MDS/AML with del5q: An acquired “laminopathy”?

Eirini P. Papapetrou

doi:10.1016/j.stem.2022.03.008

MDS/AML with del5q: An acquired “laminopathy”?

Research output: Contribution to journal › Comment/debate

Abstract

In this issue of Cell Stem Cell, Reilly et al. propose loss of LMNB1, the gene encoding lamin B1, often deleted in MDS/AML, as a novel genetic basis for the abnormal nuclear shape of neutrophils (known as acquired Pelger-Huët anomaly) and a cause of HSPC fate alterations promoting malignancy.

Original language	English
Pages (from-to)	498-499
Number of pages	2
Journal	Cell Stem Cell
Volume	29
Issue number	4
DOIs	https://doi.org/10.1016/j.stem.2022.03.008
State	Published - 7 Apr 2022

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title = "MDS/AML with del5q: An acquired “laminopathy”?",

abstract = "In this issue of Cell Stem Cell, Reilly et al. propose loss of LMNB1, the gene encoding lamin B1, often deleted in MDS/AML, as a novel genetic basis for the abnormal nuclear shape of neutrophils (known as acquired Pelger-Hu{\"e}t anomaly) and a cause of HSPC fate alterations promoting malignancy.",

author = "Papapetrou, {Eirini P.}",

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N2 - In this issue of Cell Stem Cell, Reilly et al. propose loss of LMNB1, the gene encoding lamin B1, often deleted in MDS/AML, as a novel genetic basis for the abnormal nuclear shape of neutrophils (known as acquired Pelger-Huët anomaly) and a cause of HSPC fate alterations promoting malignancy.

AB - In this issue of Cell Stem Cell, Reilly et al. propose loss of LMNB1, the gene encoding lamin B1, often deleted in MDS/AML, as a novel genetic basis for the abnormal nuclear shape of neutrophils (known as acquired Pelger-Huët anomaly) and a cause of HSPC fate alterations promoting malignancy.

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M3 - Comment/debate

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SN - 1934-5909

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SP - 498

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JO - Cell Stem Cell

JF - Cell Stem Cell

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MDS/AML with del5q: An acquired “laminopathy”?

Abstract

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