Prognostic factors in acute myeloid leukemia (AML) may be subdivided into those related to patient characteristics and general health condition, and those related to characteristics of the tumor. More »
The management of patients with acute promyelocytic leukemia (APL) has been transformed over the course of the last two decades following the introduction of successful molecularly targeted therapies—all-trans retinoic acid (ATRA) and arsenic trioxide (ATO)— which act in concert to induce degradation of the PMLRARα oncoprotein formed by the chromosomal translocation t(15;17)(q22;q21). More »
The management of leukemias and lymphomas now includes the use of many targeted therapies. Nurses need to have an understanding of the targeted therapies and their side effects so they can appropriately manage the side effects that their patients with leukemias and lymphomas may experience. More »
Preliminary findings of a phase I/II randomized clinical trial indicate that SGI-110, a novel DNA methylation inhibitor, is safe, well tolerated and efficacious in patients with acute myelogenous leukemia. More »
Recently, we showed that increased miR-181a expression was associated with improved outcomes in cytogenetically normal acute myeloid leukemia (CN-AML). Interestingly, miR-181a expression was increased in CN-AML patients harboring CEBPA mutations, which are usually biallelic and associate with better prognosis. CEBPA encodes the C/EBP transcription factor. We demonstrate here that the presence of N-terminal CEBPA mutations and miR-181a expression are linked. Indeed, the truncated C/EBP-p30 isoform, which is produced from the N-terminal mutant CEBPA gene or from the differential translation of wild-type CEBPA mRNA and is commonly believed to have no transactivation activity, binds to the miR-181a-1 promoter and up-regulates the microRNA expression. Furthermore, we show that lenalidomide, a drug approved for myelodysplasticsyndromes and multiple myeloma, enhances translation of the C/EBP-p30 isoform, resulting in higher miR-181a levels. In xenograft mouse models, ectopic miR-181a
23061809 2012 12 17 2013 02 06 1600-0609 90 1 Jan Eur. J. Haematol. 79-80 10.1111/ejh.12024 Matsuda Akira A Germing Ulrich U Miyazaki Yasushi Y eng Letter 2012 11 22 England Eur J Haematol 8703985 0902-4441 IM pathology classification diagnosis.
Treatment of relapse after allogenic stem cell transplantation (allo-SCT) is challenging. The efficacy of donor leukocyte infusions (DLI) is excellent in chronic phase chronic myeloid leukaemia but limited in other disorders. We present a patient who relapsed 10 months after reduced intensity conditioning allo-SCT for a myelodysplastic/ myeloproliferative neoplasm with myelofibrosis despite receiving escalating doses of DLI for incomplete chimerism. He finally achieved complete remission with full whole blood and T-cell donor chimerism after DLI preceded by lymphodepletion chemotherapy. This case demonstrates that chemotherapy prior to DLI is a useful approach for treating relapses of relatively slowly progressive diseases, such as myeloproliferative diseases or myelodysplasticsyndromes.
23258901 2012 12 21 2013 02 15 1528-0020 120 26 Dec 20 Blood 5247-9 10.1182/blood-2012-09-457945 Churpek Jane E JE Nickels Eric E Marquez Rafael R Rojek Katarzyna K Liu Bohao B Lorenz Rachelle R Lepore Janet J Madzo Jozef J Wickrema Amittha A Artz
Myelodysplasticsyndromes (MDS) are malignant clonal disorders of haematopoietic stem cells and their microenvironment, affecting older individuals (median age 70 years). Unique features that are associated with MDS - but which are not necessarily present in every patient with MDS - include excessive apoptosis in maturing clonal cells, a pro-inflammatory bone marrow microenvironment, specific chromosomal abnormalities, abnormal ribosomal protein biogenesis, the presence of uniparental disomy, and mutations affecting genes involved in proliferation, methylation and epigenetic modifications. Although emerging insights establish an association between molecular abnormalities and the phenotypic heterogeneity of MDS, their origin and progression remain enigmatic.