PMID- 22583069
OWN - NLM
STAT- MEDLINE
DCOM- 20121031
LR  - 20211021
IS  - 1398-9995 (Electronic)
IS  - 0105-4538 (Print)
IS  - 0105-4538 (Linking)
VI  - 67
IP  - 7
DP  - 2012 Jul
TI  - NI-1: a novel canine mastocytoma model for studying drug resistance and 
      IgER-dependent mast cell activation.
PG  - 858-68
LID - 10.1111/j.1398-9995.2012.02833.x [doi]
AB  - BACKGROUND: Advanced mast cell (MC) disorders are characterized by uncontrolled 
      growth of neoplastic MC in various organs, mediator-related symptoms, and a poor 
      prognosis. Kit mutations supposedly contribute to abnormal growth and drug 
      resistance in these patients. METHODS: We established a novel canine mastocytoma 
      cell line, NI-1, from a patient suffering from MC leukemia. RESULTS: NI-1 cells 
      were found to form mastocytoma lesions in NOD/SCID IL-2Rgamma(null) mice and to 
      harbor several homozygous Kit mutations, including missense mutations at 
      nucleotides 107(C-->T) and 1187(A-->G), a 12-bp duplication (nucleotide 1263), and a 
      12-bp deletion (nucleotide 1550). NI-1 cells expressed several MC differentiation 
      antigens, including tryptase, Kit, and a functional IgE receptor. Compared to the 
      C2 mastocytoma cell line harboring a Kit exon 11 mutation, NI-1 cells were found 
      to be less responsive against the Kit tyrosine kinase inhibitors (TKI) masitinib 
      and imatinib, but were even more sensitive against proliferation-inhibitory 
      effects of the mammalian target of rapamycin (mTOR) blocker RAD001 and 
      PI3-kinase/mTOR blocker NVP-BEZ235. The Kit-targeting multikinase inhibitors 
      PKC412 and dasatinib were also found to override TKI resistance in NI-1 cells, 
      and produced growth inhibition with reasonable IC(50) values (<0.1 muM). 
      CONCLUSION: NI-1 may serve as a useful tool to investigate IgE-dependent 
      reactions and mechanisms of abnormal growth and drug resistance in neoplastic MC 
      in advanced mastocytosis.
CI  - (c) 2012 John Wiley & Sons A/S.
FAU - Hadzijusufovic, E
AU  - Hadzijusufovic E
AD  - Department for Companion Animals and Horses, Clinic for Internal Medicine and 
      Infectious Diseases, University of Veterinary Medicine Vienna, Vienna, Austria.
FAU - Peter, B
AU  - Peter B
FAU - Herrmann, H
AU  - Herrmann H
FAU - Rulicke, T
AU  - Rulicke T
FAU - Cerny-Reiterer, S
AU  - Cerny-Reiterer S
FAU - Schuch, K
AU  - Schuch K
FAU - Kenner, L
AU  - Kenner L
FAU - Thaiwong, T
AU  - Thaiwong T
FAU - Yuzbasiyan-Gurkan, V
AU  - Yuzbasiyan-Gurkan V
FAU - Pickl, W F
AU  - Pickl WF
FAU - Willmann, M
AU  - Willmann M
FAU - Valent, P
AU  - Valent P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120515
PL  - Denmark
TA  - Allergy
JT  - Allergy
JID - 7804028
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Receptors, IgE)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
EIN - Allergy. 2018 Nov;73(11):2264. PMID: 30450571
MH  - Animals
MH  - Antineoplastic Agents/pharmacology
MH  - Apoptosis/drug effects
MH  - Caspase 3/metabolism
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Dogs
MH  - *Drug Resistance, Neoplasm
MH  - Enzyme Activation/drug effects
MH  - Histamine Release
MH  - Immunophenotyping
MH  - Male
MH  - Mast Cells/drug effects/metabolism/*pathology
MH  - Mastocytoma/genetics/*immunology/*metabolism
MH  - Mice
MH  - Mice, Inbred NOD
MH  - Mice, SCID
MH  - Mutation
MH  - Phenotype
MH  - Proto-Oncogene Proteins c-kit/genetics
MH  - Receptors, IgE/immunology/*metabolism
PMC - PMC3401908
EDAT- 2012/05/16 06:00
MHDA- 2012/11/01 06:00
CRDT- 2012/05/16 06:00
PHST- 2012/03/27 00:00 [accepted]
PHST- 2012/05/16 06:00 [entrez]
PHST- 2012/05/16 06:00 [pubmed]
PHST- 2012/11/01 06:00 [medline]
AID - 10.1111/j.1398-9995.2012.02833.x [doi]
PST - ppublish
SO  - Allergy. 2012 Jul;67(7):858-68. doi: 10.1111/j.1398-9995.2012.02833.x. Epub 2012 
      May 15.