Abstract:
:Abstract ATM gene alteration is a frequent event in pathogenesis of chronic lymphocytic leukemia (CLL) and occurs as monoallelic loss in the form of 11q23 deletion, with and without mutation in the remaining ATM allele. ATM is a principal DNA damage response gene and biallelic ATM alterations lead to ATM functional loss and chemoresistance. The introduction of new therapies, such as intensive chemoimmunotherapy and inhibition of B-cell receptor (BCR) signaling, has changed clinical responses for the majority of CLL tumors including those with 11q deletion, but it remains to be determined whether these strategies can prevent clonal evolution of tumors with biallelic ATM alterations. In this review we discuss ATM function and the consequences of its loss during CLL pathogenesis, differences in clinical behavior of tumors with monoallelic and biallelic ATM alterations, and we outline possible approaches for targeting the ATM null CLL phenotype.
journal_name
Leuk Lymphomajournal_title
Leukemia & lymphomaauthors
Stankovic T,Skowronska Adoi
10.3109/10428194.2013.829919subject
Has Abstractpub_date
2014-06-01 00:00:00pages
1227-39issue
6eissn
1042-8194issn
1029-2403journal_volume
55pub_type
杂志文章,评审abstract::The aim of this study was to evaluate the localization of collagen modifying enzymes (CMEs) on fibroblastic reticular cells (FRCs) and follicular dendritic cells (FDCs) in non-neoplastic lymphoid tissues and various malignant lymphomas. The expression of prolyl 4-hydroxylase 1 (P4H1), lysyl hydroxylase 3 (LH3), and pr...
journal_title:Leukemia & lymphoma
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journal_title:Leukemia & lymphoma
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journal_title:Leukemia & lymphoma
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journal_title:Leukemia & lymphoma
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journal_title:Leukemia & lymphoma
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journal_title:Leukemia & lymphoma
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journal_title:Leukemia & lymphoma
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journal_title:Leukemia & lymphoma
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