Mixed lineage leukemia-septin 5 fusion transcript in de novo adult acute myeloid leukemia with t(11;22)(q23;q11.2): A case report

نویسندگان

  • WEN GAO
  • TONG WANG
  • YIN WU
  • HONG XING LIU
  • YAN CHEN LI
  • WEN MING CHEN
چکیده

The current report presents a case of de novo acute myeloid leukemia (AML) in a 32-year-old male. Cytogenetic analysis showed that the karyotype of the bone marrow cells was as follows: 46,XY,t(11;22)(q23;q11.2)[13]/46,X,-Y,+10,t(11;22)(q23;q11.2)[7]/47,XY,+10,t(11;22)(q23;q11.2)[1]/46,XY[1]. Fluorescence in situ hybridization analysis using a mixed lineage leukemia (MLL)-specific probe showed a split in the MLL gene. Reverse transcription polymerase chain reaction (PCR) analysis demonstrated an MLL-septin 5 (SEPT5) fusion transcript in the patient. Nucleotide sequencing analysis of the PCR product confirmed the fusion between the MLL exon 9 and SEPT5 exon 3, and the product was 521 bp in length. The present study reviewed the clinical and molecular features of the AML with an MLL-SEPT5 fusion gene.

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

MLL-SEPT5 Fusion Transcript in Two de novo Acute Myeloid Leukemia Patients With t(11;22)(q23;q11)

Dear Editor, Rearrangements involving mixed lineage leukemia (MLL) are common chromosome aberrations in infant, pediatric and adult acute leukemia, which are generally associated with poor prognosis. To date, more than 79 partner genes have been identified [1]. MLL fusion partners can be classified into four groups: nuclear proteins (MLLT3, MLLT10, and MLLT1), cytoplasmatic proteins (GAS7, SH3G...

متن کامل

AF17q25, a putative septin family gene, fuses the MLL gene in acute myeloid leukemia with t(11;17)(q23;q25).

The t(11;17) has been described in patients with acute myeloid leukemia (AML), and the AF17 gene was previously cloned as a fusion partner of the MLL gene in t(11;17)(q23;q21)-AML. We analyzed one patient with de novo AML and one with therapy-related AML with t(11;17)(q23;q25) and identified the AF17q25 gene on chromosome 17q25, a putative septin family gene, fused with MLL. AF17q25 encoded at ...

متن کامل

Acute myeloid leukemia with KMT2A-SEPT5 translocation: A case report and review of the literature

Chromosomal rearrangement involving the KMT2A gene is one of the most common genetic alteration in acute myeloid leukemia. A total of 135 different KMT2A rearrangements have been identified, where 94 translocation partner genes are now characterized at the molecular level. Of these 94 translocation partner genes, 35 translocation partner genes occur recurrently, but only 9 specific gene fusions...

متن کامل

MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25).

MLL (ALL1, Htrx, HRX), which is located on chromosome band 11q23, frequently is rearranged in patients with therapy-related acute myeloid leukemia who previously were treated with DNA topoisomerase II inhibitors. In this study, we have identified a fusion partner of MLL in a 10-year-old female who developed therapy-related acute myeloid leukemia 17 months after treatment for Hodgkin's disease. ...

متن کامل

A Rare Case of Acute Myeloid Leukemia with Translocation (3:3) Presenting with Features of Chronic Myelomonocytic Leukemia

Background: Acute Myeloid Leukemia (AML) with translocation (3,3) is a form of AML that may present de novo or may arise from a previous myelodysplastic syndrome. It is often associated with normal or elevated peripheral blood platelet count and increased bone marrow megakaryocytes with associated multi lineage dysplasia. A subset of patients present with hepatosplenomegaly while a few cases h...

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 7  شماره 

صفحات  -

تاریخ انتشار 2014