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Mixed-phenotype acute leukemia: suboptimal treatment when the 2008/2016 WHO classification is used
Alan Pomerantz,Sergio Rodriguez-Rodriguez,Roberta Demichelis-Gomez,Georgina Barrera-Lumbreras,Olga Barrales-Benitez,Xavier Lopez-Karpovitch,Alvaro Aguayo-Gonzalez 대한혈액학회 2016 Blood Research Vol.51 No.4
BackgroundDifferent criteria have been used to diagnose mixed-phenotype acute leukemia (MPAL), which has impacted the number of individuals diagnosed with this pathology. Better out-comes have been reported when using acute lymphoblastic leukemia (ALL)-type chemo-therapy in the treatment of MPAL.MethodsWe compared the outcome of 4 groups of patients with MPAL. Group 1 included patients diagnosed using the 2008/2016 World Health Organization (WHO) classification; group 2 included patients diagnosed using the European Group for the Immunological Characterization of Leukemias (EGIL) criteria; group 3 included patients diagnosed using either the EGIL or the 2008/2016 WHO criteria; and group 4 was comprised of patients diagnosed with MPAL using the EGIL classification only.ResultsWe found a significantly worse disease-free survival (groups 1‒4) and overall survival (OS) (groups 2 and 3) when comparing MPAL patients to other acute leukemia (AL) patients. A significantly better OS was obtained in patients (groups 2‒4) treated with ALL-type che-motherapy compared to acute myeloid leukemia (AML)-type regimens.ConclusionIn light of these results, and because a trend (P=0.06) was found with regard to a better OS in group 4 when compared to other AL patients, an argument can be made that the 2008/2016 WHO classification is underpowered to diagnose all MPAL cases, potentially resulting in the suboptimal treatment of some individuals with AL.
FOXM1 mediates Dox resistance in breast cancer by enhancing DNA repair
Park, Yun-Yong,Jung, Sung Yun,Jennings, Nicholas B,Rodriguez-Aguayo, Cristian,Peng, Guang,Lee, Se-Ran,Kim, Sang Bae,Kim, Kyounghyun,Leem, Sun-Hee,Lin, Shiaw-Yih,Lopez-Berestein, Gabriel,Sood, Anil K,L Oxford University Press 2012 Carcinogenesis Vol.33 No.10
<B>Abstract</B><P>Transcription factors are direct effectors of altered signaling pathways in cancer and frequently determine clinical outcomes in cancer patients. To uncover new transcription factors that would determine clinical outcomes in breast cancer, we systematically analyzed gene expression data from breast cancer patients. Our results revealed that Forkhead box protein M1 (FOXM1) is the top-ranked survival-associated transcription factor in patients with triple-negative breast cancer. Surprisingly, silencing FOXM1 expression led breast cancer cells to become more sensitive to doxorubicin (Dox). We found that FOXM1-dependent resistance to Dox is mediated by regulating DNA repair genes. We further demonstrated that NFκB1 interacts with FOXM1 in the presence of Dox to protect breast cancer cells from DNA damage. Finally, silencing FOXM1 expression in breast cancer cells in a mouse xenograft model significantly sensitized the cells to Dox. Our systematic approaches identified an unexpected role of FOXM1 in Dox resistance by regulating DNA repair genes, and our findings provide mechanistic insights into how FOXM1 mediates resistance to Dox and evidence that FOXM1 may be a promising therapeutic target for sensitizing breast cancer cells to Dox.</P>
Chaluvally-Raghavan, P.,Zhang, F.,Pradeep, S.,Hamilton, Mark P.,Zhao, X.,Rupaimoole, R.,Moss, T.,Lu, Y.,Yu, S.,Pecot, Chad V.,Aure, Miriam R.,Peuget, S.,Rodriguez-Aguayo, C.,Han, H.D.,Zhang, D.,Venkat Cell Press 2014 CANCER CELL Vol.26 No.6
Small noncoding miRNAs represent underexplored targets of genomic aberrations and emerging therapeutic targets. The 3q26.2 amplicon is among the most frequent genomic aberrations in multiple cancer lineages including ovarian and breast cancers. We demonstrate that hsa-miR-569 (hereafter designated as miR569), which is overexpressed in a subset of ovarian and breast cancers, at least in part due to the 3q26.2 amplicon, alters cell survival and proliferation. Downregulation of TP53INP1 expression by miR569 is required for the effects of miR569 on survival and proliferation. Targeting miR569 sensitizes ovarian and breast cancer cells overexpressing miR569 to cisplatin by increasing cell death both in vitro and in vivo. Thus targeting miR569 could potentially benefit patients with the 3q26.2 amplicon and subsequent miR569 elevation.