Changes

==Morphologic Features==

==Morphologic Features==

Morphologically, biopsy or resection specimens will show a bland spindle cell proliferation arranged haphazardly in a background of collagenous stroma. Cells contain ovoid nuclei within eosinophilic cytoplasm with indistinct cell borders. Tumors can vary in cellularity and stromal collagen. On low power, branching, “staghorn” shaped vessels can often be appreciated. Mitotic counts are usually low. Myxoid and lipomatous change have been described. SFT with adipocytic component are referred to as fat-forming (lipomatous) SFTs. There is also a variant known as giant cell rich SFT, which has the classic patternless spindle cell proliferation admixed with multinucleated giant cells. Dedifferentiated SFTs will show conventional SFT transitioning to a high-grade pleomorphic variant. Heterologous elements may be present. Standard immunophenotypic expression of CD34 and STAT6 is often lost in the dedifferentiated component.  

Morphologically, biopsy or resection specimens will show a bland spindle cell proliferation arranged haphazardly in a background of collagenous stroma. Cells contain ovoid nuclei within eosinophilic cytoplasm with indistinct cell borders. Tumors can vary in cellularity and stromal collagen. On low power, branching, “staghorn” shaped vessels can often be appreciated. Mitotic counts are usually low. Myxoid and lipomatous change have been described. SFT with adipocytic component are referred to as fat-forming (lipomatous) SFTs. There is also a variant known as giant cell rich SFT, which has the classic patternless spindle cell proliferation admixed with multinucleated giant cells. Dedifferentiated SFTs will show conventional SFT transitioning to a high-grade pleomorphic variant. Heterologous elements may be present. Standard immunophenotypic expression of CD34 and STAT6 is often lost in the dedifferentiated component.  

==Immunophenotype==

==Immunophenotype<ref>Goldblum, John R, et al. ''Enzinger & Weiss’s Soft Tissue Tumors''. 7th ed., Philadelphia, PA, Elsevier, 2020, pp. 1133–1147.</ref>==

Put your text here and fill in the table <span style="color:#0070C0">(''Instruction: Can include references in the table. Do not delete table.'') </span>

Put your text here and fill in the table <span style="color:#0070C0">(''Instruction: Can include references in the table. Do not delete table.'') </span>

{| class="wikitable sortable"

{| class="wikitable sortable"

!Finding!!Marker

!Finding!!Marker

|-

|-

|Positive (universal)||CD34

|Positive||CD34

|-

|-

|Positive (universal)||STAT6 (nuclear)

|Positive||STAT6 (nuclear)

|-

|-

|Negative (universal)||

|Positive||BCL2 (30%)

|-

|-

|Negative (subset)||

|Positive||CD99 (70%)

|Actin (20%)

|S100

|Cytokeratins

|}

|}

==Chromosomal Rearrangements (Gene Fusions)==

==Chromosomal Rearrangements (Gene Fusions)==

!Notes

!Notes

|-

|-

|inv(12)(q13q13)||3'STAT6 / 5'NAB2<ref>{{Cite journal|last=Huang|first=Shih‐Chiang|last2=Li|first2=Chien‐Feng|last3=Kao|first3=Yu‐Chien|last4=Chuang|first4=I‐Chieh|last5=Tai|first5=Hui‐Chun|last6=Tsai|first6=Jen‐Wei|last7=Yu|first7=Shih‐Chen|last8=Huang|first8=Hsuan‐Ying|last9=Lan|first9=Jui|date=2016-02|title=The clinicopathological significance of  NAB 2‐ STAT 6  gene fusions in 52 cases of intrathoracic solitary fibrous tumors|url=https://onlinelibrary.wiley.com/doi/10.1002/cam4.572|journal=Cancer Medicine|language=en|volume=5|issue=2|pages=159–168|doi=10.1002/cam4.572|issn=2045-7634}}</ref><ref>{{Cite journal|last=Chmielecki|first=Juliann|last2=Crago|first2=Aimee M|last3=Rosenberg|first3=Mara|last4=O'Connor|first4=Rachael|last5=Walker|first5=Sarah R|last6=Ambrogio|first6=Lauren|last7=Auclair|first7=Daniel|last8=McKenna|first8=Aaron|last9=Heinrich|first9=Michael C|date=2013-02|title=Whole-exome sequencing identifies a recurrent NAB2-STAT6 fusion in solitary fibrous tumors|url=https://www.nature.com/articles/ng.2522|journal=Nature Genetics|language=en|volume=45|issue=2|pages=131–132|doi=10.1038/ng.2522|issn=1061-4036}}</ref><ref>{{Cite journal|last=Robinson|first=Dan R|last2=Wu|first2=Yi-Mi|last3=Kalyana-Sundaram|first3=Shanker|last4=Cao|first4=Xuhong|last5=Lonigro|first5=Robert J|last6=Sung|first6=Yun-Shao|last7=Chen|first7=Chun-Liang|last8=Zhang|first8=Lei|last9=Wang|first9=Rui|date=2013-02|title=Identification of recurrent NAB2-STAT6 gene fusions in solitary fibrous tumor by integrative sequencing|url=https://www.nature.com/articles/ng.2509|journal=Nature Genetics|language=en|volume=45|issue=2|pages=180–185|doi=10.1038/ng.2509|issn=1061-4036}}</ref><ref>{{Cite journal|last=Mohajeri|first=Arezoo|last2=Tayebwa|first2=Johnbosco|last3=Collin|first3=Anna|last4=Nilsson|first4=Jenny|last5=Magnusson|first5=Linda|last6=von Steyern|first6=Fredrik Vult|last7=Brosjö|first7=Otte|last8=Domanski|first8=Henryk A.|last9=Larsson|first9=Olle|date=2013-10|title=Comprehensive genetic analysis identifies a pathognomonic NAB2/STAT6 fusion gene, nonrandom secondary genomic imbalances, and a characteristic gene expression profile in solitary fibrous tumor|url=https://onlinelibrary.wiley.com/doi/10.1002/gcc.22083|journal=Genes, Chromosomes and Cancer|language=en|volume=52|issue=10|pages=873–886|doi=10.1002/gcc.22083|issn=1045-2257}}</ref><ref>{{Cite journal|last=Vogels|first=Rob JC|last2=Vlenterie|first2=Myrella|last3=Versleijen-Jonkers|first3=Yvonne MH|last4=Ruijter|first4=Emiel|last5=Bekers|first5=Elise M|last6=Verdijk|first6=Marian AJ|last7=Link|first7=Monique M|last8=Bonenkamp|first8=Johannes J|last9=van der Graaf|first9=Winette TA|date=2014-12|title=Solitary fibrous tumor – clinicopathologic, immunohistochemical and molecular analysis of 28 cases|url=https://diagnosticpathology.biomedcentral.com/articles/10.1186/s13000-014-0224-6|journal=Diagnostic Pathology|language=en|volume=9|issue=1|doi=10.1186/s13000-014-0224-6|issn=1746-1596}}</ref><ref>{{Cite journal|last=Akaike|first=Keisuke|last2=Kurisaki-Arakawa|first2=Aiko|last3=Hara|first3=Kieko|last4=Suehara|first4=Yoshiyuki|last5=Takagi|first5=Tatsuya|last6=Mitani|first6=Keiko|last7=Kaneko|first7=Kazuo|last8=Yao|first8=Takashi|last9=Saito|first9=Tsuyoshi|date=2015-03|title=Distinct clinicopathological features of NAB2-STAT6 fusion gene variants in solitary fibrous tumor with emphasis on the acquisition of highly malignant potential|url=https://linkinghub.elsevier.com/retrieve/pii/S0046817714004912|journal=Human Pathology|language=en|volume=46|issue=3|pages=347–356|doi=10.1016/j.humpath.2014.11.018}}</ref>||NA||55-100%

|inv(12)(q13q13)||3'STAT6 / 5'NAB2<ref>{{Cite journal|last=Huang|first=Shih‐Chiang|last2=Li|first2=Chien‐Feng|last3=Kao|first3=Yu‐Chien|last4=Chuang|first4=I‐Chieh|last5=Tai|first5=Hui‐Chun|last6=Tsai|first6=Jen‐Wei|last7=Yu|first7=Shih‐Chen|last8=Huang|first8=Hsuan‐Ying|last9=Lan|first9=Jui|date=2016-02|title=The clinicopathological significance of  NAB 2‐ STAT 6  gene fusions in 52 cases of intrathoracic solitary fibrous tumors|url=https://onlinelibrary.wiley.com/doi/10.1002/cam4.572|journal=Cancer Medicine|language=en|volume=5|issue=2|pages=159–168|doi=10.1002/cam4.572|issn=2045-7634}}</ref><ref>{{Cite journal|last=Chmielecki|first=Juliann|last2=Crago|first2=Aimee M|last3=Rosenberg|first3=Mara|last4=O'Connor|first4=Rachael|last5=Walker|first5=Sarah R|last6=Ambrogio|first6=Lauren|last7=Auclair|first7=Daniel|last8=McKenna|first8=Aaron|last9=Heinrich|first9=Michael C|date=2013-02|title=Whole-exome sequencing identifies a recurrent NAB2-STAT6 fusion in solitary fibrous tumors|url=https://www.nature.com/articles/ng.2522|journal=Nature Genetics|language=en|volume=45|issue=2|pages=131–132|doi=10.1038/ng.2522|issn=1061-4036}}</ref><ref>{{Cite journal|last=Robinson|first=Dan R|last2=Wu|first2=Yi-Mi|last3=Kalyana-Sundaram|first3=Shanker|last4=Cao|first4=Xuhong|last5=Lonigro|first5=Robert J|last6=Sung|first6=Yun-Shao|last7=Chen|first7=Chun-Liang|last8=Zhang|first8=Lei|last9=Wang|first9=Rui|date=2013-02|title=Identification of recurrent NAB2-STAT6 gene fusions in solitary fibrous tumor by integrative sequencing|url=https://www.nature.com/articles/ng.2509|journal=Nature Genetics|language=en|volume=45|issue=2|pages=180–185|doi=10.1038/ng.2509|issn=1061-4036}}</ref><ref>{{Cite journal|last=Mohajeri|first=Arezoo|last2=Tayebwa|first2=Johnbosco|last3=Collin|first3=Anna|last4=Nilsson|first4=Jenny|last5=Magnusson|first5=Linda|last6=von Steyern|first6=Fredrik Vult|last7=Brosjö|first7=Otte|last8=Domanski|first8=Henryk A.|last9=Larsson|first9=Olle|date=2013-10|title=Comprehensive genetic analysis identifies a pathognomonic NAB2/STAT6 fusion gene, nonrandom secondary genomic imbalances, and a characteristic gene expression profile in solitary fibrous tumor|url=https://onlinelibrary.wiley.com/doi/10.1002/gcc.22083|journal=Genes, Chromosomes and Cancer|language=en|volume=52|issue=10|pages=873–886|doi=10.1002/gcc.22083|issn=1045-2257}}</ref><ref>{{Cite journal|last=Vogels|first=Rob JC|last2=Vlenterie|first2=Myrella|last3=Versleijen-Jonkers|first3=Yvonne MH|last4=Ruijter|first4=Emiel|last5=Bekers|first5=Elise M|last6=Verdijk|first6=Marian AJ|last7=Link|first7=Monique M|last8=Bonenkamp|first8=Johannes J|last9=van der Graaf|first9=Winette TA|date=2014-12|title=Solitary fibrous tumor – clinicopathologic, immunohistochemical and molecular analysis of 28 cases|url=https://diagnosticpathology.biomedcentral.com/articles/10.1186/s13000-014-0224-6|journal=Diagnostic Pathology|language=en|volume=9|issue=1|doi=10.1186/s13000-014-0224-6|issn=1746-1596}}</ref><ref name=":0">{{Cite journal|last=Akaike|first=Keisuke|last2=Kurisaki-Arakawa|first2=Aiko|last3=Hara|first3=Kieko|last4=Suehara|first4=Yoshiyuki|last5=Takagi|first5=Tatsuya|last6=Mitani|first6=Keiko|last7=Kaneko|first7=Kazuo|last8=Yao|first8=Takashi|last9=Saito|first9=Tsuyoshi|date=2015-03|title=Distinct clinicopathological features of NAB2-STAT6 fusion gene variants in solitary fibrous tumor with emphasis on the acquisition of highly malignant potential|url=https://linkinghub.elsevier.com/retrieve/pii/S0046817714004912|journal=Human Pathology|language=en|volume=46|issue=3|pages=347–356|doi=10.1016/j.humpath.2014.11.018}}</ref>||NA||55-100%

|Yes

|Yes

|Unknown

|Unknown

|}

|}

==Gene Mutations (SNV / INDEL)==

==Gene Mutations (SNV / INDEL)==

There are multiple genes with single nucleotide variations that have been reported only in metastatic solitary fibrous tumor tissues including TP53 and APAF1.<ref>{{Cite journal|last=Park|first=Hyung Kyu|last2=Yu|first2=Dan Bi|last3=Sung|first3=Minjung|last4=Oh|first4=Ensel|last5=Kim|first5=Mingi|last6=Song|first6=Ji-Young|last7=Lee|first7=Mi-Sook|last8=Jung|first8=Kyungsoo|last9=Noh|first9=Ka-Won|date=2019|title=Molecular changes in solitary fibrous tumor progression|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6746689/|journal=Journal of Molecular Medicine (Berlin, Germany)|volume=97|issue=10|pages=1413–1425|doi=10.1007/s00109-019-01815-8|issn=0946-2716|pmc=6746689|pmid=31321477}}</ref>

There are multiple genes with single nucleotide variations that have been reported only in metastatic solitary fibrous tumor tissues including TP53 and APAF1.<ref name=":1">{{Cite journal|last=Park|first=Hyung Kyu|last2=Yu|first2=Dan Bi|last3=Sung|first3=Minjung|last4=Oh|first4=Ensel|last5=Kim|first5=Mingi|last6=Song|first6=Ji-Young|last7=Lee|first7=Mi-Sook|last8=Jung|first8=Kyungsoo|last9=Noh|first9=Ka-Won|date=2019|title=Molecular changes in solitary fibrous tumor progression|url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6746689/|journal=Journal of Molecular Medicine (Berlin, Germany)|volume=97|issue=10|pages=1413–1425|doi=10.1007/s00109-019-01815-8|issn=0946-2716|pmc=6746689|pmid=31321477}}</ref>  

{| class="wikitable sortable"

{| class="wikitable sortable"

|-

|-

|-

|-

|TERT

|TERT

|<span class="blue-text">EXAMPLE:</span> TSG

|Oncogene

|13-28% <ref>{{Cite journal|last=Bahrami|first=Armita|last2=Lee|first2=Seungjae|last3=Schaefer|first3=Inga-Marie|last4=Boland|first4=Jennifer M|last5=Patton|first5=Kurt T|last6=Pounds|first6=Stanley|last7=Fletcher|first7=Christopher D|date=2016-12|title=TERT promoter mutations and prognosis in solitary fibrous tumor|url=https://linkinghub.elsevier.com/retrieve/pii/S0893395222023328|journal=Modern Pathology|language=en|volume=29|issue=12|pages=1511–1522|doi=10.1038/modpathol.2016.126}}</ref><ref>{{Cite journal|last=Liu|first=Xiaoli|last2=Bishop|first2=Justin|last3=Shan|first3=Yuan|last4=Pai|first4=Sara|last5=Liu|first5=Dingxie|last6=Murugan|first6=Avaniyapuram Kannan|last7=Sun|first7=Hui|last8=El-Naggar|first8=Adel K|last9=Xing|first9=Mingzhao|date=2013-08|title=Highly prevalent TERT promoter mutations in aggressive thyroid cancers|url=https://erc.bioscientifica.com/view/journals/erc/20/4/603.xml|journal=Endocrine-Related Cancer|volume=20|issue=4|pages=603–610|doi=10.1530/ERC-13-0210|issn=1351-0088|pmc=PMC3782569|pmid=23766237}}</ref><ref>{{Cite journal|last=Killela|first=Patrick J.|last2=Reitman|first2=Zachary J.|last3=Jiao|first3=Yuchen|last4=Bettegowda|first4=Chetan|last5=Agrawal|first5=Nishant|last6=Diaz|first6=Luis A.|last7=Friedman|first7=Allan H.|last8=Friedman|first8=Henry|last9=Gallia|first9=Gary L.|date=2013-04-09|title=TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal|url=https://pnas.org/doi/full/10.1073/pnas.1303607110|journal=Proceedings of the National Academy of Sciences|language=en|volume=110|issue=15|pages=6021–6026|doi=10.1073/pnas.1303607110|issn=0027-8424|pmc=PMC3625331|pmid=23530248}}</ref><ref>{{Cite journal|last=Koelsche|first=Christian|last2=Renner|first2=Marcus|last3=Hartmann|first3=Wolfgang|last4=Brandt|first4=Regine|last5=Lehner|first5=Burkhard|last6=Waldburger|first6=Nina|last7=Alldinger|first7=Ingo|last8=Schmitt|first8=Thomas|last9=Egerer|first9=Gerlinde|date=2014-12|title=TERT promoter hotspot mutations are recurrent in myxoid liposarcomas but rare in other soft tissue sarcoma entities|url=https://jeccr.biomedcentral.com/articles/10.1186/1756-9966-33-33|journal=Journal of Experimental & Clinical Cancer Research|language=en|volume=33|issue=1|doi=10.1186/1756-9966-33-33|issn=1756-9966}}</ref>

|13-29% <ref name=":3">{{Cite journal|last=Bahrami|first=Armita|last2=Lee|first2=Seungjae|last3=Schaefer|first3=Inga-Marie|last4=Boland|first4=Jennifer M|last5=Patton|first5=Kurt T|last6=Pounds|first6=Stanley|last7=Fletcher|first7=Christopher D|date=2016-12|title=TERT promoter mutations and prognosis in solitary fibrous tumor|url=https://linkinghub.elsevier.com/retrieve/pii/S0893395222023328|journal=Modern Pathology|language=en|volume=29|issue=12|pages=1511–1522|doi=10.1038/modpathol.2016.126}}</ref><ref>{{Cite journal|last=Liu|first=Xiaoli|last2=Bishop|first2=Justin|last3=Shan|first3=Yuan|last4=Pai|first4=Sara|last5=Liu|first5=Dingxie|last6=Murugan|first6=Avaniyapuram Kannan|last7=Sun|first7=Hui|last8=El-Naggar|first8=Adel K|last9=Xing|first9=Mingzhao|date=2013-08|title=Highly prevalent TERT promoter mutations in aggressive thyroid cancers|url=https://erc.bioscientifica.com/view/journals/erc/20/4/603.xml|journal=Endocrine-Related Cancer|volume=20|issue=4|pages=603–610|doi=10.1530/ERC-13-0210|issn=1351-0088|pmc=PMC3782569|pmid=23766237}}</ref><ref>{{Cite journal|last=Killela|first=Patrick J.|last2=Reitman|first2=Zachary J.|last3=Jiao|first3=Yuchen|last4=Bettegowda|first4=Chetan|last5=Agrawal|first5=Nishant|last6=Diaz|first6=Luis A.|last7=Friedman|first7=Allan H.|last8=Friedman|first8=Henry|last9=Gallia|first9=Gary L.|date=2013-04-09|title=TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal|url=https://pnas.org/doi/full/10.1073/pnas.1303607110|journal=Proceedings of the National Academy of Sciences|language=en|volume=110|issue=15|pages=6021–6026|doi=10.1073/pnas.1303607110|issn=0027-8424|pmc=PMC3625331|pmid=23530248}}</ref><ref>{{Cite journal|last=Koelsche|first=Christian|last2=Renner|first2=Marcus|last3=Hartmann|first3=Wolfgang|last4=Brandt|first4=Regine|last5=Lehner|first5=Burkhard|last6=Waldburger|first6=Nina|last7=Alldinger|first7=Ingo|last8=Schmitt|first8=Thomas|last9=Egerer|first9=Gerlinde|date=2014-12|title=TERT promoter hotspot mutations are recurrent in myxoid liposarcomas but rare in other soft tissue sarcoma entities|url=https://jeccr.biomedcentral.com/articles/10.1186/1756-9966-33-33|journal=Journal of Experimental & Clinical Cancer Research|language=en|volume=33|issue=1|doi=10.1186/1756-9966-33-33|issn=1756-9966}}</ref><ref name=":2">{{Cite journal|last=Demicco|first=Elizabeth G.|last2=Wani|first2=Khalida|last3=Ingram|first3=Davis|last4=Wagner|first4=Michael|last5=Maki|first5=Robert G.|last6=Rizzo|first6=Anthony|last7=Meeker|first7=Alan|last8=Lazar|first8=Alexander J.|last9=Wang|first9=Wei-Lien|date=2018-11|title=TERT promoter mutations in solitary fibrous tumour|url=https://pubmed.ncbi.nlm.nih.gov/29985536|journal=Histopathology|volume=73|issue=5|pages=843–851|doi=10.1111/his.13703|issn=1365-2559|pmid=29985536}}</ref>

|

|

|

|

|No

|No

|Yes

|Yes<ref name=":0" /><ref name=":3" /><ref name=":2" /><ref>{{Cite journal|last=Park|first=Hyung Kyu|last2=Yu|first2=Dan Bi|last3=Sung|first3=Minjung|last4=Oh|first4=Ensel|last5=Kim|first5=Mingi|last6=Song|first6=Ji-Young|last7=Lee|first7=Mi-Sook|last8=Jung|first8=Kyungsoo|last9=Noh|first9=Ka-Won|date=2019-10|title=Molecular changes in solitary fibrous tumor progression|url=https://pubmed.ncbi.nlm.nih.gov/31321477|journal=Journal of Molecular Medicine (Berlin, Germany)|volume=97|issue=10|pages=1413–1425|doi=10.1007/s00109-019-01815-8|issn=1432-1440|pmc=6746689|pmid=31321477}}</ref><ref>{{Cite journal|last=Bahrami|first=Armita|last2=Lee|first2=Seungjae|last3=Schaefer|first3=Inga-Marie|last4=Boland|first4=Jennifer M.|last5=Patton|first5=Kurt T.|last6=Pounds|first6=Stanley|last7=Fletcher|first7=Christopher D.|date=2016-12|title=TERT promoter mutations and prognosis in solitary fibrous tumor|url=https://pubmed.ncbi.nlm.nih.gov/27562490|journal=Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc|volume=29|issue=12|pages=1511–1522|doi=10.1038/modpathol.2016.126|issn=1530-0285|pmc=5731237|pmid=27562490}}</ref>

|No

|No

|

|

|}<br />

|No

|Yes<ref name=":1" />

==Epigenomic Alterations==

==Epigenomic Alterations==

Not Applicable

Not Applicable

==Genes and Main Pathways Involved==

==Genes and Main Pathways Involved==

{| class="wikitable sortable"

{| class="wikitable sortable"

|-

|-

|}

|}

==Genetic Diagnostic Testing Methods==

==Genetic Diagnostic Testing Methods==

Ancillary studies such as immunohistochemistry and molecular tests are useful in differentiating soft tissue tumors. SFTs have historically been diagnosed by morphology and strong diffuse CD34 positivity. Additional immunohistochemical phenotype previously used for identification included expression of Bcl2, CD99, and vimentin and absence of expression of epithelial, muscle, and neural markers. However, the introduction of STAT6 (signal transducer and activator of transcription 6) immunostain now dominates due to its high sensitivity and specificity. STAT6 expression is demonstrated by nuclear staining. Molecular testing by next generation sequencing is also highly useful in detecting the NAB2::STAT6 fusion. Breakapart fluorescence in situ hybridization (FISH) probe for STAT6 can detect rearrangement of this gene.  In the context of SFT, the rearrangement of the ''STAT6'' gene is highly suggestive for the presence of ''NAB2-STAT6'' fusion. [https://pubmed.ncbi.nlm.nih.gov/27802414/ A dual color dual fusion probe targeting both genes would be a direct confirmation for ''NAB2-STAT6'' fusion.]

Ancillary studies such as immunohistochemistry and molecular tests are useful in differentiating soft tissue tumors. SFTs have historically been diagnosed by morphology and strong diffuse CD34 positivity. Additional immunohistochemical phenotype previously used for identification included expression of Bcl2, CD99, and vimentin and absence of expression of epithelial, muscle, and neural markers. However, the introduction of STAT6 (signal transducer and activator of transcription 6) immunostain now dominates due to its high sensitivity and specificity. STAT6 expression is demonstrated by nuclear staining. Next generation sequencing (NGS) using mRNA is also highly useful in detecting the NAB2::STAT6 fusion. Breakapart fluorescence in situ hybridization (FISH) probe for STAT6 can detect rearrangement of this gene.  In the context of SFT, the rearrangement of the ''STAT6'' gene is highly suggestive for the presence of ''NAB2-STAT6'' fusion. [https://pubmed.ncbi.nlm.nih.gov/27802414/ A dual color dual fusion probe targeting both genes would be a direct confirmation for ''NAB2-STAT6'' fusion.]

==Familial Forms==

==Familial Forms==

Not Applicable

Not Applicable

==Notes==

==Notes==

<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page.  If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage).  Additional global feedback or concerns are also welcome.

<nowiki>*</nowiki>Primary authors will typically be those that initially create and complete the content of a page.  If a subsequent user modifies the content and feels the effort put forth is of high enough significance to warrant listing in the authorship section, please contact the CCGA coordinators (contact information provided on the homepage).  Additional global feedback or concerns are also welcome.