Widespread over-expression of the non-clustered homeobox gene HLX in acute myeloid leukemia.

نویسنده

  • Stefan Fröhling
چکیده

Immunohistochemical analysis of skin tissue biopsies from an individual with acute graft-versus-host-disease. Scattered ICOS+ activated lymphocytes were observed at the dermo-epidermal junction, superficial dermis and around the adnexal follicular epithelium. Figure taken from the article by Maria Cuzzola and colleagues on page 1532. Widespread over-expression of the non-clustered homeobox gene HLX in acute myeloid leukemia Stefan Fröhling Is it time to abandon RHAMM/HMMR as a candidate antigen for immunotherapy of acute myeloid leukemia? Dolores J. Schendel Survivin: a new player during erythroblast maturation Wataru Nunomura and Kenichi Sawada Production of the effector cytokine interleukin-17, rather than interferon-γ, is more strongly associated with autoimmune hemolytic anemia An observational, prospective, two-cohort comparison of a fixed versus variable dosing strategy of prothrombin complex concentrate to counteract vitamin K antagonists in 240 bleeding emergencies

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

HLX in AML: novel prognostic and therapeutic target

Acute myeloid leukemia (AML) is an aggressive hematological malignancy with poor clinical outcome in most subtypes of the disease. Less than one third of patients achieve durable remission with current treatment regimens, and prognostication and risk stratification are challenging. We recently reported that a new non-clustered homeobox gene, H2.0-like homeobox (HLX), regulates early hematopoies...

متن کامل

Enforced expression of Hlx homeobox gene prompts myeloid cell maturation and altered adherence properties of T cells.

Within the hematopoietic compartment, the murine Hlx homeobox gene is expressed in myeloid cells, most prominently in macrophages and granulocytes, and in immature B-lymphoid cells but not in erythroid, mast, or T-lymphoid cells. The level of Hlx mRNA increased with induced differentiation of the promyelocytic lines WEHI-3B and HL-60. To address its biologic action more directly, Hlx expression...

متن کامل

Gene Identification from Microarray Data for Diagnosis of Acute Myeloid and Lymphoblastic Leukemia Using a Sparse Gene Selection Method

Background: Microarray experiments can simultaneously determine the expression of thousands of genes. Identification of potential genes from microarray data for diagnosis of cancer is important. This study aimed to identify genes for the diagnosis of acute myeloid and lymphoblastic leukemia using a sparse feature selection method. Materials and Methods: In this descriptive study, the expressio...

متن کامل

Evaluation of the CD123 Expression and FLT3 Gene Mutations in Patients with Acute Myeloid Leukemia

Background and Objective: Identification of cytogenetic and molecular changes plays an important role in acute myeloid leukemia (AML) patients. Thus, they are used in classification, prognosis and treatment of the disease. The CD123 expression and FLT3 gene mutations are also the variations that may assist in prognosis and treatment of patients with AML.Methods:</...

متن کامل

Alterations of adiponectin gene expression in bone marrow of acute myeloid leukemia

Background: Acute myeloid leukemia (AML) is characterized by the proliferation of myeloid precursors and abnormal differentiation of hematopoietic stem cells, which results in the accumulation of immature cells in the bone marrow (BM). The accumulation of these cells in the bone marrow causes molecular and cellular changes in the microenvironment of the bone marrow. The adiponectin hormone orig...

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:
  • Haematologica

دوره 97 10  شماره 

صفحات  -

تاریخ انتشار 2012