Impact of the Injection Site on Growth Characteristics, Phenotype and Sensitivity towards Cytarabine of Twenty Acute Leukaemia Patient-Derived Xenograft Models.
acute leukaemia
cytarabine
flow cytometry
patient-derived xenografts
tumour microenvironment
Journal
Cancers
ISSN: 2072-6694
Titre abrégé: Cancers (Basel)
Pays: Switzerland
ID NLM: 101526829
Informations de publication
Date de publication:
25 05 2020
25 05 2020
Historique:
received:
28
04
2020
revised:
22
05
2020
accepted:
23
05
2020
entrez:
30
5
2020
pubmed:
30
5
2020
medline:
30
5
2020
Statut:
epublish
Résumé
Rodent models have contributed significantly to the understanding of haematological malignancies. One important model system in this context are patient-derived xenografts (PDX). In the current study, we examined 20 acute leukaemia PDX models for growth behaviour, infiltration in haemopoietic organs and sensitivity towards cytarabine. PDX were injected intratibially (i.t.), intrasplenicaly (i.s.) or subcutaneously (s.c.) into immune compromised mice. For 18/20 models the engraftment capacity was independent of the implantation site. Two models could exclusively be propagated in one or two specific settings. The implantation site did influence tumour growth kinetics as median overall survival differed within one model depending on the injection route. The infiltration pattern was similar in i.t. and i.s. models. In contrast to the s.c. implantation, only one model displayed circulating leukaemic cells outside of the locally growing tumour mass. Cytarabine was active in all four tested models. Nevertheless, the degree of sensitivity was specific for an individual model and implantation site. In summary, all three application routes turned out to be feasible for the propagation of PDX. Nevertheless, the distinct differences between the settings highlight the need for well characterized platforms to ensure the meaningful interpretation of data generated using those powerful tools.
Identifiants
pubmed: 32466316
pii: cancers12051349
doi: 10.3390/cancers12051349
pmc: PMC7281503
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : Deutsche Forschungsgemeinschaft
ID : CRC 992 MEDEP C04, FOR 2674, LU 429/16-1), JCLS (R14/25)
Références
Cancer Biol Ther. 2012 Oct;13(12):1158-64
pubmed: 22892848
Haematologica. 2017 May;102(5):854-864
pubmed: 28183848
Blood. 2013 Mar 21;121(12):e90-7
pubmed: 23349390
Expert Opin Drug Discov. 2016 Nov;11(11):1081-1091
pubmed: 27562952
Blood. 2002 Nov 1;100(9):3175-82
pubmed: 12384415
Leukemia. 2003 Apr;17(4):760-3
pubmed: 12682634
Nucleic Acids Res. 2015 Jul 1;43(W1):W566-70
pubmed: 25969447
Int J Cancer. 2019 Apr 15;144(8):1941-1953
pubmed: 30350310
Cancer Res. 2011 Dec 1;71(23):7141-4
pubmed: 22088964
Leukemia. 2017 Jan;31(1):151-158
pubmed: 27363283
Nucleic Acids Res. 2019 Jan 8;47(D1):D1073-D1079
pubmed: 30535239
Blood. 2017 Feb 16;129(7):811-822
pubmed: 28064238
Int J Oncol. 2012 Dec;41(6):2047-56
pubmed: 23007607
J Vis Exp. 2016 Jul 29;(113):
pubmed: 27501218
Cancer Cell. 2016 Apr 11;29(4):574-586
pubmed: 27070704
J Cancer Res Clin Oncol. 2018 Jul;144(7):1239-1251
pubmed: 29721667
PLoS One. 2015 Mar 20;10(3):e0120925
pubmed: 25793878
J Immunol. 2005 May 15;174(10):6477-89
pubmed: 15879151
Blood. 2006 May 1;107(9):3481-5
pubmed: 16455952
Leukemia. 2000 May;14(5):889-97
pubmed: 10803522
PLoS One. 2013 Nov 06;8(11):e79939
pubmed: 24223204
J Bone Oncol. 2019 Aug 20;19:100257
pubmed: 31871882
Clin Cancer Res. 1997 Dec;3(12 Pt 2):2598-604
pubmed: 9815664
Ann Oncol. 1994 May;5(5):415-22
pubmed: 8075048
Leukemia. 2009 Nov;23(11):2109-17
pubmed: 19626050
Cancer. 2014 Dec 1;120 Suppl 23:3755-7
pubmed: 25412387
Cancer. 2006 Nov 1;107(9):2099-107
pubmed: 17019734
J Hematol Oncol. 2009 Dec 29;2:51
pubmed: 20040095
Sci Rep. 2015 Aug 17;5:13054
pubmed: 26278963
CA Cancer J Clin. 2018 Nov;68(6):394-424
pubmed: 30207593
Nature. 1968 Jan 27;217(5126):370-1
pubmed: 5639157