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Tytuł pozycji:

ABCB1 SNP predicts outcome in patients with acute myeloid leukemia treated with Gemtuzumab ozogamicin: a report from Children's Oncology Group AAML0531 Trial.

Tytuł:
ABCB1 SNP predicts outcome in patients with acute myeloid leukemia treated with Gemtuzumab ozogamicin: a report from Children's Oncology Group AAML0531 Trial.
Autorzy:
Rafiee R; Department of Pharmacotherapy and Translational Research, Center for Pharmacogenomics, College of Pharmacy, University of Florida, Gainesville, FL, USA.
Chauhan L; Department of Pharmacotherapy and Translational Research, Center for Pharmacogenomics, College of Pharmacy, University of Florida, Gainesville, FL, USA.
Alonzo TA; Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Wang YC; Children's Oncology Group, Monrovia, CA, USA.
Elmasry A; Mansoura University, Mansoura, Egypt.
Loken MR; Hematologics Inc, Seattle, USA.
Pollard J; Dana-Farber/Boston Children's Cancer Center and Blood Disorders Center, Boston, MA, USA.; Harvard Medical School, Boston, MA, USA.
Aplenc R; Division of Oncology, Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Raimondi S; Department of Pathology, St. Jude Children's Hospital, Memphis, TN, USA.
Hirsch BA; Children's Hospitals and Clinic of Minnesota, University of Minnesota, Minneapolis, MN, USA.
Bernstein ID; Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
Gamis AS; Division of Hematology/Oncology/Bone Marrow Transplantation, Children's Mercy Hospitals and Clinics, Kansas City, MO, USA.
Meshinchi S; Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA, USA.
Lamba JK; Department of Pharmacotherapy and Translational Research, Center for Pharmacogenomics, College of Pharmacy, University of Florida, Gainesville, FL, USA. .
Źródło:
Blood cancer journal [Blood Cancer J] 2019 May 21; Vol. 9 (6), pp. 51. Date of Electronic Publication: 2019 May 21.
Typ publikacji:
Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: New York, NY : Nature Pub. Group
MeSH Terms:
Biomarkers, Tumor*
Polymorphism, Single Nucleotide*
Antineoplastic Agents, Immunological/*therapeutic use
Gemtuzumab/*therapeutic use
Leukemia, Myeloid, Acute/*drug therapy
Leukemia, Myeloid, Acute/*genetics
ATP Binding Cassette Transporter, Subfamily B/genetics ; Adolescent ; Adult ; Alleles ; Antineoplastic Agents, Immunological/administration & dosage ; Antineoplastic Agents, Immunological/adverse effects ; Child ; Child, Preschool ; Female ; Gemtuzumab/administration & dosage ; Gemtuzumab/adverse effects ; Genotype ; Humans ; Infant ; Infant, Newborn ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/mortality ; Male ; Prognosis ; Recurrence ; Treatment Outcome ; Young Adult
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Grant Information:
R01 CA132946 United States CA NCI NIH HHS; R01 CA133881 United States CA NCI NIH HHS; U10 CA098413 United States CA NCI NIH HHS; U10 CA098543 United States CA NCI NIH HHS; U10 CA180899 United States CA NCI NIH HHS; U10 CA180886 United States CA NCI NIH HHS; R21 CA155524 United States CA NCI NIH HHS
Substance Nomenclature:
0 (ABCB1 protein, human)
0 (ATP Binding Cassette Transporter, Subfamily B)
0 (Antineoplastic Agents, Immunological)
0 (Biomarkers, Tumor)
93NS566KF7 (Gemtuzumab)
Entry Date(s):
Date Created: 20190523 Date Completed: 20200219 Latest Revision: 20210109
Update Code:
20240104
PubMed Central ID:
PMC6529443
DOI:
10.1038/s41408-019-0211-y
PMID:
31113932
Czasopismo naukowe
Gemtuzumab-ozogamicin (GO), a humanized-anti-CD33 antibody linked with the toxin-calicheamicin-γ is a reemerging and promising drug for AML. Calicheamicin a key element of GO, induces DNA-damage and cell-death once the linked CD33-antibody facilitates its uptake. Calicheamicin efflux by the drug-transporter PgP-1 have been implicated in GO response thus in this study, we evaluated impact of ABCB1-SNPs on GO response. Genomic-DNA samples from 942 patients randomized to receive standard therapy with or without addition of GO (COG-AAML0531) were genotyped for ABCB1-SNPs. Our most interesting results show that for rs1045642, patients with minor-T-allele (CT/TT) had better outcome as compared to patients with CC genotype in GO-arm (Event-free survival-EFS: p = 0.022; and risk of relapse-RR, p = 0.007). In contrast, no difference between genotypes was observed for any of the clinical endpoints within No-GO arm (all p > 0.05). Consistent results were obtained when genotype groups were compared by GO and No-GO arms. The in vitro evaluation using HL60-cells further demonstrated consistent impact of rs1045642-T-allele on calicheamicin induced DNA-damage and cell-viability. Our results show the significance of ABCB1 SNPs on GO response in AML and warrants the need to investigate this in other cohorts. Once validated, ABCB1-SNPs in conjunction with CD33-SNPs can open up opportunities to personalize GO-therapy.

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