C-kit receptor (CD0117) expression in acute leukemia

Valverde, Leila; Matutes, E.; Farahat, Nahla; Heffernan, Amelia Jiménez; Owusu-Ankomah, K; Morilla, Ricardo; Catovsky, Daniel

doi:10.1007/bf00663010

Cited by 28 publications

(5 citation statements)

References 24 publications

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“…C-kit expression appears to be a rare event in lymphoblastic leukemia of B-lineage, however. 39 Valverde et al, 47 found only one of 23 ALL cells of different types positive for c-kit expression and Morita et al 48 found no c-kit expression in 44 lymphoid blast preparations from pediatric leukemia patients and 20 cell lines of erythroid and lymphoid lineages. Whether c-kit is biologically active by transducing a growth signal in the T-lymphoblastic cells was not studied by these investigators.…”

Section: Discussionmentioning

confidence: 99%

Expression and regulation of c-kit receptor and response to stem cell factor in childhood malignant T-lymphoblastic cells

et al. 1998

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Section: Discussionmentioning

confidence: 99%

Expression and regulation of c-kit receptor and response to stem cell factor in childhood malignant T-lymphoblastic cells

et al. 1998

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“…The human stem cell factor (SCF) receptor c-KIT (CD 117) is expressed on the majority of AML blast cells whereas it is missing on acute lymphatic leukemia (ALL) cells [107]. It can easily be detected by flow cytometry and thus has become an important diagnostic tool in the differential diagnosis of AML and ALL.…”

Section: Genetic Abnormalities In Upstream Receptorsmentioning

confidence: 99%

Signaling Through RAS-RAF-MEK-ERK: from Basics to Bedside

Zebisch¹,

Czernilofsky²,

Kéri³

et al. 2007

CMC

105

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Aberrant signaling caused by mutations in the RAS-RAF-MEK-ERK pathway and its upstream activators critically contributes to human tumor development. Strategies, which aim at inhibiting hyperactive signaling molecules, appear conceptually straight forward, but their translation into clinical practice has been hampered by many setbacks. Understanding structure, function and regulation of this intracellular pathway as well as its crosstalk with other signaling activities in the cell will be essential to ensure reasonable usage of new therapeutic possibilities. This review provides an understanding of this signaling cascade as revealed by genetic and biochemical approaches and discusses the existing or arising possibilities to interfere with unphysiological activation in cancer. Signaling aberrations and signal transduction therapies will be discussed exemplary for two types of hematological neoplasia, acute myeloid leukemia (AML) and the myelodysplastic syndromes (MDS). In the future understanding the role of tumor stem cells, both as a source of tumor recurrence and tumor heterogeneity, the signals controlling their fate as well as epigenetic changes in cancer will be the next critical steps to further advance the applicability of these novel therapeutic strategies.

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“…A higher frequency of nonsilent genetic changes has been demonstrated in a selected group of tested AML-CBF leukemia patients. Expression of KIT was indicated only in 6.3% of ALL, which corresponds to reports of other authors [27,28,29]. …”

Section: Discussionmentioning

confidence: 52%

The Overexpression of <b><i>KIT</i></b> Proto-Oncogene in Acute Leukemic Cells Is Not Necessarily Caused by the Gene Mutation

Szatkowski

Hellmann²

2014

Acta Haematol

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KIT is detected in a variety of cells, also in acute leukemia. Inhibition of wild-type KIT is not always satisfactory. The aim of this work was to evaluate the frequency of the most common KIT mutations in acute myeloid leukemia (AML) and determine the correlation between mutation and expression level. Samples were obtained from 75 patients with AL. CD117 presence was shown in 45 of 51 patients with AML and in 1 of 16 patients with acute lymphocytic leukemia (ALL). Asp816Val mutation was found in 3.5% of cases of AML and Val560Gly mutation in 1 sample with acute biclonal leukemia. Other genetic changes were found in 15 of 57 samples with AML: polymorphisms Met541Leu in 14% of cases, Lys546Lys in 7% and 1 case of acute biclonal leukemia, Ile798Ile in 5.3% of cases, Met541Leu in 1 acute biphenotypic leukemia and in 6.3% of ALL. Polymorphism Lys546Lys was also shown in 1 case of acute biclonal leukemia. Nonsilent genetic changes were detected in a total of 23% cases with core binding factor leukemia. There was no statistical significance between KIT expression and genetic changes. There was no correlation between the incidence and types of KIT mutations and its expression on cells in AML.

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C-kit receptor (CD0117) expression in acute leukemia

Cited by 28 publications

References 24 publications

Expression and regulation of c-kit receptor and response to stem cell factor in childhood malignant T-lymphoblastic cells

Expression and regulation of c-kit receptor and response to stem cell factor in childhood malignant T-lymphoblastic cells

Signaling Through RAS-RAF-MEK-ERK: from Basics to Bedside

The Overexpression of <b><i>KIT</i></b> Proto-Oncogene in Acute Leukemic Cells Is Not Necessarily Caused by the Gene Mutation

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