Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics. Export

@article{citeulike:4845475, abstract = {ABSTRACT: Acute myeloid leukemia (AML) is a heterogenous disorder that results from a block in the differentiation of hematopoietic progenitor cells along with uncontrolled proliferation. In approximately sixty percent of cases, specific recurrent chromosomal aberrations can be identified by modern cytogenetic techniques. This cytogenetic information is the single most important tool to classify patients at their initial diagnosis into three prognostic categories: favorable, intermediate, and poor risk. Currently, favorable risk AML patients are usually treated with contemporary chemotherapy while poor risk AML patients receive allogeneic stem cell transplantation if suitable stem cell donors exist. The largest subgroup of AML patients (approximately forty percent) have no identifiable cytogenetic abnormalities and are classified as intermediate risk. The optimal therapeutic strategies for these patients are still largely unclear. Recently, it is becoming increasingly evident that it is possible to identify a subgroup of poorer risk patients among those with normal cytogenic AML (NC-AML). Molecular risk stratification for NC-AML patients may be possible due to mutations of NPM1, FLT3, MLL, and CEBPalpha as well as alterations in expression levels of BAALC, MN1, ERG, and AF1q. Further prospective studies are needed to confirm if poorer risk NC-AML patients have improved clinical outcomes after more aggressive therapy.}, author = {Gregory, Tara K. and Wald, David and Chen, Yichu and Vermaat, Johanna M. and Xiong, Yin and Tse, William}, citeulike-article-id = {4845475}, citeulike-linkout-0 = {http://dx.doi.org/10.1186/1756-8722-2-23}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19490647}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19490647}, doi = {10.1186/1756-8722-2-23}, issn = {1756-8722}, journal = {Journal of hematology \& oncology}, keywords = {genetics, medicine}, month = {June}, number = {1}, posted-at = {2009-06-14 14:31:35}, priority = {2}, title = {Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics.}, url = {http://dx.doi.org/10.1186/1756-8722-2-23}, volume = {2}, year = {2009} }

TY - JOUR ID - citeulike:4845475 L3 - citeulike-article-id:4845475 N2 - ABSTRACT: Acute myeloid leukemia (AML) is a heterogenous disorder that results from a block in the differentiation of hematopoietic progenitor cells along with uncontrolled proliferation. In approximately sixty percent of cases, specific recurrent chromosomal aberrations can be identified by modern cytogenetic techniques. This cytogenetic information is the single most important tool to classify patients at their initial diagnosis into three prognostic categories: favorable, intermediate, and poor risk. Currently, favorable risk AML patients are usually treated with contemporary chemotherapy while poor risk AML patients receive allogeneic stem cell transplantation if suitable stem cell donors exist. The largest subgroup of AML patients (approximately forty percent) have no identifiable cytogenetic abnormalities and are classified as intermediate risk. The optimal therapeutic strategies for these patients are still largely unclear. Recently, it is becoming increasingly evident that it is possible to identify a subgroup of poorer risk patients among those with normal cytogenic AML (NC-AML). Molecular risk stratification for NC-AML patients may be possible due to mutations of NPM1, FLT3, MLL, and CEBPalpha as well as alterations in expression levels of BAALC, MN1, ERG, and AF1q. Further prospective studies are needed to confirm if poorer risk NC-AML patients have improved clinical outcomes after more aggressive therapy. IS - 1 JF - Journal of hematology & oncology SN - 1756-8722 TI - Molecular prognostic markers for adult acute myeloid leukemia with normal cytogenetics. VL - 2 KW - genetics KW - medicine AU - Gregory, Tara AU - Wald, David AU - Chen, Yichu AU - Vermaat, Johanna AU - Xiong, Yin AU - Tse, William PY - 2009/06/02/ UR - http://dx.doi.org/10.1186/1756-8722-2-23 ER -