic myelomonocytic leukemia and acute myeloid leukemia, but not in acute lymphoblastic leukemia or chronic lymphocytic leukemiaRoss L Levine
Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
Blood 106:3377-9. 2005..These data indicate that the JAK2V617F allele is present in acute and chronic myeloid malignancies but not in lymphoid malignancies...
- Single-cell profiling identifies aberrant STAT5 activation in myeloid malignancies with specific clinical and biologic correlatesNikesh Kotecha
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
Cancer Cell 14:335-43. 2008..This signature was a specific feature involving JAK-STAT signaling, suggesting a critical role of this pathway in the biological mechanism of this disorder and indicating potential targets for future therapies...
- Gene expression signatures define novel oncogenic pathways in T cell acute lymphoblastic leukemiaAdolfo A Ferrando
Department of Pediatric Oncology, Dana Farber Cancer Institute and Harvard Medical School, Boston, MA 02142, USA
Cancer Cell 1:75-87. 2002..Our results illustrate the power of gene expression profiles to elucidate transformation pathways relevant to human leukemia...
- Congenital leukemia cutis with subsequent development of leukemiaInga Hofmann Zhang
Department of Pediatrics, University of California San Francisco, California 94143 0519, USA
J Am Acad Dermatol 54:S22-7. 2006..The patient died of refractory leukemia and secondary fungal disease. This case report supports the observation that leukemia cutis with an 11q23 rearrangement should be treated aggressively...
- Prenatal origin of TEL-AML1-positive acute lymphoblastic leukemia in children born in CaliforniaCliona M McHale
School of Public Health, University of California, Berkeley 94720 7360, USA
Genes Chromosomes Cancer 37:36-43. 2003..Secondary changes were also similar to those described previously, with deletion of the second TEL allele being the most common. Other secondary changes included duplication of the fusion gene, trisomy 21, and monosomy X...