LAUSR

the hotspots identified in the earlier study [3]. The ALL patient (a 6-year-old girl) with the LEPROTL1 mutation was diagnosed as having B lymphoblastic leukemia with t(12; 21)(p13;q22);TEL-AML1 (ETV6RUNX1). Cytogenetic analysis of the bone marrow demonstrated the following karyotype in detail: 46,XX,del(11)(q14q21),t(11; 1 8 ) ( p 1 5 ; q 1 2 ) , a d d ( 1 2 ) ( p 1 1 . 2 ) [ 3 ] / 46,XX[17].ish t(12; 21)(p13;q22)(ETV6+, RUNX1+;RUNX1 + 1,ETV6 + 1)[20]. After chemotherapy, she achieved complete remission and has been healthy for 2.5 years without relapse. While the specificity of SSCP used in this study was addressed by the recurrent sequencing of positives with the earlier data, its sensitivity was not. It is possible that the negative mutation status could be a result of the failure of SSCP to detect a specific variant. Under suitable conditions, SSCP is capable of detecting > 90% of mutations occurring within any sequence, and the sensitivity of PCR-SSCP is generally believed to be high if the fragments are < 200 bp [6]. Because we analyzed the samples with products < 200 bp by SSCP, it is unlikely that we would miss the LEPROTL1 mutations. One goal of this study was to identify whether the promoter mutation found in Dear Editor, The leptin receptor overlapping transcript-like 1 gene (LEPROTL1) encodes a membrane protein [1, 2]. To date, the only known function of this gene product is to suppress growth hormone activity in the liver [2]. The cancer-related functions of LEPROTL1 remain unknown. According to the Human Protein Atlas database (www.proteinatlas.org), LEPROTL1 is widely expressed in human tissues, but its expression in most cancer types is negative, suggesting that loss of LEPROTL1 could be related to tumorigenesis. A recent study analyzed genome-wide somatic mutations in promoters in breast cancers and identified promoter mutations in several genes [3], including LEPROTL1, which resulted in its decreased expression, suggesting a loss of function [3]. Interestingly, the promoter mutations repeatedly occur at 2 hotspots (chr8: 29952919 and chr8: 29952921). Alterations in promoter regions such as somatic mutation and aberrant methylation are known to play a role in cancer pathogenesis [4]. Together, these data suggest that promoter mutation in the LEPROTL1 gene might be prevalent and play a role in the development of breast cancer as well as other cancers. For this study, we analyzed somatic promoter mutations of the LEPROTL1 gene using genomic DNA from bone marrow aspirates of 1,011 hematologic tumors (acute myelogenous leukemia [AML], acute lymphoblastic leukemia [ALL], mulLetter to the Editor