CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons
Calreticulin ( CALR ) mutations were recently described in JAK2 and MPL unmutated primary myelofibrosis (PMF) and essential thrombocythemia. In the current study, we compared the clinical, cytogenetic and molecular features of patients with PMF with or without CALR , JAK2 or MPL mutations. Among 254...
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| Veröffentlicht in: | Leukemia 2014-07, Vol.28 (7), p.1472-1477 |
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| creator | Tefferi, A Lasho, T L Finke, C M Knudson, R A Ketterling, R Hanson, C H Maffioli, M Caramazza, D Passamonti, F Pardanani, A |
| description | Calreticulin (
CALR
) mutations were recently described in
JAK2
and
MPL
unmutated primary myelofibrosis (PMF) and essential thrombocythemia. In the current study, we compared the clinical, cytogenetic and molecular features of patients with PMF with or without
CALR
,
JAK2
or
MPL
mutations. Among 254 study patients, 147 (58%) harbored
JAK2
, 63 (25%)
CALR
and 21 (8.3%)
MPL
mutations; 22 (8.7%) patients were negative for all three mutations, whereas one patient expressed both
JAK2
and
CALR
mutations. Study patients were also screened for
ASXL1
(31%),
EZH2
(6%),
IDH
(4%),
SRSF2
(12%),
SF3B1
(7%) and
U2AF1
(16%) mutations. In univariate analysis,
CALR
mutations were associated with younger age (
P |
| doi_str_mv | 10.1038/leu.2014.3 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1554952510</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A377776865</galeid><sourcerecordid>A377776865</sourcerecordid><originalsourceid>FETCH-LOGICAL-c646t-2d76377bc88751577e6557274611f21b03da42bf784626a251844ba2b87ec7ce3</originalsourceid><addsrcrecordid>eNqNkl1rFDEUhgdR7LZ64w-QgCCizppk8rXeLaV-riii1yGTObNNyUzWJFPYf2-GrdqqiOQikPOcN-dN3qp6QPCS4Ea98DAtKSZs2dyqFoRJUXPOye1qgZWStVhRdlQdp3SB8VwUd6sjyhimRNBFNZyuN5_RZULv1u_pvH_4tKmHKZsMHQoR5eh2HuoRtia7S0DDHnzoXRtDcuklst6Nzhr_HNl9DlsYITuLzNihIXiwkzcR2TDsTHQpjOledac3PsH9q_2k-vrq7Mvpm3rz8fXbMkltBRO5pp0UjZStLfNzwqUEwbmkkglCekpa3HSG0baXigkqDOVEMdYa2ioJVlpoTqonB91dDN8mSFkPLlnw3owQpqQJ52zFSx_-D5SxhtKVkgV99Bt6EaY4FiOaCsYlk0XyX1TRaiRVjaK_qK3xoN3YhxyNna_W62JdSqHErLX8C1VWB4OzYYTelfMbDY-vNZyD8fk8BT9lV17_Jvj0ANrykylCr3fRDSbuNcF6TpUuqdJzqnRT4IdXlqZ2gO4n-iNGBXh2AFIpjVuI1zz_KfcdE4nQ1g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1543728382</pqid></control><display><type>article</type><title>CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons</title><source>MEDLINE</source><source>Springer Journals</source><source>Springer Nature - Connect here FIRST to enable access</source><source>EZB Electronic Journals Library</source><creator>Tefferi, A ; Lasho, T L ; Finke, C M ; Knudson, R A ; Ketterling, R ; Hanson, C H ; Maffioli, M ; Caramazza, D ; Passamonti, F ; Pardanani, A</creator><creatorcontrib>Tefferi, A ; Lasho, T L ; Finke, C M ; Knudson, R A ; Ketterling, R ; Hanson, C H ; Maffioli, M ; Caramazza, D ; Passamonti, F ; Pardanani, A</creatorcontrib><description>Calreticulin (
CALR
) mutations were recently described in
JAK2
and
MPL
unmutated primary myelofibrosis (PMF) and essential thrombocythemia. In the current study, we compared the clinical, cytogenetic and molecular features of patients with PMF with or without
CALR
,
JAK2
or
MPL
mutations. Among 254 study patients, 147 (58%) harbored
JAK2
, 63 (25%)
CALR
and 21 (8.3%)
MPL
mutations; 22 (8.7%) patients were negative for all three mutations, whereas one patient expressed both
JAK2
and
CALR
mutations. Study patients were also screened for
ASXL1
(31%),
EZH2
(6%),
IDH
(4%),
SRSF2
(12%),
SF3B1
(7%) and
U2AF1
(16%) mutations. In univariate analysis,
CALR
mutations were associated with younger age (
P
<0.0001), higher platelet count (
P
<0.0001) and lower DIPSS-plus score (
P
=0.02).
CALR
-mutated patients were also less likely to be anemic, require transfusions or display leukocytosis. Spliceosome mutations were infrequent (
P
=0.0001) in
CALR
-mutated patients, but no other molecular or cytogenetic associations were evident. In multivariable analysis,
CALR
mutations had a favorable impact on survival that was independent of both DIPSS-plus risk and
ASXL1
mutation status (
P
=0.001; HR 3.4 for triple-negative and 2.2 for
JAK2
-mutated). Triple-negative patients also displayed inferior LFS (
P
=0.003). The current study identifies ‘CALR
–
ASXL1
+
’ and ‘triple-negative’ as high-risk molecular signatures in PMF.</description><identifier>ISSN: 0887-6924</identifier><identifier>EISSN: 1476-5551</identifier><identifier>DOI: 10.1038/leu.2014.3</identifier><identifier>PMID: 24402162</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/208/2489/144 ; 631/208/737 ; 692/699/67/1990/2331 ; 692/700/1750 ; Aged ; Aged, 80 and over ; Calreticulin ; Calreticulin - genetics ; Cancer ; Cancer Research ; Chromosome Aberrations ; Critical Care Medicine ; Cytogenetics ; DNA Mutational Analysis ; Female ; Gene Expression ; Gene mutations ; Genetic aspects ; Genetic research ; Hematology ; Hemoglobin ; Humans ; Identification and classification ; Intensive ; Internal Medicine ; Janus kinase 2 ; Janus Kinase 2 - genetics ; Leukemia ; Leukocytes ; Leukocytosis ; Male ; Medical prognosis ; Medicine ; Medicine & Public Health ; Middle Aged ; Mutation ; Myelofibrosis ; Oncology ; Oncology, Experimental ; original-article ; Patients ; Primary Myelofibrosis - diagnosis ; Primary Myelofibrosis - genetics ; Primary Myelofibrosis - mortality ; Prognosis ; Proteins ; Receptors, Thrombopoietin - genetics</subject><ispartof>Leukemia, 2014-07, Vol.28 (7), p.1472-1477</ispartof><rights>Macmillan Publishers Limited 2014</rights><rights>COPYRIGHT 2014 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jul 2014</rights><rights>Macmillan Publishers Limited 2014.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c646t-2d76377bc88751577e6557274611f21b03da42bf784626a251844ba2b87ec7ce3</citedby><cites>FETCH-LOGICAL-c646t-2d76377bc88751577e6557274611f21b03da42bf784626a251844ba2b87ec7ce3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/leu.2014.3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/leu.2014.3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24402162$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tefferi, A</creatorcontrib><creatorcontrib>Lasho, T L</creatorcontrib><creatorcontrib>Finke, C M</creatorcontrib><creatorcontrib>Knudson, R A</creatorcontrib><creatorcontrib>Ketterling, R</creatorcontrib><creatorcontrib>Hanson, C H</creatorcontrib><creatorcontrib>Maffioli, M</creatorcontrib><creatorcontrib>Caramazza, D</creatorcontrib><creatorcontrib>Passamonti, F</creatorcontrib><creatorcontrib>Pardanani, A</creatorcontrib><title>CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons</title><title>Leukemia</title><addtitle>Leukemia</addtitle><addtitle>Leukemia</addtitle><description>Calreticulin (
CALR
) mutations were recently described in
JAK2
and
MPL
unmutated primary myelofibrosis (PMF) and essential thrombocythemia. In the current study, we compared the clinical, cytogenetic and molecular features of patients with PMF with or without
CALR
,
JAK2
or
MPL
mutations. Among 254 study patients, 147 (58%) harbored
JAK2
, 63 (25%)
CALR
and 21 (8.3%)
MPL
mutations; 22 (8.7%) patients were negative for all three mutations, whereas one patient expressed both
JAK2
and
CALR
mutations. Study patients were also screened for
ASXL1
(31%),
EZH2
(6%),
IDH
(4%),
SRSF2
(12%),
SF3B1
(7%) and
U2AF1
(16%) mutations. In univariate analysis,
CALR
mutations were associated with younger age (
P
<0.0001), higher platelet count (
P
<0.0001) and lower DIPSS-plus score (
P
=0.02).
CALR
-mutated patients were also less likely to be anemic, require transfusions or display leukocytosis. Spliceosome mutations were infrequent (
P
=0.0001) in
CALR
-mutated patients, but no other molecular or cytogenetic associations were evident. In multivariable analysis,
CALR
mutations had a favorable impact on survival that was independent of both DIPSS-plus risk and
ASXL1
mutation status (
P
=0.001; HR 3.4 for triple-negative and 2.2 for
JAK2
-mutated). Triple-negative patients also displayed inferior LFS (
P
=0.003). The current study identifies ‘CALR
–
ASXL1
+
’ and ‘triple-negative’ as high-risk molecular signatures in PMF.</description><subject>631/208/2489/144</subject><subject>631/208/737</subject><subject>692/699/67/1990/2331</subject><subject>692/700/1750</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Calreticulin</subject><subject>Calreticulin - genetics</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Chromosome Aberrations</subject><subject>Critical Care Medicine</subject><subject>Cytogenetics</subject><subject>DNA Mutational Analysis</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene mutations</subject><subject>Genetic aspects</subject><subject>Genetic research</subject><subject>Hematology</subject><subject>Hemoglobin</subject><subject>Humans</subject><subject>Identification and classification</subject><subject>Intensive</subject><subject>Internal Medicine</subject><subject>Janus kinase 2</subject><subject>Janus Kinase 2 - genetics</subject><subject>Leukemia</subject><subject>Leukocytes</subject><subject>Leukocytosis</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Myelofibrosis</subject><subject>Oncology</subject><subject>Oncology, Experimental</subject><subject>original-article</subject><subject>Patients</subject><subject>Primary Myelofibrosis - diagnosis</subject><subject>Primary Myelofibrosis - genetics</subject><subject>Primary Myelofibrosis - mortality</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Receptors, Thrombopoietin - genetics</subject><issn>0887-6924</issn><issn>1476-5551</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkl1rFDEUhgdR7LZ64w-QgCCizppk8rXeLaV-riii1yGTObNNyUzWJFPYf2-GrdqqiOQikPOcN-dN3qp6QPCS4Ea98DAtKSZs2dyqFoRJUXPOye1qgZWStVhRdlQdp3SB8VwUd6sjyhimRNBFNZyuN5_RZULv1u_pvH_4tKmHKZsMHQoR5eh2HuoRtia7S0DDHnzoXRtDcuklst6Nzhr_HNl9DlsYITuLzNihIXiwkzcR2TDsTHQpjOledac3PsH9q_2k-vrq7Mvpm3rz8fXbMkltBRO5pp0UjZStLfNzwqUEwbmkkglCekpa3HSG0baXigkqDOVEMdYa2ioJVlpoTqonB91dDN8mSFkPLlnw3owQpqQJ52zFSx_-D5SxhtKVkgV99Bt6EaY4FiOaCsYlk0XyX1TRaiRVjaK_qK3xoN3YhxyNna_W62JdSqHErLX8C1VWB4OzYYTelfMbDY-vNZyD8fk8BT9lV17_Jvj0ANrykylCr3fRDSbuNcF6TpUuqdJzqnRT4IdXlqZ2gO4n-iNGBXh2AFIpjVuI1zz_KfcdE4nQ1g</recordid><startdate>20140701</startdate><enddate>20140701</enddate><creator>Tefferi, A</creator><creator>Lasho, T L</creator><creator>Finke, C M</creator><creator>Knudson, R A</creator><creator>Ketterling, R</creator><creator>Hanson, C H</creator><creator>Maffioli, M</creator><creator>Caramazza, D</creator><creator>Passamonti, F</creator><creator>Pardanani, A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7RV</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20140701</creationdate><title>CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons</title><author>Tefferi, A ; Lasho, T L ; Finke, C M ; Knudson, R A ; Ketterling, R ; Hanson, C H ; Maffioli, M ; Caramazza, D ; Passamonti, F ; Pardanani, A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c646t-2d76377bc88751577e6557274611f21b03da42bf784626a251844ba2b87ec7ce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>631/208/2489/144</topic><topic>631/208/737</topic><topic>692/699/67/1990/2331</topic><topic>692/700/1750</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Calreticulin</topic><topic>Calreticulin - genetics</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Chromosome Aberrations</topic><topic>Critical Care Medicine</topic><topic>Cytogenetics</topic><topic>DNA Mutational Analysis</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene mutations</topic><topic>Genetic aspects</topic><topic>Genetic research</topic><topic>Hematology</topic><topic>Hemoglobin</topic><topic>Humans</topic><topic>Identification and classification</topic><topic>Intensive</topic><topic>Internal Medicine</topic><topic>Janus kinase 2</topic><topic>Janus Kinase 2 - genetics</topic><topic>Leukemia</topic><topic>Leukocytes</topic><topic>Leukocytosis</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Myelofibrosis</topic><topic>Oncology</topic><topic>Oncology, Experimental</topic><topic>original-article</topic><topic>Patients</topic><topic>Primary Myelofibrosis - diagnosis</topic><topic>Primary Myelofibrosis - genetics</topic><topic>Primary Myelofibrosis - mortality</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Receptors, Thrombopoietin - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tefferi, A</creatorcontrib><creatorcontrib>Lasho, T L</creatorcontrib><creatorcontrib>Finke, C M</creatorcontrib><creatorcontrib>Knudson, R A</creatorcontrib><creatorcontrib>Ketterling, R</creatorcontrib><creatorcontrib>Hanson, C H</creatorcontrib><creatorcontrib>Maffioli, M</creatorcontrib><creatorcontrib>Caramazza, D</creatorcontrib><creatorcontrib>Passamonti, F</creatorcontrib><creatorcontrib>Pardanani, A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Leukemia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tefferi, A</au><au>Lasho, T L</au><au>Finke, C M</au><au>Knudson, R A</au><au>Ketterling, R</au><au>Hanson, C H</au><au>Maffioli, M</au><au>Caramazza, D</au><au>Passamonti, F</au><au>Pardanani, A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons</atitle><jtitle>Leukemia</jtitle><stitle>Leukemia</stitle><addtitle>Leukemia</addtitle><date>2014-07-01</date><risdate>2014</risdate><volume>28</volume><issue>7</issue><spage>1472</spage><epage>1477</epage><pages>1472-1477</pages><issn>0887-6924</issn><eissn>1476-5551</eissn><abstract>Calreticulin (
CALR
) mutations were recently described in
JAK2
and
MPL
unmutated primary myelofibrosis (PMF) and essential thrombocythemia. In the current study, we compared the clinical, cytogenetic and molecular features of patients with PMF with or without
CALR
,
JAK2
or
MPL
mutations. Among 254 study patients, 147 (58%) harbored
JAK2
, 63 (25%)
CALR
and 21 (8.3%)
MPL
mutations; 22 (8.7%) patients were negative for all three mutations, whereas one patient expressed both
JAK2
and
CALR
mutations. Study patients were also screened for
ASXL1
(31%),
EZH2
(6%),
IDH
(4%),
SRSF2
(12%),
SF3B1
(7%) and
U2AF1
(16%) mutations. In univariate analysis,
CALR
mutations were associated with younger age (
P
<0.0001), higher platelet count (
P
<0.0001) and lower DIPSS-plus score (
P
=0.02).
CALR
-mutated patients were also less likely to be anemic, require transfusions or display leukocytosis. Spliceosome mutations were infrequent (
P
=0.0001) in
CALR
-mutated patients, but no other molecular or cytogenetic associations were evident. In multivariable analysis,
CALR
mutations had a favorable impact on survival that was independent of both DIPSS-plus risk and
ASXL1
mutation status (
P
=0.001; HR 3.4 for triple-negative and 2.2 for
JAK2
-mutated). Triple-negative patients also displayed inferior LFS (
P
=0.003). The current study identifies ‘CALR
–
ASXL1
+
’ and ‘triple-negative’ as high-risk molecular signatures in PMF.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24402162</pmid><doi>10.1038/leu.2014.3</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0887-6924 |
| ispartof | Leukemia, 2014-07, Vol.28 (7), p.1472-1477 |
| issn | 0887-6924 1476-5551 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1554952510 |
| source | MEDLINE; Springer Journals; Springer Nature - Connect here FIRST to enable access; EZB Electronic Journals Library |
| subjects | 631/208/2489/144 631/208/737 692/699/67/1990/2331 692/700/1750 Aged Aged, 80 and over Calreticulin Calreticulin - genetics Cancer Cancer Research Chromosome Aberrations Critical Care Medicine Cytogenetics DNA Mutational Analysis Female Gene Expression Gene mutations Genetic aspects Genetic research Hematology Hemoglobin Humans Identification and classification Intensive Internal Medicine Janus kinase 2 Janus Kinase 2 - genetics Leukemia Leukocytes Leukocytosis Male Medical prognosis Medicine Medicine & Public Health Middle Aged Mutation Myelofibrosis Oncology Oncology, Experimental original-article Patients Primary Myelofibrosis - diagnosis Primary Myelofibrosis - genetics Primary Myelofibrosis - mortality Prognosis Proteins Receptors, Thrombopoietin - genetics |
| title | CALR vs JAK2 vs MPL-mutated or triple-negative myelofibrosis: clinical, cytogenetic and molecular comparisons |
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