High expression of miR-125b-2 and SNORD116 noncoding RNA clusters characterize ERG-related B cell precursor acute lymphoblastic leukemia

نویسندگان

  • Elena Vendramini
  • Marco Giordan
  • Emanuela Giarin
  • Barbara Michielotto
  • Grazia Fazio
  • Gianni Cazzaniga
  • Andrea Biondi
  • Daniela Silvestri
  • Maria Grazia Valsecchi
  • Martina U. Muckenthaler
  • Andreas E. Kulozik
  • Valter Gattei
  • Shai Izraeli
  • Giuseppe Basso
  • Geertruy te Kronnie
چکیده

ERG-related leukemia is a B cell precursor acute lymphoblastic leukemia (BCP ALL) subtype characterized by aberrant expression of DUX4 and ERG transcription factors, and highly recurrent ERG intragenic deletions. ERG-related patients have remarkably favorable outcome despite a high incidence of inauspicious IKZF1 aberrations.We describe clinical and genomic features of the ERG-related cases in an unselected cohort of B-other BCP ALL pediatric patients enrolled in the AIEOP ALL 2000 therapeutic protocol. We report a small noncoding RNA signature specific of ERG-related group, with up-regulation of miR-125b-2 cluster on chromosome 21 and several snoRNAs in the Prader-Willi locus at 15q11.2, including the orphan SNORD116 cluster.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

MiR-125b and miR-99a encoded on chromosome 21 co-regulate vincristine resistance in childhood acute megakaryoblastic leukemia.

To the Editor: MicroRNAs (miRNAs) are small, non-coding RNA of 20–22 nucleotides in length which can silence specific target genes through direct mRNA degradation, translational repression, or both. miRNAs are involved in several cellular processes like cell cycle, apoptosis, drug resistance and differentiation. In 2011, Schotte et al. reported different miRNA signatures in pediatric acute lymp...

متن کامل

miR-125b regulates differentiation and metabolic reprogramming of T cell acute lymphoblastic leukemia by directly targeting A20

T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematopoietic malignancy. Although it has been reported that overexpression of miR-125b leads to T-ALL development, the underlying mechanisms of miR-125b action are still unclear. The goal of this study is to delineate the role of miR-125b in T-ALL development. We found that miR-125b is highly expressed in undifferentiated leukemic T ...

متن کامل

بررسی بیان ژن های CCDC26 و C-Kit در رده های سلولی لوسمی لنفوبلاستیک حاد

Background and Aim: Acute Lymphoblastic Leukemia is the most common cancer in children and is one of the main causes of their mortality. In this study, we examined the expression of long noncoding RNA CCDC26 gene and its downstream C-Kit gene in acute lymphocytic Leukemia cell line. Materials and Methods: This is an experimental study. In this study, the acute Lymphoblastic Leukemia cell lines...

متن کامل

Changes in Expression of miR-1297 and PTEN Tumor Suppressor Gene in T-cell Acute Lymphoblastic Leukemia

Background and purpose: T-cell acute lymphoblastic leukemia (T-ALL) is a type of blood malignancy caused by changes in the precursors of T lymphocyte cells. The PTEN gene is one of the most common tumor suppressor genes that mutates in most human cancers, including T-ALL. Therefore, it is important to identify miRNAs that target the PTEN gene in T-ALL. For this purpose, in the present study, mi...

متن کامل

MicroRNA miR-125b causes leukemia.

MicroRNA miR-125b has been implicated in several kinds of leukemia. The chromosomal translocation t(2;11)(p21;q23) found in patients with myelodysplasia and acute myeloid leukemia leads to an overexpression of miR-125b of up to 90-fold normal. Moreover, miR-125b is also up-regulated in patients with B-cell acute lymphoblastic leukemia carrying the t(11;14)(q24;q32) translocation. To decipher th...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره 8  شماره 

صفحات  -

تاریخ انتشار 2017