The calreticulin (CALR) exon 9 mutations are promising targets for cancer immune therapy

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Standard

The calreticulin (CALR) exon 9 mutations are promising targets for cancer immune therapy. / Holmstrom, M. O.; Martinenaite, E.; Ahmad, S. M.; Met, O.; Friese, C.; Kjaer, L.; Riley, C. H.; Straten, P. thor; Svane, I. M.; Hasselbalch, H. C.; Andersen, M. H.

I: Leukemia, Bind 32, Nr. 2, 01.02.2018, s. 429-437.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Holmstrom, MO, Martinenaite, E, Ahmad, SM, Met, O, Friese, C, Kjaer, L, Riley, CH, Straten, PT, Svane, IM, Hasselbalch, HC & Andersen, MH 2018, 'The calreticulin (CALR) exon 9 mutations are promising targets for cancer immune therapy', Leukemia, bind 32, nr. 2, s. 429-437. https://doi.org/10.1038/leu.2017.214

APA

Holmstrom, M. O., Martinenaite, E., Ahmad, S. M., Met, O., Friese, C., Kjaer, L., Riley, C. H., Straten, P. T., Svane, I. M., Hasselbalch, H. C., & Andersen, M. H. (2018). The calreticulin (CALR) exon 9 mutations are promising targets for cancer immune therapy. Leukemia, 32(2), 429-437. https://doi.org/10.1038/leu.2017.214

Vancouver

Holmstrom MO, Martinenaite E, Ahmad SM, Met O, Friese C, Kjaer L o.a. The calreticulin (CALR) exon 9 mutations are promising targets for cancer immune therapy. Leukemia. 2018 feb. 1;32(2):429-437. https://doi.org/10.1038/leu.2017.214

Author

Holmstrom, M. O. ; Martinenaite, E. ; Ahmad, S. M. ; Met, O. ; Friese, C. ; Kjaer, L. ; Riley, C. H. ; Straten, P. thor ; Svane, I. M. ; Hasselbalch, H. C. ; Andersen, M. H. / The calreticulin (CALR) exon 9 mutations are promising targets for cancer immune therapy. I: Leukemia. 2018 ; Bind 32, Nr. 2. s. 429-437.

Bibtex

@article{abde5b9cfb3f48df947df206d0514772,
title = "The calreticulin (CALR) exon 9 mutations are promising targets for cancer immune therapy",
abstract = "The calreticulin (CALR) exon 9 mutations are found in ∼30% of patients with essential thrombocythemia and primary myelofibrosis. Recently, we reported spontaneous immune responses against the CALR mutations. Here, we describe that CALR-mutant (CALRmut)-specific T cells are able to specifically recognize CALRmut cells. First, we established a T-cell culture specific for a CALRmut epitope. These specific T cells were able to recognize several epitopes in the CALRmut C terminus. Next, we established a CALRmut-specific CD4+ T-cell clone by limiting dilution. These CD4+ T cells recognized autologous CALRmut monocytes and hematopoietic stem cells, and T-cell recognition of target cells was dependent on the presence of CALR. Furthermore, we showed that the CALRmut response was human leukocyte antigen (HLA)-DR restricted. Finally, we demonstrated that the CALRmut-specific CD4+ T cells, despite their phenotype, were cytotoxic to autologous CALRmut cells, and that the cytotoxicity was mediated by degranulation of the T cells. In conclusion, the CALR exon 9 mutations are targets for specific T cells and thus are promising targets for cancer immune therapy such as peptide vaccination in patients harboring CALR exon 9 mutations.",
author = "Holmstrom, {M. O.} and E. Martinenaite and Ahmad, {S. M.} and O. Met and C. Friese and L. Kjaer and Riley, {C. H.} and Straten, {P. thor} and Svane, {I. M.} and Hasselbalch, {H. C.} and Andersen, {M. H.}",
year = "2018",
month = feb,
day = "1",
doi = "10.1038/leu.2017.214",
language = "English",
volume = "32",
pages = "429--437",
journal = "Leukemia",
issn = "0887-6924",
publisher = "nature publishing group",
number = "2",

}

RIS

TY - JOUR

T1 - The calreticulin (CALR) exon 9 mutations are promising targets for cancer immune therapy

AU - Holmstrom, M. O.

AU - Martinenaite, E.

AU - Ahmad, S. M.

AU - Met, O.

AU - Friese, C.

AU - Kjaer, L.

AU - Riley, C. H.

AU - Straten, P. thor

AU - Svane, I. M.

AU - Hasselbalch, H. C.

AU - Andersen, M. H.

PY - 2018/2/1

Y1 - 2018/2/1

N2 - The calreticulin (CALR) exon 9 mutations are found in ∼30% of patients with essential thrombocythemia and primary myelofibrosis. Recently, we reported spontaneous immune responses against the CALR mutations. Here, we describe that CALR-mutant (CALRmut)-specific T cells are able to specifically recognize CALRmut cells. First, we established a T-cell culture specific for a CALRmut epitope. These specific T cells were able to recognize several epitopes in the CALRmut C terminus. Next, we established a CALRmut-specific CD4+ T-cell clone by limiting dilution. These CD4+ T cells recognized autologous CALRmut monocytes and hematopoietic stem cells, and T-cell recognition of target cells was dependent on the presence of CALR. Furthermore, we showed that the CALRmut response was human leukocyte antigen (HLA)-DR restricted. Finally, we demonstrated that the CALRmut-specific CD4+ T cells, despite their phenotype, were cytotoxic to autologous CALRmut cells, and that the cytotoxicity was mediated by degranulation of the T cells. In conclusion, the CALR exon 9 mutations are targets for specific T cells and thus are promising targets for cancer immune therapy such as peptide vaccination in patients harboring CALR exon 9 mutations.

AB - The calreticulin (CALR) exon 9 mutations are found in ∼30% of patients with essential thrombocythemia and primary myelofibrosis. Recently, we reported spontaneous immune responses against the CALR mutations. Here, we describe that CALR-mutant (CALRmut)-specific T cells are able to specifically recognize CALRmut cells. First, we established a T-cell culture specific for a CALRmut epitope. These specific T cells were able to recognize several epitopes in the CALRmut C terminus. Next, we established a CALRmut-specific CD4+ T-cell clone by limiting dilution. These CD4+ T cells recognized autologous CALRmut monocytes and hematopoietic stem cells, and T-cell recognition of target cells was dependent on the presence of CALR. Furthermore, we showed that the CALRmut response was human leukocyte antigen (HLA)-DR restricted. Finally, we demonstrated that the CALRmut-specific CD4+ T cells, despite their phenotype, were cytotoxic to autologous CALRmut cells, and that the cytotoxicity was mediated by degranulation of the T cells. In conclusion, the CALR exon 9 mutations are targets for specific T cells and thus are promising targets for cancer immune therapy such as peptide vaccination in patients harboring CALR exon 9 mutations.

U2 - 10.1038/leu.2017.214

DO - 10.1038/leu.2017.214

M3 - Journal article

C2 - 28676668

VL - 32

SP - 429

EP - 437

JO - Leukemia

JF - Leukemia

SN - 0887-6924

IS - 2

ER -

ID: 190648096