Prognostic relevance of RUNX1 mutations in T-cell acute lymphoblastic leukemia

Großmann, Vera; Kern, Wolfgang; Harbich, Stefan; Alpermann, Tamara; Jeromin, Sabine; Schnittger, Susanne; Haferlach, Claudia; Haferlach, Torsten; Kohlmann, Alexander

doi:10.3324/haematol.2011.043919

Cited by 67 publications

(54 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…First, Grossman and colleagues performed a systematic screening of RUNX1 in 128 ALL patients. 135 They identified 17 different RUNX1 mutations distributed throughout the RHD and TAD in 15 patients, 13 with T-ALL (18%) and 2 with B-ALL (7%). Interestingly, 2 of the 13 T-ALL patients had biallelic RUNX1 mutations.…”

Section: Runx1 Somatic Mutations In Amlmentioning

confidence: 99%

Role of RUNX1 in hematological malignancies

Sood

Kamikubo

Liu

2017

Blood

378

319

View full text Add to dashboard Cite

RUNX1 is a member of the core-binding factor family of transcription factors and is indispensable for the establishment of definitive hematopoiesis in vertebrates. RUNX1 is one of the most frequently mutated genes in a variety of hematological malignancies. Germ line mutations in RUNX1 cause familial platelet disorder with associated myeloid malignancies. Somatic mutations and chromosomal rearrangements involving RUNX1 are frequently observed in myelodysplastic syndrome and leukemias of myeloid and lymphoid lineages, that is, acute myeloid leukemia, acute lymphoblastic leukemia, and chronic myelomonocytic leukemia. More recent studies suggest that the wild-type RUNX1 is required for growth and survival of certain types of leukemia cells. The purpose of this review is to discuss the current status of our understanding about the role of RUNX1 in hematological malignancies.

show abstract

Section: Runx1 Somatic Mutations In Amlmentioning

confidence: 99%

Role of RUNX1 in hematological malignancies

Sood

Kamikubo

Liu

2017

Blood

378

319

View full text Add to dashboard Cite

show abstract

“…22,47 The identification of HDAC1-and HDAC2-negative tumor specimen in various other tumor types 48,49 encourages the analysis of T-cell lymphomas for HDAC1 or HDAC2 expression.…”

Section: Discussionmentioning

confidence: 99%

Dosage-dependent tumor suppression by histone deacetylases 1 and 2 through regulation of c-Myc collaborating genes and p53 function

Heideman¹,

Wilting²,

Yanover³

et al. 2013

Blood

View full text Add to dashboard Cite

show abstract

“…A recent systems biology study that aimed at deciphering the transcriptional regulatory network controlled by TLX1 and TLX3 in the pathogenesis T-ALL revealed a prominent role for RUNX1 in the control of the oncogenic program downstream of the TLX1 and TLX3 HOX transcription factor oncogenes (100). Moreover, loss-of-function mutations in RUNX1 can be found in immature T-ALL samples, suggesting a tumor suppressor role for RUNX1 in T cell transformation (33,100,101).…”

Section: Loss Of Transcription Factor Tumor Suppressor Genesmentioning

confidence: 99%

The molecular basis of T cell acute lymphoblastic leukemia

Vlierberghe¹,

Ferrando²

2012

J. Clin. Invest.

438

395

View full text Add to dashboard Cite

T cell acute lymphoblastic leukemias (T-ALLs) arise from the malignant transformation of hematopoietic progenitors primed toward T cell development, as result of a multistep oncogenic process involving constitutive activation of NOTCH signaling and genetic alterations in transcription factors, signaling oncogenes, and tumor suppressors. Notably, these genetic alterations define distinct molecular groups of T-ALL with specific gene expression signatures and clinicobiological features. This review summarizes recent advances in our understanding of the molecular genetics of T-ALL.

show abstract

Prognostic relevance of RUNX1 mutations in T-cell acute lymphoblastic leukemia

Cited by 67 publications

References 20 publications

Role of RUNX1 in hematological malignancies

Role of RUNX1 in hematological malignancies

Dosage-dependent tumor suppression by histone deacetylases 1 and 2 through regulation of c-Myc collaborating genes and p53 function

The molecular basis of T cell acute lymphoblastic leukemia

Contact Info

Product

Resources

About