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Recurrent fusion of PCM1 to JAK2 in atypical chronic myeloid leukemia and acute leukemia associated with the t(8;9)(p21-22;p23-24)

Recurrent fusion of PCM1 to JAK2 in atypical chronic myeloid leukemia and acute leukemia associated with the t(8;9)(p21-22;p23-24)
Recurrent fusion of PCM1 to JAK2 in atypical chronic myeloid leukemia and acute leukemia associated with the t(8;9)(p21-22;p23-24)
We have identified a novel, recurrent t(8;9)(p21–22;p23–24) in six patients with diverse hematological malignancies: atypical CML (n=4), secondary AML following idiopathic myelofibrosis (n=1) and pre B-ALL (n=1). Because of the involvement of several different tyrosine kinases in atypical CML, we focused our analysis on this class of gene. Initial FISH studies of one patient indicated that the janus kinase 2 gene (JAK2), located at 9p24, was disrupted. RACE-PCR was then used to identify the 8p21 partner gene as PCM1, a large centrosomal protein that contains multiple coiled-coil domains. RT-PCR and FISH analysis confirmed the fusion in this case, and also identified PCM1-JAK2 in the five other t(8;9) patients (RT-PCR and FISH, n=4; RT-PCR only, n=1; FISH only, n=1). Four different types of in-frame mRNA junction were identified, but in all cases the chimeric mRNA is predicted to encode a protein that retains several of the predicted coiled-coil domains from PCM1 and the entire tyrosine kinase domain of JAK2. Reciprocal JAK2-PCM1 mRNA could not be amplified in any patient. Clinically, 4 patients displayed CML-like hyperplasia with variable degrees of myelofibrosis and eosinophilia. Similar to typical CML, the clinical course of these patients was variable: one is alive 11 months after allogeneic stem cell transplantation, one transformed to acute leukemia 5 years after diagnosis, one died 4 days after presentation and one achieved a major cytogenetic response with interferon but died due to neurodegenerative disease and pneumonia at 7.5 years. Of the two remaining patients, one presented with secondary AML following idiopathic myelofibrosis and remains in remission 15 years after diagnosis following intensive chemotherapy and maintenance with interferon. The final patient died shortly after induction therapy for pre B-ALL. In conclusion, PCM1-JAK2 is a novel recurrent fusion gene in hematological malignancies that is likely to deregulate hemopoiesis in a manner similar to BCR-ABL. Patients with PCM1-JAK2 disease are attractive targets for signal transduction therapy.
england, time, germany, leukemia, hematology, human
0006-4971
809A-810A
Reiter, Andreas
ffa23e84-4a13-4cb5-aaf0-3fafe25dbede
Walz, Christoph
b8d235ac-2a38-41e7-a22f-e0bb78719b19
Watmore, Ann
95ae2283-7a3c-43b1-a03c-c88acc182399
Schoch, Claudia
21cdc88a-2968-4cae-b0e9-0d7ad89b26f8
Blau, Ilona
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Telford, Nick
fd0a72a1-0d9d-4dda-a9bb-7e83a1001218
Aruliah, Shilani
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Yin, John
34754100-be8e-4386-b8f4-97a308c4d945
Vanstraelen, Danny
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Barker, Helen
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Taylor, Peter
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O'Driscoli, Aisling
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Schlegelberger, Brigitte
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Berger, Ute
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Hochhaus, Andreas
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Hehlmann, Rüdiger
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Chase, Andrew
a40a09c2-3073-4655-ba0b-a802e34914b5
Cross, Nicholas C.P.
f87650da-b908-4a34-b31b-d62c5f186fe4
Reiter, Andreas
ffa23e84-4a13-4cb5-aaf0-3fafe25dbede
Walz, Christoph
b8d235ac-2a38-41e7-a22f-e0bb78719b19
Watmore, Ann
95ae2283-7a3c-43b1-a03c-c88acc182399
Schoch, Claudia
21cdc88a-2968-4cae-b0e9-0d7ad89b26f8
Blau, Ilona
87dbae59-c1e4-467e-b461-662e05a6ef6f
Telford, Nick
fd0a72a1-0d9d-4dda-a9bb-7e83a1001218
Aruliah, Shilani
a618ce91-70c0-45b5-8976-9bf21765bf62
Yin, John
34754100-be8e-4386-b8f4-97a308c4d945
Vanstraelen, Danny
10c808e2-40ad-4b85-a4b5-a33262923abf
Barker, Helen
89c74c6b-0438-472e-b08e-9b81051bc110
Taylor, Peter
0ccfe683-1eeb-483b-82bb-27a9ad727e69
O'Driscoli, Aisling
d1e637fa-26ff-4e39-90e0-726683245dcf
Schlegelberger, Brigitte
5a42d72a-138f-454a-a865-4269f809b743
Berger, Ute
a343755b-a56e-413d-9f14-a0d70f9b4597
Hochhaus, Andreas
b37b9b7d-85ff-455e-994d-fcc2adf94088
Hehlmann, Rüdiger
790dac9f-3d0a-4388-b038-b5bbd07359c4
Chase, Andrew
a40a09c2-3073-4655-ba0b-a802e34914b5
Cross, Nicholas C.P.
f87650da-b908-4a34-b31b-d62c5f186fe4

Reiter, Andreas, Walz, Christoph, Watmore, Ann, Schoch, Claudia, Blau, Ilona, Telford, Nick, Aruliah, Shilani, Yin, John, Vanstraelen, Danny, Barker, Helen, Taylor, Peter, O'Driscoli, Aisling, Schlegelberger, Brigitte, Berger, Ute, Hochhaus, Andreas, Hehlmann, Rüdiger, Chase, Andrew and Cross, Nicholas C.P. (2004) Recurrent fusion of PCM1 to JAK2 in atypical chronic myeloid leukemia and acute leukemia associated with the t(8;9)(p21-22;p23-24). Blood, 104 (11), 809A-810A.

Record type: Article

Abstract

We have identified a novel, recurrent t(8;9)(p21–22;p23–24) in six patients with diverse hematological malignancies: atypical CML (n=4), secondary AML following idiopathic myelofibrosis (n=1) and pre B-ALL (n=1). Because of the involvement of several different tyrosine kinases in atypical CML, we focused our analysis on this class of gene. Initial FISH studies of one patient indicated that the janus kinase 2 gene (JAK2), located at 9p24, was disrupted. RACE-PCR was then used to identify the 8p21 partner gene as PCM1, a large centrosomal protein that contains multiple coiled-coil domains. RT-PCR and FISH analysis confirmed the fusion in this case, and also identified PCM1-JAK2 in the five other t(8;9) patients (RT-PCR and FISH, n=4; RT-PCR only, n=1; FISH only, n=1). Four different types of in-frame mRNA junction were identified, but in all cases the chimeric mRNA is predicted to encode a protein that retains several of the predicted coiled-coil domains from PCM1 and the entire tyrosine kinase domain of JAK2. Reciprocal JAK2-PCM1 mRNA could not be amplified in any patient. Clinically, 4 patients displayed CML-like hyperplasia with variable degrees of myelofibrosis and eosinophilia. Similar to typical CML, the clinical course of these patients was variable: one is alive 11 months after allogeneic stem cell transplantation, one transformed to acute leukemia 5 years after diagnosis, one died 4 days after presentation and one achieved a major cytogenetic response with interferon but died due to neurodegenerative disease and pneumonia at 7.5 years. Of the two remaining patients, one presented with secondary AML following idiopathic myelofibrosis and remains in remission 15 years after diagnosis following intensive chemotherapy and maintenance with interferon. The final patient died shortly after induction therapy for pre B-ALL. In conclusion, PCM1-JAK2 is a novel recurrent fusion gene in hematological malignancies that is likely to deregulate hemopoiesis in a manner similar to BCR-ABL. Patients with PCM1-JAK2 disease are attractive targets for signal transduction therapy.

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More information

Published date: November 2004
Keywords: england, time, germany, leukemia, hematology, human

Identifiers

Local EPrints ID: 60155
URI: http://eprints.soton.ac.uk/id/eprint/60155
ISSN: 0006-4971
PURE UUID: a9725c8e-f10c-415d-a117-7217a72f1b13
ORCID for Andrew Chase: ORCID iD orcid.org/0000-0001-6617-9953
ORCID for Nicholas C.P. Cross: ORCID iD orcid.org/0000-0001-5481-2555

Catalogue record

Date deposited: 05 Sep 2008
Last modified: 23 Jul 2022 01:49

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Contributors

Author: Andreas Reiter
Author: Christoph Walz
Author: Ann Watmore
Author: Claudia Schoch
Author: Ilona Blau
Author: Nick Telford
Author: Shilani Aruliah
Author: John Yin
Author: Danny Vanstraelen
Author: Helen Barker
Author: Peter Taylor
Author: Aisling O'Driscoli
Author: Brigitte Schlegelberger
Author: Ute Berger
Author: Andreas Hochhaus
Author: Rüdiger Hehlmann
Author: Andrew Chase ORCID iD

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