Asset Details
MbrlCatalogueTitleDetail
Do you wish to reserve the book?
Monosomal karyotype and chromosome 17p loss or TP53 mutations in decitabine-treated patients with acute myeloid leukemia
by
Germing Ulrich
, Kuendgen Andrea
, Ganser, Arnold
, Döhner Hartmut
, Hagemeijer, Anne
, Döhner Konstanze
, Wijermans, Pierre W
, Pantic Milena
, Hackanson Björn
, Pfeifer Dietmar
, Wehrle Julius
, Duyster Justus
, Lübbert, Michael
, Ihorst Gabriele
, Bullinger Lars
, Platzbecker Uwe
, Becker, Heiko
, Rüter, Björn H
in
Leukemia
/ Mutation
/ Patients
/ Response rates
2020
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
You are currently in the queue to collect this book. You will be notified once it is your turn to collect the book.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Monosomal karyotype and chromosome 17p loss or TP53 mutations in decitabine-treated patients with acute myeloid leukemia
by
Germing Ulrich
, Kuendgen Andrea
, Ganser, Arnold
, Döhner Hartmut
, Hagemeijer, Anne
, Döhner Konstanze
, Wijermans, Pierre W
, Pantic Milena
, Hackanson Björn
, Pfeifer Dietmar
, Wehrle Julius
, Duyster Justus
, Lübbert, Michael
, Ihorst Gabriele
, Bullinger Lars
, Platzbecker Uwe
, Becker, Heiko
, Rüter, Björn H
in
Leukemia
/ Mutation
/ Patients
/ Response rates
2020
Oops! Something went wrong.
While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Monosomal karyotype and chromosome 17p loss or TP53 mutations in decitabine-treated patients with acute myeloid leukemia
by
Germing Ulrich
, Kuendgen Andrea
, Ganser, Arnold
, Döhner Hartmut
, Hagemeijer, Anne
, Döhner Konstanze
, Wijermans, Pierre W
, Pantic Milena
, Hackanson Björn
, Pfeifer Dietmar
, Wehrle Julius
, Duyster Justus
, Lübbert, Michael
, Ihorst Gabriele
, Bullinger Lars
, Platzbecker Uwe
, Becker, Heiko
, Rüter, Björn H
in
Leukemia
/ Mutation
/ Patients
/ Response rates
2020
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Monosomal karyotype and chromosome 17p loss or TP53 mutations in decitabine-treated patients with acute myeloid leukemia
Journal Article
Monosomal karyotype and chromosome 17p loss or TP53 mutations in decitabine-treated patients with acute myeloid leukemia
2020
Request Book From Autostore
and Choose the Collection Method
Overview
TP53 aberrations reportedly predict favorable responses to decitabine (DAC) in acute myeloid leukemia (AML). We evaluated clinical features and outcomes associated with chromosome 17p loss or TP53 gene mutations in older, unfit DAC-treated AML patients in a phase II trial. Of 178 patients, 25 had loss of 17p in metaphase cytogenetics; 24 of these had a complex (CK+) and 21 a monosomal karyotype (MK+). In analyses in all patients and restricted to CK+ and MK+ patients, 17p loss tended to associate with higher rates of complete remission (CR), partial remission (PR), or antileukemic effect (ALE). Despite favorable response rates, there was no significant OS difference between patients with or without loss of 17p in the entire cohort or in the CK+ and MK+ cohort. TP53 mutations were identified in eight of 45 patients with material available. Five of the eight TP53-mutated patients had 17p loss. TP53-mutated patients had similar rates of CR/PR/ALE but shorter OS than those with TP53 wild type (P = 0.036). Moreover, patients with a subclone based on mutation data had shorter OS than those without (P = 0.05); only one patient with TP53-mutated AML had a subclone. In conclusion, 17p loss conferred a favorable impact on response rates, even among CK+ and MK+ patients that however could not be maintained. The effect of TP53 mutations appeared to be different; however, patient numbers were low. Future research needs to further dissect the impact of the various TP53 aberrations in HMA-based combination therapies. The limited duration of favorable responses to HMA treatment in adverse-risk genetics AML should prompt physicians to advance allografting for eligible patients in a timely fashion.
Publisher
Springer Nature B.V
Subject
This website uses cookies to ensure you get the best experience on our website.