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Promyelocytic leukemia protein

About: Promyelocytic leukemia protein is a research topic. Over the lifetime, 1760 publications have been published within this topic receiving 95918 citations. The topic is also known as: MYL & PP8675.


Papers
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Journal ArticleDOI
23 Aug 1991-Cell
TL;DR: Because patients with APL can be induced into remission with high dose RA therapy, it is proposed that the nonliganded PML-RAR protein is a new class of dominant negative oncogene product.

1,429 citations

Journal ArticleDOI
11 Oct 1990-Nature
TL;DR: It is reported that, in one APL-derived cell line, the RARα gene has been translocated to a locus, myl, on chromosome 15, resulting in the synthesis of a myl/RARα fusion messenger RNA, which strongly implicate retinoic acid receptor α in leukaemogenesis.
Abstract: RETINOIC acid is a vitamin A derivative with striking effects on development and cell differentiation1–3. Several nuclear retinoic acid receptors (RARs), acting as ligand-inducible transcription factors, have been characterized4–8 and indirect evidence suggests that they have distinct roles9–11. One of the most intriguing properties of retinoic acid is its ability to induce in vivo differentiation of acute promyelocytic leukaemia (APL) cells into mature granulocytes, leading to morphological complete remissions12–13. Because the RARα gene maps to chromosome 17q21 (ref. 14), close to the t(15;17) (q21–qll–22) translocation specifically associated with APL15, we analysed RARα gene structure and expression in APL cells. We report here that, in one APL-derived cell line, the RARα gene has been translocated to a locus, myl, on chromosome 15, resulting in the synthesis of a myl/RARα fusion messenger RNA. Using two probes located on either side of the cloned breakpoint, we have found genomic rearrangements of one or other locus in six patients out of eight, demonstrating that the RARα and/or myl genes are frequently rearranged in APL and the breakpoints are clustered. These findings strongly implicate retinoic acid receptor α in leukaemogenesis.

1,323 citations

Journal ArticleDOI
23 Aug 1991-Cell
TL;DR: In APL, the t(15;17) translocation generates an RAR mutant that could contribute to leukemogenesis through interference with promyelocytic differentiation, and this gene product contains a novel zinc finger motif common to several DNA-binding proteins.

1,321 citations

Journal ArticleDOI
01 Nov 1987-Blood
TL;DR: The HL-60 cell line, derived from a single patient with acute promyelocytic leukemia, provides a unique in vitro model system for studying the cellular and molecular events involved in the proliferation and differentiation of normal and leukemic cells of the granulocyte/monocyte/macrophage lineage.

1,193 citations

Journal ArticleDOI
15 May 1999-Blood
TL;DR: The elucidation of the molecular basis of acute promyelocytic leukemia emerged as a paradigm for the connection between the bench and bedside and it became apparent that APL was, among the forms of acute myeloid leukemia, uniquely sensitive to all

1,022 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202356
202237
202120
202023
201925
201821