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2 edition of Understanding RAR[alpha] chimeric proteins associated with acute promyelocytic leukemia found in the catalog.

Understanding RAR[alpha] chimeric proteins associated with acute promyelocytic leukemia

Jeff L. Hummel

Understanding RAR[alpha] chimeric proteins associated with acute promyelocytic leukemia

evidence supporting the deregulation of NPM in APL.

by Jeff L. Hummel

  • 219 Want to read
  • 31 Currently reading

Published .
Written in English


Edition Notes

Thesis (Ph.D.) -- University of Toronto, 2002.

The Physical Object
Pagination235 leaves.
Number of Pages235
ID Numbers
Open LibraryOL19480380M
ISBN 100612784185

PML—RAR (retinoic acid receptor)α is the hallmark protein of acute promyelocytic leukaemia, a highly malignant subtype of acute myeloid leukaemia that accounts for approximately 10% of all AML. Resistance to treatment in patients with acute promyelocytic leukemia is rare. The authors describe the development of resistance to arsenic through a mutation in the allele of PML that is not rear.

Acute Myeleoid Leukemia Acute Myeleoid Leukemia Research Papers delve into how this type of blood cancer develops. Acute Myeleoid Leukemia is a cancer of the blood which is heterogenous in nature, making it rather difficult to consistently Myeleoid Leukemia is characterized by a differentiation block at the promyelocytic stage and by a reciprocal translocation affecting .   APL with t(V;17)(V;q12): Involves RAR alpha and either PLZF / ZBTB16 (11q23), NUMA (11q13), NPM (5q31) or STAT5b genes (Leukemia ;) Table 3: cytogenetic abnormalities in APL (eMedicine: Acute Myeloid Leukemia (AML) Workup [Accessed 2 April, ]): Translocation Genes Involved All-Trans-Retinoic Acid Response.

Recurrent chromosomal translocations involving the RAR alpha locus on chromosome 17 are the hallmark of acute promyelocytic leukemia (APL). The RAR alpha gene fuses to . Gheath Alatrash, Jeffrey J. Molldrem, in Immune Biology of Allogeneic Hematopoietic Stem Cell Transplantation, PML-RARα. The promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARα) fusion that is caused by translocation to (15;17) is a hallmark feature of acute promyelocytic leukemia (APL).The fusion protein caused by this translocation functions as an abnormal retinoid.


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Understanding RAR[alpha] chimeric proteins associated with acute promyelocytic leukemia by Jeff L. Hummel Download PDF EPUB FB2

Acute promyelocytic leukemia (APML, APL) is a subtype of acute myeloid leukemia (AML), a cancer of the white blood cells. In APL, there is an abnormal accumulation of immature granulocytes called disease is characterized by a chromosomal translocation involving the retinoic acid receptor alpha (RARα or RARA) gene and is distinguished from other forms of AML by its Specialty: Hematology and oncology.

1. Introduction. Acute promyelocytic leukemia (APL) is a unique entity in acute myeloid malignancies typically characterized by the balanced translocation t (15; 17)(q;q) and resultant PML-RARA fusion gene [1,2].The PML-RARA protein product has been identified as the primary driver responsible for nearly all cases of APL, and enhanced understanding of the mechanism by which Cited by: 3.

Acute promyelocytic leukemia is a distinguished subset of acute myeloid leukemia which is characterized by fusion gene transcript PML-RAR-alpha and high cure rates with treatment. This entity was first described in in patients with severe bleeding tendencies with fibrinolysis, rapid deterioration of the clinical condition, and the presence of promyelocytes in peripheral blood and bone Author: Shashank R.

Cingam, Nebu V. Koshy. acute promyelocytic leukemia (apl) is a subtype of acute myeloid leukemia, a cancer that affects stem cells. in apl, the leukemia cells contain special proteins.

Introduction. Acute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia (AML) characterized by distinctive morphology of blast cells, 1,2 a life-threatening coagulopathy, 3 and a specific balanced reciprocal translocation t(15;17), 4 which fuses the PML (promyelocyte) gene on chromosome 15 to the RARα (retinoic acid receptor-α) gene on Cited by: The mutation that causes acute promyelocytic leukemia involves two genes, the PML gene on chromosome 15 and the RARA gene on chromosome A rearrangement of genetic material (translocation) between chromosomes 15 written as t(15;17), fuses part of the PML gene with part of the RARA gene.

The protein produced from this fused gene is known as PML-RARα. Acute promyelocytic leukemia (APL) has been recognized as a distinct clinical entity for over 40 years.

Although relatively rare among hematopoietic malignancies (approximately 10% of AML cases. Acute promyelocytic leukemia (APL) is a distinct subset of acute myeloid leukemia (AML) associated with peculiar biologic and clinical features and requiring specific management.

At the genetic level, APL is featured by a unique chromosome translocation t(15;17) which results in the PML–RARα gene fusion and chimeric protein. Acute promyelocytic leukemia (APL) is an aggressive type of acute myeloid leukemia in which there are too many immature blood-forming cells (promyelocytes) in the blood and bone marrow.

This build up of promyelocytes leads to a shortage of normal white and red blood cells and platelets in the body. The signs and symptoms of APL include an. The vast majority of APL patients bear t(15;17)(q24;q21) involving the promyelocytic leukemia (PML) gene at chromosome band 15q24 and the retinoic acid receptor alpha (RARA) gene at 17q21, generating an aberrant PML-RARA fusion gene.

1, 2 However, in a subset of APL patients, a t(15;17)(q24;q21) and PML-RARA fusion cannot be detected. 3 Many. Leuk Lymphoma. Apr;45(4) The PML-RARalpha fusion protein and targeted therapy for acute promyelocytic leukemia.

Jing Y(1). Author information: (1)Division of Hematology/Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, NYUSA. @ Acute promyelocytic leukemia (APL) is an unique subtype of acute myeloid leukemia.

PML-RAR Alpha. The PML– retinoic acid receptor alpha (RARα) fusion that is caused by translocation t(15; 17) is a hallmark feature of acute promyelocytic leukemia (APL). The fusion protein caused by this translocation functions as an abnormal retinoid receptor with. Transcription factors and kinases such as retinoic acid receptor-alpha (RARα), acute myeloid leukemia 1 (AML1), CAAT/enhancer-binding protein α (C/EBPα), c-myc, and c.

M. Ruthardt, U. Testa, C. Nervi, et te effects of the acute promyelocytic leukemia PML-retinoic acid receptor alpha (RAR alpha) and PLZF-RAR alpha fusion proteins on retinoic acid signalling Mol Cell Biol, 17 (), pp. Acute promyelocytic leukemia (APL) is distinguished from other acute myeloid leukemias (AMLs) by cytogenetic, clinical, as well as biological characteristics.

The hallmark of. leads to the juxtaposition of promyelocytic leukemia gene (PML) with the retinoic acid receptor alpha gene (RAR)2 in a head-to-tail configuration.3 The PML/RAR chimeric protein causes transcrip-tional repression and blocks differentiation of cells that leads to leu-kemogenesis.4,5 The clinical association of APL with hyperfibrino.

Acute promyelocytic leukemia (APL) is characterized by a block in differentiation and accumulation of promyelocytes in the bone marrow and blood. The majority of APL patients harbor the t() translocation leading to expression of the fusion protein promyelocytic-retinoic acid receptor α.

Book Editor(s): Hussain I. Saba MD, PHD Acute promyelocytic leukemia (APL) is a specific type of AML characterized by the morphology of blasts, t(15;17) translocation, PML‐RAR alpha gene fusion and coagulopathy combining DIC and fibrinolysis. All‐trans retinoic acid (ATRA), and arsenic trioxide (ATO), have greatly improved the treatment.

Cao Y, Yuan R, Wang Y, Chen R, Huang M, Zhou J. A New Chromosome Translocation t(7;16)(q31,q22) Change during an Acute Promyelocytic Leukemia Relapse. Cytogenet Genome Res. May Jurcic JG, Soignet SL, Maslak AP.

Diagnosis and treatment of acute promyelocytic leukemia. Curr Oncol Rep. Sep. 9(5) The mechanism(s) by which acute promyelocytic leukemia (APL) cells acquire resistance to all-trans retinoic acid (ATRA) is poorly understood. We describe here an APL cell line, named NB, that. PML/RARA Fusion Gene.

In the process of analyzing the RARA gene in the t(15;17)(q22;qq12) translocation specifically associated with acute promyelocytic leukemia (APL), de The et al.

() identified a novel gene on chromosome 15 involved with the RARA gene in formation of a fusion product. This gene, which they called MYL, was transcribed in the same direction as RARA on the.The PML-RAR alpha fusion mRNA generated by the t(15;17) translocation in acute promyelocytic leukemia encodes a functionally altered RAR.

Cell. ;66(4) 5. de Thé H, Chomienne C, Lanotte M, Degos L, Dejean A. The t(15;17) translocation of acute promyelocytic leukaemia fuses the retinoic acid receptor alpha gene to a novel transcribed.Abstract.

In this chapter, our goal is to review and summarize current knowledge of the molecular biology of acute promyelocytic leukemia (APL). The cure of up to 75% of patients with APL [1, 2] represents a remarkable and fascinating success story in medicine, and the treatment of APL with retinoic acid serves as a paradigm for the use of differentiation therapy in other types of human cancers.