HAEM5:Hepatosplenic T-cell lymphoma: Difference between revisions

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==Epigenomic Alterations==

''AIM1'' is dramatically reduced in HSTL likely due to promoter methylation<ref name=":5" />

*''AIM1'' is dramatically reduced in HSTL likely due to promoter methylation<ref name=":5" />

*Suggest ''AIM1'' may play a role as a tumor suppressor gene in HSTL oncogenesis<ref name=":5">Travert M, Huang Y, De Leval L, Martin-Garcia N, Delfau-Larue MH, Berger F, Bosq J, Brière J, Soulier J, Macintyre E, Marafioti T. Molecular features of hepatosplenic T-cell lymphoma unravels potential novel therapeutic targets. Blood, The Journal of the American Society of Hematology. 2012 Jun 14;119(24):5795-806.</ref>

**Suggest ''AIM1'' may play a role as a tumor suppressor gene in HSTL oncogenesis<ref name=":5">Travert M, Huang Y, De Leval L, Martin-Garcia N, Delfau-Larue MH, Berger F, Bosq J, Brière J, Soulier J, Macintyre E, Marafioti T. Molecular features of hepatosplenic T-cell lymphoma unravels potential novel therapeutic targets. Blood, The Journal of the American Society of Hematology. 2012 Jun 14;119(24):5795-806.</ref>

Eight consistently hypermethylated genes (''BCL11B'', ''CD5'', ''CXCR6'', ''GIMAP7'', ''LTA'', SEPT9, ''UBAC2'', ''UXS1'') and four consistently hypomethylated genes (''ADARB1'', ''NFIC'', ''NR1H3'', ''ST3GAL3'') in HSTL<ref name=":6">{{Cite journal|last=Bergmann|first=Anke K.|last2=Fataccioli|first2=Virginie|last3=Castellano|first3=Giancarlo|last4=Martin-Garcia|first4=Nadine|last5=Pelletier|first5=Laura|last6=Ammerpohl|first6=Ole|last7=Bergmann|first7=Juri|last8=Bhat|first8=Jaydeep|last9=Pau|first9=Enrique Carrillo-de Santa|date=03 2019|title=DNA methylation profiling of hepatosplenic T-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/30337361|journal=Haematologica|volume=104|issue=3|pages=e104–e107|doi=10.3324/haematol.2018.196196|issn=1592-8721|pmc=6395348|pmid=30337361}}</ref>.

*Hypermethylated genes (''LTA'', ''CD5'', ''CXCR6'', ''GIMAP7'', ''BCL11B'' and ''SEPT9)'' are relevant to the pathobiology of T-cell leukemias/lymphomas, and are hypermethylated at active promoter sites mainly around transcription start sites<ref name=":6" />.

*Eight consistently hypermethylated genes (''BCL11B'', ''CD5'', ''CXCR6'', ''GIMAP7'', ''LTA'', SEPT9, ''UBAC2'', ''UXS1'') and four consistently hypomethylated genes (''ADARB1'', ''NFIC'', ''NR1H3'', ''ST3GAL3'') in HSTL<ref name=":6">{{Cite journal|last=Bergmann|first=Anke K.|last2=Fataccioli|first2=Virginie|last3=Castellano|first3=Giancarlo|last4=Martin-Garcia|first4=Nadine|last5=Pelletier|first5=Laura|last6=Ammerpohl|first6=Ole|last7=Bergmann|first7=Juri|last8=Bhat|first8=Jaydeep|last9=Pau|first9=Enrique Carrillo-de Santa|date=03 2019|title=DNA methylation profiling of hepatosplenic T-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/30337361|journal=Haematologica|volume=104|issue=3|pages=e104–e107|doi=10.3324/haematol.2018.196196|issn=1592-8721|pmc=6395348|pmid=30337361}}</ref>.

**Hypermethylation of CpGs around transcription start sites shows a lack of protein expression of CD5 and CXCR6 by immunohistochemistry in HSTL, compared to normal lymphocytes<ref name=":6" />.

**Hypermethylated genes (''LTA'', ''CD5'', ''CXCR6'', ''GIMAP7'', ''BCL11B'' and ''SEPT9)'' are relevant to the pathobiology of T-cell leukemias/lymphomas, and are hypermethylated at active promoter sites mainly around transcription start sites<ref name=":6" />.

**Note: This finding is not specific to HSTL and can be seen in other T-cell lymphomas<ref name=":6" />

***Hypermethylation of CpGs around transcription start sites shows a lack of protein expression of CD5 and CXCR6 by immunohistochemistry in HSTL, compared to normal lymphocytes<ref name=":6" />.

A single study has shown use of IFNα2c therapy-induced changes in CpG methylation<ref name=":7">{{Cite journal|last=Bhat|first=Jaydeep|last2=Bergmann|first2=Anke K.|last3=Waschina|first3=Silvio|last4=Nerl|first4=Christoph|last5=Kaleta|first5=Christoph|last6=Siebert|first6=Reiner|last7=Ammerpohl|first7=Ole|last8=Kabelitz|first8=Dieter|date=2021-05|title=DNA methylation profile of a hepatosplenic gamma/delta T-cell lymphoma patient associated with response to interferon-α therapy|url=https://pubmed.ncbi.nlm.nih.gov/32820235|journal=Cellular & Molecular Immunology|volume=18|issue=5|pages=1332–1335|doi=10.1038/s41423-020-0518-4|issn=2042-0226|pmc=8093208|pmid=32820235}}</ref>

****Note: This finding is not specific to HSTL and can be seen in other T-cell lymphomas<ref name=":6" />

*CpG methylation changes have the potential to serve as biomarkers of drug responses and/or disease progression<ref name=":7" />

*A single study has shown use of IFNα2c therapy-induced changes in CpG methylation<ref name=":7">{{Cite journal|last=Bhat|first=Jaydeep|last2=Bergmann|first2=Anke K.|last3=Waschina|first3=Silvio|last4=Nerl|first4=Christoph|last5=Kaleta|first5=Christoph|last6=Siebert|first6=Reiner|last7=Ammerpohl|first7=Ole|last8=Kabelitz|first8=Dieter|date=2021-05|title=DNA methylation profile of a hepatosplenic gamma/delta T-cell lymphoma patient associated with response to interferon-α therapy|url=https://pubmed.ncbi.nlm.nih.gov/32820235|journal=Cellular & Molecular Immunology|volume=18|issue=5|pages=1332–1335|doi=10.1038/s41423-020-0518-4|issn=2042-0226|pmc=8093208|pmid=32820235}}</ref>

**CpG methylation changes have the potential to serve as biomarkers of drug responses and/or disease progression<ref name=":7" />

==Genes and Main Pathways Involved==

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==Familial Forms==

N/A

*N/A

==Additional Information==

@@ Line 230: / Line 230: @@
 ==Epigenomic Alterations==
+''AIM1'' is dramatically reduced in HSTL likely due to promoter methylation<ref name=":5" />
-*''AIM1'' is dramatically reduced in HSTL likely due to promoter methylation<ref name=":5" />
+*Suggest ''AIM1'' may play a role as a tumor suppressor gene in HSTL oncogenesis<ref name=":5">Travert M, Huang Y, De Leval L, Martin-Garcia N, Delfau-Larue MH, Berger F, Bosq J, Brière J, Soulier J, Macintyre E, Marafioti T. Molecular features of hepatosplenic T-cell lymphoma unravels potential novel therapeutic targets. Blood, The Journal of the American Society of Hematology. 2012 Jun 14;119(24):5795-806.</ref>
-**Suggest ''AIM1'' may play a role as a tumor suppressor gene in HSTL oncogenesis<ref name=":5">Travert M, Huang Y, De Leval L, Martin-Garcia N, Delfau-Larue MH, Berger F, Bosq J, Brière J, Soulier J, Macintyre E, Marafioti T. Molecular features of hepatosplenic T-cell lymphoma unravels potential novel therapeutic targets. Blood, The Journal of the American Society of Hematology. 2012 Jun 14;119(24):5795-806.</ref>
+Eight consistently hypermethylated genes (''BCL11B'', ''CD5'', ''CXCR6'', ''GIMAP7'', ''LTA'', SEPT9, ''UBAC2'', ''UXS1'') and four consistently hypomethylated genes (''ADARB1'', ''NFIC'', ''NR1H3'', ''ST3GAL3'') in HSTL<ref name=":6">{{Cite journal|last=Bergmann|first=Anke K.|last2=Fataccioli|first2=Virginie|last3=Castellano|first3=Giancarlo|last4=Martin-Garcia|first4=Nadine|last5=Pelletier|first5=Laura|last6=Ammerpohl|first6=Ole|last7=Bergmann|first7=Juri|last8=Bhat|first8=Jaydeep|last9=Pau|first9=Enrique Carrillo-de Santa|date=03 2019|title=DNA methylation profiling of hepatosplenic T-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/30337361|journal=Haematologica|volume=104|issue=3|pages=e104–e107|doi=10.3324/haematol.2018.196196|issn=1592-8721|pmc=6395348|pmid=30337361}}</ref>.
+*Hypermethylated genes (''LTA'', ''CD5'', ''CXCR6'', ''GIMAP7'', ''BCL11B'' and ''SEPT9)'' are relevant to the pathobiology of T-cell leukemias/lymphomas, and are hypermethylated at active promoter sites mainly around transcription start sites<ref name=":6" />.
-*Eight consistently hypermethylated genes (''BCL11B'', ''CD5'', ''CXCR6'', ''GIMAP7'', ''LTA'', SEPT9, ''UBAC2'', ''UXS1'') and four consistently hypomethylated genes (''ADARB1'', ''NFIC'', ''NR1H3'', ''ST3GAL3'') in HSTL<ref name=":6">{{Cite journal|last=Bergmann|first=Anke K.|last2=Fataccioli|first2=Virginie|last3=Castellano|first3=Giancarlo|last4=Martin-Garcia|first4=Nadine|last5=Pelletier|first5=Laura|last6=Ammerpohl|first6=Ole|last7=Bergmann|first7=Juri|last8=Bhat|first8=Jaydeep|last9=Pau|first9=Enrique Carrillo-de Santa|date=03 2019|title=DNA methylation profiling of hepatosplenic T-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/30337361|journal=Haematologica|volume=104|issue=3|pages=e104–e107|doi=10.3324/haematol.2018.196196|issn=1592-8721|pmc=6395348|pmid=30337361}}</ref>.
+**Hypermethylation of CpGs around transcription start sites shows a lack of protein expression of CD5 and CXCR6 by immunohistochemistry in HSTL, compared to normal lymphocytes<ref name=":6" />.
-**Hypermethylated genes (''LTA'', ''CD5'', ''CXCR6'', ''GIMAP7'', ''BCL11B'' and ''SEPT9)'' are relevant to the pathobiology of T-cell leukemias/lymphomas, and are hypermethylated at active promoter sites mainly around transcription start sites<ref name=":6" />.
+**Note: This finding is not specific to HSTL and can be seen in other T-cell lymphomas<ref name=":6" />
-***Hypermethylation of CpGs around transcription start sites shows a lack of protein expression of CD5 and CXCR6 by immunohistochemistry in HSTL, compared to normal lymphocytes<ref name=":6" />.
+A single study has shown use of IFNα2c therapy-induced changes in CpG methylation<ref name=":7">{{Cite journal|last=Bhat|first=Jaydeep|last2=Bergmann|first2=Anke K.|last3=Waschina|first3=Silvio|last4=Nerl|first4=Christoph|last5=Kaleta|first5=Christoph|last6=Siebert|first6=Reiner|last7=Ammerpohl|first7=Ole|last8=Kabelitz|first8=Dieter|date=2021-05|title=DNA methylation profile of a hepatosplenic gamma/delta T-cell lymphoma patient associated with response to interferon-α therapy|url=https://pubmed.ncbi.nlm.nih.gov/32820235|journal=Cellular & Molecular Immunology|volume=18|issue=5|pages=1332–1335|doi=10.1038/s41423-020-0518-4|issn=2042-0226|pmc=8093208|pmid=32820235}}</ref>
-****Note: This finding is not specific to HSTL and can be seen in other T-cell lymphomas<ref name=":6" />
+*CpG methylation changes have the potential to serve as biomarkers of drug responses and/or disease progression<ref name=":7" />
-*A single study has shown use of IFNα2c therapy-induced changes in CpG methylation<ref name=":7">{{Cite journal|last=Bhat|first=Jaydeep|last2=Bergmann|first2=Anke K.|last3=Waschina|first3=Silvio|last4=Nerl|first4=Christoph|last5=Kaleta|first5=Christoph|last6=Siebert|first6=Reiner|last7=Ammerpohl|first7=Ole|last8=Kabelitz|first8=Dieter|date=2021-05|title=DNA methylation profile of a hepatosplenic gamma/delta T-cell lymphoma patient associated with response to interferon-α therapy|url=https://pubmed.ncbi.nlm.nih.gov/32820235|journal=Cellular & Molecular Immunology|volume=18|issue=5|pages=1332–1335|doi=10.1038/s41423-020-0518-4|issn=2042-0226|pmc=8093208|pmid=32820235}}</ref>
-**CpG methylation changes have the potential to serve as biomarkers of drug responses and/or disease progression<ref name=":7" />
 ==Genes and Main Pathways Involved==
@@ Line 321: / Line 318: @@
 ==Familial Forms==
+N/A
-*N/A
 ==Additional Information==