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Conference Paper: Epigenetic inactivation of the miR-34a in hematological malignancies

TitleEpigenetic inactivation of the miR-34a in hematological malignancies
Authors
KeywordsMalignancy
Issue Date2010
Citation
The 15th Congress of the European Hematology Association (EHA), Barcelona, Spain, 10-13 June 2010. How to Cite?
AbstractBACKGROUND : miR-34a is a transcriptional target of p53, and implicated in carcinogenesis. AIM: We studied the role of miR-34a methylation in a panel of hematological malignancies including acute leukemia (AML, ALL), chronic leukemia (CLL and CML), multiple myeloma (MM) and non-Hodgkin's lymphoma (NHL). METHODS: The methylation status of miR-34a promoter was studied in 12 cell lines and 188 diagnostic samples by methylation-specific PCR. RESULTS: miR-34a promoter was unmethylated in normal controls but methylated in 75% lymphoma and 37% myeloma cell lines. Hypomethylating treatment led to re-expression of pri-miR-34a transcript in lymphoma cells with homozygous miR-34a methylation. In primary samples at diagnosis, miR-34a methylation was detected in 4% CLL, 5.5% MM samples, and 18.8% of NHL at diagnosis but none of ALL, AML and CML (p=0.011). In MM patients with paired samples, miR-34a methylation status remained unchanged at progression. Amongst lymphoid malignancies, miR-34a was preferentially methylated in NHL (p=0.018), in particular natural killer/T cell (NK/T cell) lymphoma. SUMMARY: Amongst hematological malignancies, miR-34a methylation is preferentially hypermethylated in NHL, in particular NK/T cell lymphoma, in a tumor-specific manner, therefore the role of miR-34a in lymphomagenesis warrants further study.
DescriptionPoster Session I: Developmental Biology & Genomics
Persistent Identifierhttp://hdl.handle.net/10722/126433

 

DC FieldValueLanguage
dc.contributor.authorChim, JCSen_HK
dc.contributor.authorWong, KYen_HK
dc.contributor.authorQi, Yen_HK
dc.date.accessioned2010-10-31T12:28:20Z-
dc.date.available2010-10-31T12:28:20Z-
dc.date.issued2010en_HK
dc.identifier.citationThe 15th Congress of the European Hematology Association (EHA), Barcelona, Spain, 10-13 June 2010.en_HK
dc.identifier.urihttp://hdl.handle.net/10722/126433-
dc.descriptionPoster Session I: Developmental Biology & Genomics-
dc.description.abstractBACKGROUND : miR-34a is a transcriptional target of p53, and implicated in carcinogenesis. AIM: We studied the role of miR-34a methylation in a panel of hematological malignancies including acute leukemia (AML, ALL), chronic leukemia (CLL and CML), multiple myeloma (MM) and non-Hodgkin's lymphoma (NHL). METHODS: The methylation status of miR-34a promoter was studied in 12 cell lines and 188 diagnostic samples by methylation-specific PCR. RESULTS: miR-34a promoter was unmethylated in normal controls but methylated in 75% lymphoma and 37% myeloma cell lines. Hypomethylating treatment led to re-expression of pri-miR-34a transcript in lymphoma cells with homozygous miR-34a methylation. In primary samples at diagnosis, miR-34a methylation was detected in 4% CLL, 5.5% MM samples, and 18.8% of NHL at diagnosis but none of ALL, AML and CML (p=0.011). In MM patients with paired samples, miR-34a methylation status remained unchanged at progression. Amongst lymphoid malignancies, miR-34a was preferentially methylated in NHL (p=0.018), in particular natural killer/T cell (NK/T cell) lymphoma. SUMMARY: Amongst hematological malignancies, miR-34a methylation is preferentially hypermethylated in NHL, in particular NK/T cell lymphoma, in a tumor-specific manner, therefore the role of miR-34a in lymphomagenesis warrants further study.-
dc.languageengen_HK
dc.relation.ispartofCongress of the European Hematology Association-
dc.subjectMalignancy-
dc.titleEpigenetic inactivation of the miR-34a in hematological malignanciesen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailChim, JCS: jcschim@hku.hken_HK
dc.identifier.emailQi, Y: blackfin561@163.comen_HK
dc.identifier.hkuros172209en_HK
dc.description.otherThe 15th Congress of the European Hematology Association (EHA), Barcelona, Spain, 10-13 June 2010.-

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