Special Issue "Leukemia"
QuicklinksA special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: 31 July 2012
Special Issue Editor
Guest Editor
Dr. Charles H. Lawrie
Lymphoid Malignancy Research Group, Nuffield Department of Clinical Laboratory Sciences, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DU, UK
Website: http://www.ndcls.ox.ac.uk/ResGroups.php?GID=29
E-Mail: charles.lawrie@ndcls.ox.ac.uk
Phone: +44 1865 220344
Interests: cancer; lymphoma; leukemia; microarray; microRNA; biomarkers; non-coding RNA
Special Issue Information
Dear Colleagues,
Leukemia (leukaemia- British spelling) is a malignancy of the blood originating from immature leukocytes (lymphoid and myeloid). It is the most common form of childhood cancer (~1/3 of cases) and accounts for >44,000 new diagnoses and >22,000 mortalities annually in the US alone. Recent advances in both laboratory and clinic continue to improve the outcome for patients. This special edition of Cancers gives an opportunity to describe recent original research in the field of leukemia, the development or application of new platforms or insights, and/or reviews of the field. We are particularly interested in genomics, leukemia stem cell research, novel therapeutics, epidemiological studies and new biomarker studies. If you would like to discuss an idea for a paper before committing please contact the guest editor.
Dr. Charles Lawrie
Guest Editor
Submission
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed Open Access quarterly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 500 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.
Keywords
- acute lymphoblastic leukemia (ALL)
- chronic lymphocytic leukemia (CLL)
- acute myelogenous leukemia (AML)
- chronic myelogenous leukemia (CML)
- hairy cell leukemia (HCL)
- T-cell prolymphocytic leukemia (T-PLL)
- large granular lymphocytic leukemia
- adult T-cell leukemia
- human T-lymphotropic virus (HTLV)
Published Papers
Planned Papers
Title: Molecular and Epigenetic Mechanisms of MLL1 in Human Leukaemogenesis
Authors: Erica Ballabio and Thomas A. Milne
Affiliation: MRC Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital Headington, Oxford, OX3 9DS, UK; E-Mail: thomas.milne@imm.ox.ac.uk
Abstract: Epigenetics is often defined as heritable changes in gene expression or chromosome stability that don't alter the underlying DNA sequence. Epigenetic changes are established through multiple mechanisms that include DNA methylation, non-coding RNAs and the covalent modification of specific residues on histone proteins. It is becoming clear not only that aberrant epigenetic changes are common in many human diseases such as leukaemia, but that these changes by their very nature are malleable, and thus are amenable to treatment. Epigenetic therapies have so far focused on the use of Histone deacetylase (HDAC) inhibitors and DNA methyltransferase inhibitors, which tend to have more general and widespread effects on gene regulation in the cell. However, if a unique molecular pathway can be identified, epigenetic diseases are excellent candidates for the development of more targeted therapies that focus on specific gene targets, individual binding domains, or specific enzymatic activities. Designing effective targeted therapies depends on a clear understanding of the role of epigenetic mutations during disease progression. The Mixed Lineage Leukaemia 1 (MLL1) protein is an example of an epigenetic protein that controls gene activation in part by methylating histone 3 on lysine 4. MLL1 is required for normal development, but is also mutated in a subset of aggressive human leukaemias and thus provides a useful model for studying the link between epigenetic cell memory and human disease. The most common MLL1 mutations fuse the MLL1 gene in frame with over 64 different partner genes creating novel fusion proteins. In this review, we summarise recent work that argues MLL1 fusion proteins function through a single molecular pathway, but we also highlight important data that instead suggests multiple independent mechanisms underlie MLL1 mediated leukaemogenesis.
Last update: 16 May 2012