HAEM5:Myeloid/lymphoid neoplasms with other tyrosine kinase fusion genes: Difference between revisions
| [pending revision] | [pending revision] |
| Line 68: | Line 68: | ||
!Clinical Relevance Details/Other Notes | !Clinical Relevance Details/Other Notes | ||
|- | |- | ||
|'' | |''FGFR2''||''ETV6::FGFR2'' <ref>{{Cite journal|last=Carll|first=Timothy|last2=Patel|first2=Anand|last3=Derman|first3=Benjamin|last4=Hyjek|first4=Elizabeth|last5=Lager|first5=Angela|last6=Wanjari|first6=Pankhuri|last7=Segal|first7=Jeremy|last8=Odenike|first8=Olatoyosi|last9=Fidai|first9=Shiraz|date=2020-10-13|title=Diagnosis and treatment of mixed phenotype (T-myeloid/lymphoid) acute leukemia with novel ETV6-FGFR2 rearrangement|url=https://pubmed.ncbi.nlm.nih.gov/33049052|journal=Blood Advances|volume=4|issue=19|pages=4924–4928|doi=10.1182/bloodadvances.2019001282|issn=2473-9537|pmc=7556145|pmid=33049052}}</ref>||Fusion between exon 4 of ''ETV6'' (upstream) and exon 5 of ''FGFR2'' (downstream).||Cryptic rearrangement detected by FISH involving chromosomes 10 and 12 | ||
|Rare < 5% | |Rare < 5% | ||
|D, P, T | |D, P, T | ||
| Line 74: | Line 74: | ||
|This fusion suggests abnormal FGFR2 expression. Aberrant The ''FGFR2'' activation resulting from ''ETV6::FGFR2'' may respond to ''FGFR1,2,3'' tyrosine kinase inhibitors (TKIs). <ref>{{Cite journal|last=Katoh|first=Masaru|date=2019-02|title=Fibroblast growth factor receptors as treatment targets in clinical oncology|url=https://pubmed.ncbi.nlm.nih.gov/30367139|journal=Nature Reviews. Clinical Oncology|volume=16|issue=2|pages=105–122|doi=10.1038/s41571-018-0115-y|issn=1759-4782|pmid=30367139}}</ref> This rearrangement exhibited aggressive clinical behavior, demonstrating resistance to both conventional and intensive chemotherapy, as well as allogeneic stem cell transplantation.<ref>{{Cite journal|last=Carll|first=Timothy|last2=Patel|first2=Anand|last3=Derman|first3=Benjamin|last4=Hyjek|first4=Elizabeth|last5=Lager|first5=Angela|last6=Wanjari|first6=Pankhuri|last7=Segal|first7=Jeremy|last8=Odenike|first8=Olatoyosi|last9=Fidai|first9=Shiraz|date=2020-10-13|title=Diagnosis and treatment of mixed phenotype (T-myeloid/lymphoid) acute leukemia with novel ETV6-FGFR2 rearrangement|url=https://pubmed.ncbi.nlm.nih.gov/33049052|journal=Blood Advances|volume=4|issue=19|pages=4924–4928|doi=10.1182/bloodadvances.2019001282|issn=2473-9537|pmc=7556145|pmid=33049052}}</ref> The prognosis remains unclear due to the limited number of cases. | |This fusion suggests abnormal FGFR2 expression. Aberrant The ''FGFR2'' activation resulting from ''ETV6::FGFR2'' may respond to ''FGFR1,2,3'' tyrosine kinase inhibitors (TKIs). <ref>{{Cite journal|last=Katoh|first=Masaru|date=2019-02|title=Fibroblast growth factor receptors as treatment targets in clinical oncology|url=https://pubmed.ncbi.nlm.nih.gov/30367139|journal=Nature Reviews. Clinical Oncology|volume=16|issue=2|pages=105–122|doi=10.1038/s41571-018-0115-y|issn=1759-4782|pmid=30367139}}</ref> This rearrangement exhibited aggressive clinical behavior, demonstrating resistance to both conventional and intensive chemotherapy, as well as allogeneic stem cell transplantation.<ref>{{Cite journal|last=Carll|first=Timothy|last2=Patel|first2=Anand|last3=Derman|first3=Benjamin|last4=Hyjek|first4=Elizabeth|last5=Lager|first5=Angela|last6=Wanjari|first6=Pankhuri|last7=Segal|first7=Jeremy|last8=Odenike|first8=Olatoyosi|last9=Fidai|first9=Shiraz|date=2020-10-13|title=Diagnosis and treatment of mixed phenotype (T-myeloid/lymphoid) acute leukemia with novel ETV6-FGFR2 rearrangement|url=https://pubmed.ncbi.nlm.nih.gov/33049052|journal=Blood Advances|volume=4|issue=19|pages=4924–4928|doi=10.1182/bloodadvances.2019001282|issn=2473-9537|pmc=7556145|pmid=33049052}}</ref> The prognosis remains unclear due to the limited number of cases. | ||
|- | |- | ||
|'' | |''LYN'' | ||
|''ETV6::LYN'' <ref>{{Cite journal|last=Telford|first=N.|last2=Alexander|first2=S.|last3=McGinn|first3=O. J.|last4=Williams|first4=M.|last5=Wood|first5=K. M.|last6=Bloor|first6=A.|last7=Saha|first7=V.|date=2016-04-08|title=Myeloproliferative neoplasm with eosinophilia and T-lymphoblastic lymphoma with ETV6-LYN gene fusion|url=https://pubmed.ncbi.nlm.nih.gov/27058227|journal=Blood Cancer Journal|volume=6|issue=4|pages=e412|doi=10.1038/bcj.2016.11|issn=2044-5385|pmc=4855251|pmid=27058227}}</ref><ref>{{Cite journal|last=Ma|first=Edmond S. K.|last2=Wan|first2=Thomas S. K.|last3=Au|first3=Chun Hang|last4=Ho|first4=Dona N.|last5=Ma|first5=Shing Yan|last6=Ng|first6=Margaret H. L.|last7=Chan|first7=Tsun Leung|date=2017-12|title=Next-generation sequencing and molecular cytogenetic characterization of ETV6-LYN fusion due to chromosomes 1, 8 and 12 rearrangement in acute myeloid leukemia|url=https://pubmed.ncbi.nlm.nih.gov/29153093|journal=Cancer Genetics|volume=218-219|pages=15–19|doi=10.1016/j.cancergen.2017.09.001|issn=2210-7762|pmid=29153093}}</ref><ref>{{Cite journal|last=Tanaka|first=H.|last2=Takeuchi|first2=M.|last3=Takeda|first3=Y.|last4=Sakai|first4=S.|last5=Abe|first5=D.|last6=Ohwada|first6=C.|last7=Sakaida|first7=E.|last8=Shimizu|first8=N.|last9=Saito|first9=Y.|date=2010-01|title=Identification of a novel TEL-Lyn fusion gene in primary myelofibrosis|url=https://pubmed.ncbi.nlm.nih.gov/19710703|journal=Leukemia|volume=24|issue=1|pages=197–200|doi=10.1038/leu.2009.167|issn=1476-5551|pmid=19710703}}</ref> | |''ETV6::LYN'' <ref>{{Cite journal|last=Telford|first=N.|last2=Alexander|first2=S.|last3=McGinn|first3=O. J.|last4=Williams|first4=M.|last5=Wood|first5=K. M.|last6=Bloor|first6=A.|last7=Saha|first7=V.|date=2016-04-08|title=Myeloproliferative neoplasm with eosinophilia and T-lymphoblastic lymphoma with ETV6-LYN gene fusion|url=https://pubmed.ncbi.nlm.nih.gov/27058227|journal=Blood Cancer Journal|volume=6|issue=4|pages=e412|doi=10.1038/bcj.2016.11|issn=2044-5385|pmc=4855251|pmid=27058227}}</ref><ref>{{Cite journal|last=Ma|first=Edmond S. K.|last2=Wan|first2=Thomas S. K.|last3=Au|first3=Chun Hang|last4=Ho|first4=Dona N.|last5=Ma|first5=Shing Yan|last6=Ng|first6=Margaret H. L.|last7=Chan|first7=Tsun Leung|date=2017-12|title=Next-generation sequencing and molecular cytogenetic characterization of ETV6-LYN fusion due to chromosomes 1, 8 and 12 rearrangement in acute myeloid leukemia|url=https://pubmed.ncbi.nlm.nih.gov/29153093|journal=Cancer Genetics|volume=218-219|pages=15–19|doi=10.1016/j.cancergen.2017.09.001|issn=2210-7762|pmid=29153093}}</ref><ref>{{Cite journal|last=Tanaka|first=H.|last2=Takeuchi|first2=M.|last3=Takeda|first3=Y.|last4=Sakai|first4=S.|last5=Abe|first5=D.|last6=Ohwada|first6=C.|last7=Sakaida|first7=E.|last8=Shimizu|first8=N.|last9=Saito|first9=Y.|date=2010-01|title=Identification of a novel TEL-Lyn fusion gene in primary myelofibrosis|url=https://pubmed.ncbi.nlm.nih.gov/19710703|journal=Leukemia|volume=24|issue=1|pages=197–200|doi=10.1038/leu.2009.167|issn=1476-5551|pmid=19710703}}</ref> | ||
|Fusion between exon 5 in ''ETV6'' to exon 8 in ''LYN'' (5′ to 3′ orientation to produce an in-frame chimeric fusion) | |Fusion between exon 5 in ''ETV6'' to exon 8 in ''LYN'' (5′ to 3′ orientation to produce an in-frame chimeric fusion) | ||
| Line 83: | Line 83: | ||
|Resistant to intensive chemotherapy or stem cell transplant, the disease progressed rapidly to terminal AML.<ref>{{Cite journal|last=Telford|first=N.|last2=Alexander|first2=S.|last3=McGinn|first3=O. J.|last4=Williams|first4=M.|last5=Wood|first5=K. M.|last6=Bloor|first6=A.|last7=Saha|first7=V.|date=2016-04-08|title=Myeloproliferative neoplasm with eosinophilia and T-lymphoblastic lymphoma with ETV6-LYN gene fusion|url=https://pubmed.ncbi.nlm.nih.gov/27058227|journal=Blood Cancer Journal|volume=6|issue=4|pages=e412|doi=10.1038/bcj.2016.11|issn=2044-5385|pmc=4855251|pmid=27058227}}</ref> Prognosis is not well defined due to the small number of cases. | |Resistant to intensive chemotherapy or stem cell transplant, the disease progressed rapidly to terminal AML.<ref>{{Cite journal|last=Telford|first=N.|last2=Alexander|first2=S.|last3=McGinn|first3=O. J.|last4=Williams|first4=M.|last5=Wood|first5=K. M.|last6=Bloor|first6=A.|last7=Saha|first7=V.|date=2016-04-08|title=Myeloproliferative neoplasm with eosinophilia and T-lymphoblastic lymphoma with ETV6-LYN gene fusion|url=https://pubmed.ncbi.nlm.nih.gov/27058227|journal=Blood Cancer Journal|volume=6|issue=4|pages=e412|doi=10.1038/bcj.2016.11|issn=2044-5385|pmc=4855251|pmid=27058227}}</ref> Prognosis is not well defined due to the small number of cases. | ||
|- | |- | ||
|'' | |''NTRK3'' | ||
|''ETV6::NTRK3''<ref>{{Cite journal|last=Reshmi|first=Shalini C.|last2=Harvey|first2=Richard C.|last3=Roberts|first3=Kathryn G.|last4=Stonerock|first4=Eileen|last5=Smith|first5=Amy|last6=Jenkins|first6=Heather|last7=Chen|first7=I.-Ming|last8=Valentine|first8=Marc|last9=Liu|first9=Yu|date=2017-06-22|title=Targetable kinase gene fusions in high-risk B-ALL: a study from the Children's Oncology Group|url=https://pubmed.ncbi.nlm.nih.gov/28408464|journal=Blood|volume=129|issue=25|pages=3352–3361|doi=10.1182/blood-2016-12-758979|issn=1528-0020|pmc=5482101|pmid=28408464}}</ref><ref>{{Cite journal|last=Roberts|first=Kathryn G.|last2=Li|first2=Yongjin|last3=Payne-Turner|first3=Debbie|last4=Harvey|first4=Richard C.|last5=Yang|first5=Yung-Li|last6=Pei|first6=Deqing|last7=McCastlain|first7=Kelly|last8=Ding|first8=Li|last9=Lu|first9=Charles|date=2014-09-11|title=Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/25207766|journal=The New England Journal of Medicine|volume=371|issue=11|pages=1005–1015|doi=10.1056/NEJMoa1403088|issn=1533-4406|pmc=4191900|pmid=25207766}}</ref> | |''ETV6::NTRK3''<ref>{{Cite journal|last=Reshmi|first=Shalini C.|last2=Harvey|first2=Richard C.|last3=Roberts|first3=Kathryn G.|last4=Stonerock|first4=Eileen|last5=Smith|first5=Amy|last6=Jenkins|first6=Heather|last7=Chen|first7=I.-Ming|last8=Valentine|first8=Marc|last9=Liu|first9=Yu|date=2017-06-22|title=Targetable kinase gene fusions in high-risk B-ALL: a study from the Children's Oncology Group|url=https://pubmed.ncbi.nlm.nih.gov/28408464|journal=Blood|volume=129|issue=25|pages=3352–3361|doi=10.1182/blood-2016-12-758979|issn=1528-0020|pmc=5482101|pmid=28408464}}</ref><ref>{{Cite journal|last=Roberts|first=Kathryn G.|last2=Li|first2=Yongjin|last3=Payne-Turner|first3=Debbie|last4=Harvey|first4=Richard C.|last5=Yang|first5=Yung-Li|last6=Pei|first6=Deqing|last7=McCastlain|first7=Kelly|last8=Ding|first8=Li|last9=Lu|first9=Charles|date=2014-09-11|title=Targetable kinase-activating lesions in Ph-like acute lymphoblastic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/25207766|journal=The New England Journal of Medicine|volume=371|issue=11|pages=1005–1015|doi=10.1056/NEJMoa1403088|issn=1533-4406|pmc=4191900|pmid=25207766}}</ref> | ||
|Fusion between ''ETV6'' and ''NTRK3'' (5′ to 3′ orientation) | |Fusion between ''ETV6'' and ''NTRK3'' (5′ to 3′ orientation) | ||
| Line 94: | Line 94: | ||
|ALK | |ALK | ||
|''RANBP2::ALK''<ref>{{Cite journal|last=Röttgers|first=S.|last2=Gombert|first2=M.|last3=Teigler-Schlegel|first3=A.|last4=Busch|first4=K.|last5=Gamerdinger|first5=U.|last6=Slany|first6=R.|last7=Harbott|first7=J.|last8=Borkhardt|first8=A.|date=2010-06|title=ALK fusion genes in children with atypical myeloproliferative leukemia|url=https://pubmed.ncbi.nlm.nih.gov/20428197|journal=Leukemia|volume=24|issue=6|pages=1197–1200|doi=10.1038/leu.2010.18|issn=1476-5551|pmid=20428197}}</ref><ref>{{Cite journal|last=Lim|first=Ji-Hun|last2=Jang|first2=Seongsoo|last3=Park|first3=Chan-Jeoung|last4=Cho|first4=Young-Uk|last5=Lee|first5=Je-Hwan|last6=Lee|first6=Kyoo-Hyung|last7=Lee|first7=Jin-Ok|last8=Shin|first8=Jong-Yeon|last9=Kim|first9=Jong-Il|date=2014|title=RANBP2-ALK fusion combined with monosomy 7 in acute myelomonocytic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/24613277|journal=Cancer Genetics|volume=207|issue=1-2|pages=40–45|doi=10.1016/j.cancergen.2013.12.003|issn=2210-7762|pmid=24613277}}</ref> | |''RANBP2::ALK''<ref>{{Cite journal|last=Röttgers|first=S.|last2=Gombert|first2=M.|last3=Teigler-Schlegel|first3=A.|last4=Busch|first4=K.|last5=Gamerdinger|first5=U.|last6=Slany|first6=R.|last7=Harbott|first7=J.|last8=Borkhardt|first8=A.|date=2010-06|title=ALK fusion genes in children with atypical myeloproliferative leukemia|url=https://pubmed.ncbi.nlm.nih.gov/20428197|journal=Leukemia|volume=24|issue=6|pages=1197–1200|doi=10.1038/leu.2010.18|issn=1476-5551|pmid=20428197}}</ref><ref>{{Cite journal|last=Lim|first=Ji-Hun|last2=Jang|first2=Seongsoo|last3=Park|first3=Chan-Jeoung|last4=Cho|first4=Young-Uk|last5=Lee|first5=Je-Hwan|last6=Lee|first6=Kyoo-Hyung|last7=Lee|first7=Jin-Ok|last8=Shin|first8=Jong-Yeon|last9=Kim|first9=Jong-Il|date=2014|title=RANBP2-ALK fusion combined with monosomy 7 in acute myelomonocytic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/24613277|journal=Cancer Genetics|volume=207|issue=1-2|pages=40–45|doi=10.1016/j.cancergen.2013.12.003|issn=2210-7762|pmid=24613277}}</ref> | ||
|exon 18 of ''RANBP2'' and exon 20 of ''ALK'' (5′ to 3′ orientation).<ref>{{Cite journal|last=Lim|first=Ji-Hun|last2=Jang|first2=Seongsoo|last3=Park|first3=Chan-Jeoung|last4=Cho|first4=Young-Uk|last5=Lee|first5=Je-Hwan|last6=Lee|first6=Kyoo-Hyung|last7=Lee|first7=Jin-Ok|last8=Shin|first8=Jong-Yeon|last9=Kim|first9=Jong-Il|date=2014|title=RANBP2-ALK fusion combined with monosomy 7 in acute myelomonocytic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/24613277|journal=Cancer Genetics|volume=207|issue=1-2|pages=40–45|doi=10.1016/j.cancergen.2013.12.003|issn=2210-7762|pmid=24613277}}</ref> Leads to constitutive autophosphorylation of ''ALK'' tyrosine kinase and activating downstream signaling.<ref>{{Cite journal|last=Maesako|first=Yoshitomo|last2=Izumi|first2=Kiyotaka|last3=Okamori|first3=Satoshi|last4=Takeoka|first4=Kayo|last5=Kishimori|first5=Chiyuki|last6=Okumura|first6=Atsuko|last7=Honjo|first7=Gen|last8=Akasaka|first8=Takashi|last9=Ohno|first9=Hitoshi|date=2014-02|title=inv(2)(p23q13)/RAN-binding protein 2 (RANBP2)-ALK fusion gene in myeloid leukemia that developed in an elderly woman|url=https://pubmed.ncbi.nlm.nih.gov/24307515|journal=International Journal of Hematology|volume=99|issue=2|pages=202–207|doi=10.1007/s12185-013-1482-x|issn=1865-3774|pmid=24307515}}</ref> | |exon 18 of ''RANBP2'' and exon 20 of ''ALK'' (5′ to 3′ orientation).<ref>{{Cite journal|last=Lim|first=Ji-Hun|last2=Jang|first2=Seongsoo|last3=Park|first3=Chan-Jeoung|last4=Cho|first4=Young-Uk|last5=Lee|first5=Je-Hwan|last6=Lee|first6=Kyoo-Hyung|last7=Lee|first7=Jin-Ok|last8=Shin|first8=Jong-Yeon|last9=Kim|first9=Jong-Il|date=2014|title=RANBP2-ALK fusion combined with monosomy 7 in acute myelomonocytic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/24613277|journal=Cancer Genetics|volume=207|issue=1-2|pages=40–45|doi=10.1016/j.cancergen.2013.12.003|issn=2210-7762|pmid=24613277}}</ref> Leads to constitutive autophosphorylation of ''ALK'' tyrosine kinase and activating downstream signaling.<ref>{{Cite journal|last=Maesako|first=Yoshitomo|last2=Izumi|first2=Kiyotaka|last3=Okamori|first3=Satoshi|last4=Takeoka|first4=Kayo|last5=Kishimori|first5=Chiyuki|last6=Okumura|first6=Atsuko|last7=Honjo|first7=Gen|last8=Akasaka|first8=Takashi|last9=Ohno|first9=Hitoshi|date=2014-02|title=inv(2)(p23q13)/RAN-binding protein 2 (RANBP2)-ALK fusion gene in myeloid leukemia that developed in an elderly woman|url=https://pubmed.ncbi.nlm.nih.gov/24307515|journal=International Journal of Hematology|volume=99|issue=2|pages=202–207|doi=10.1007/s12185-013-1482-x|issn=1865-3774|pmid=24307515}}</ref> | ||
|inv(2)(p23q13) / t(2;2)(p23;q13)<ref>{{Cite journal|last=Röttgers|first=S.|last2=Gombert|first2=M.|last3=Teigler-Schlegel|first3=A.|last4=Busch|first4=K.|last5=Gamerdinger|first5=U.|last6=Slany|first6=R.|last7=Harbott|first7=J.|last8=Borkhardt|first8=A.|date=2010-06|title=ALK fusion genes in children with atypical myeloproliferative leukemia|url=https://pubmed.ncbi.nlm.nih.gov/20428197|journal=Leukemia|volume=24|issue=6|pages=1197–1200|doi=10.1038/leu.2010.18|issn=1476-5551|pmid=20428197}}</ref> <ref>{{Cite journal|last=Lim|first=Ji-Hun|last2=Jang|first2=Seongsoo|last3=Park|first3=Chan-Jeoung|last4=Cho|first4=Young-Uk|last5=Lee|first5=Je-Hwan|last6=Lee|first6=Kyoo-Hyung|last7=Lee|first7=Jin-Ok|last8=Shin|first8=Jong-Yeon|last9=Kim|first9=Jong-Il|date=2014|title=RANBP2-ALK fusion combined with monosomy 7 in acute myelomonocytic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/24613277|journal=Cancer Genetics|volume=207|issue=1-2|pages=40–45|doi=10.1016/j.cancergen.2013.12.003|issn=2210-7762|pmid=24613277}}</ref> | |inv(2)(p23q13) / t(2;2)(p23;q13)<ref>{{Cite journal|last=Röttgers|first=S.|last2=Gombert|first2=M.|last3=Teigler-Schlegel|first3=A.|last4=Busch|first4=K.|last5=Gamerdinger|first5=U.|last6=Slany|first6=R.|last7=Harbott|first7=J.|last8=Borkhardt|first8=A.|date=2010-06|title=ALK fusion genes in children with atypical myeloproliferative leukemia|url=https://pubmed.ncbi.nlm.nih.gov/20428197|journal=Leukemia|volume=24|issue=6|pages=1197–1200|doi=10.1038/leu.2010.18|issn=1476-5551|pmid=20428197}}</ref> <ref>{{Cite journal|last=Lim|first=Ji-Hun|last2=Jang|first2=Seongsoo|last3=Park|first3=Chan-Jeoung|last4=Cho|first4=Young-Uk|last5=Lee|first5=Je-Hwan|last6=Lee|first6=Kyoo-Hyung|last7=Lee|first7=Jin-Ok|last8=Shin|first8=Jong-Yeon|last9=Kim|first9=Jong-Il|date=2014|title=RANBP2-ALK fusion combined with monosomy 7 in acute myelomonocytic leukemia|url=https://pubmed.ncbi.nlm.nih.gov/24613277|journal=Cancer Genetics|volume=207|issue=1-2|pages=40–45|doi=10.1016/j.cancergen.2013.12.003|issn=2210-7762|pmid=24613277}}</ref> | ||
|Rare < 5% | |Rare < 5% | ||
| Line 102: | Line 102: | ||
|- | |- | ||
| | | | ||
''RET'' | |||
|''BCR::RET''<ref>{{Cite journal|last=Ballerini|first=P.|last2=Struski|first2=S.|last3=Cresson|first3=C.|last4=Prade|first4=N.|last5=Toujani|first5=S.|last6=Deswarte|first6=C.|last7=Dobbelstein|first7=S.|last8=Petit|first8=A.|last9=Lapillonne|first9=H.|date=2012-11|title=RET fusion genes are associated with chronic myelomonocytic leukemia and enhance monocytic differentiation|url=https://pubmed.ncbi.nlm.nih.gov/22513837|journal=Leukemia|volume=26|issue=11|pages=2384–2389|doi=10.1038/leu.2012.109|issn=1476-5551|pmid=22513837}}</ref> | |||
| | | | ||
|t(10;22)(q11;q11)<ref>{{Cite journal|last=Ballerini|first=P.|last2=Struski|first2=S.|last3=Cresson|first3=C.|last4=Prade|first4=N.|last5=Toujani|first5=S.|last6=Deswarte|first6=C.|last7=Dobbelstein|first7=S.|last8=Petit|first8=A.|last9=Lapillonne|first9=H.|date=2012-11|title=RET fusion genes are associated with chronic myelomonocytic leukemia and enhance monocytic differentiation|url=https://pubmed.ncbi.nlm.nih.gov/22513837|journal=Leukemia|volume=26|issue=11|pages=2384–2389|doi=10.1038/leu.2012.109|issn=1476-5551|pmid=22513837}}</ref> | |||
| | | | ||
| | | | ||
| | |||
| | |||
Sensitive to Sorafenib, an inhibitor to tyrosine kinase activity. | |||
<br /> | |||
|- | |||
| | |||
''RET'' | |||
|''FGFR1OP::RET''<ref>{{Cite journal|last=Ballerini|first=P.|last2=Struski|first2=S.|last3=Cresson|first3=C.|last4=Prade|first4=N.|last5=Toujani|first5=S.|last6=Deswarte|first6=C.|last7=Dobbelstein|first7=S.|last8=Petit|first8=A.|last9=Lapillonne|first9=H.|date=2012-11|title=RET fusion genes are associated with chronic myelomonocytic leukemia and enhance monocytic differentiation|url=https://pubmed.ncbi.nlm.nih.gov/22513837|journal=Leukemia|volume=26|issue=11|pages=2384–2389|doi=10.1038/leu.2012.109|issn=1476-5551|pmid=22513837}}</ref> | |||
|Fusion between ''FGFR1OP'' exon 12 with ''RET'' exon 12.<ref>{{Cite journal|last=Ballerini|first=P.|last2=Struski|first2=S.|last3=Cresson|first3=C.|last4=Prade|first4=N.|last5=Toujani|first5=S.|last6=Deswarte|first6=C.|last7=Dobbelstein|first7=S.|last8=Petit|first8=A.|last9=Lapillonne|first9=H.|date=2012-11|title=RET fusion genes are associated with chronic myelomonocytic leukemia and enhance monocytic differentiation|url=https://pubmed.ncbi.nlm.nih.gov/22513837|journal=Leukemia|volume=26|issue=11|pages=2384–2389|doi=10.1038/leu.2012.109|issn=1476-5551|pmid=22513837}}</ref> | |||
|t(6;10)(q27;q11)<ref>{{Cite journal|last=Ballerini|first=P.|last2=Struski|first2=S.|last3=Cresson|first3=C.|last4=Prade|first4=N.|last5=Toujani|first5=S.|last6=Deswarte|first6=C.|last7=Dobbelstein|first7=S.|last8=Petit|first8=A.|last9=Lapillonne|first9=H.|date=2012-11|title=RET fusion genes are associated with chronic myelomonocytic leukemia and enhance monocytic differentiation|url=https://pubmed.ncbi.nlm.nih.gov/22513837|journal=Leukemia|volume=26|issue=11|pages=2384–2389|doi=10.1038/leu.2012.109|issn=1476-5551|pmid=22513837}}</ref> | |||
| | | | ||
| | | | ||