HAEM5:Extranodal NK/T-cell lymphoma: Difference between revisions

← Older edit Newer edit →

VisualWikitext

@@ Line 50: / Line 50: @@
 |CTLA4-CD28
 |CTLA4-CD28
-|This fusion promotes tumor cell growth and survival by redirecting immune checkpoint signals
+|This fusion promotes tumor cell growth and survival by redirecting immune checkpoint signals<ref>{{Cite journal|last=Yoo|first=Hae Yong|last2=Kim|first2=Pora|last3=Kim|first3=Won Seog|last4=Lee|first4=Seung Ho|last5=Kim|first5=Sangok|last6=Kang|first6=So Young|last7=Jang|first7=Hye Yoon|last8=Lee|first8=Jong-Eun|last9=Kim|first9=Jaesang|date=2016-06-01|title=Frequent CTLA4-CD28 gene fusion in diverse types of T-cell lymphoma|url=https://haematologica.org/article/view/7742|journal=Haematologica|language=en|volume=101|issue=6|pages=757–763|doi=10.3324/haematol.2015.139253|issn=1592-8721|pmc=5013939|pmid=26819049}}</ref>
 |Chromosome 2q33
 |29%
@@ Line 68: / Line 68: @@
 |6
 |Loss
-|n/a
+|~2.6 Mb interval within 6q21–q25<ref>{{Cite journal|last=De Mel|first=Sanjay|last2=Soon|first2=Gwyneth Shook-Ting|last3=Mok|first3=Yingting|last4=Chung|first4=Tae-Hoon|last5=Jeyasekharan|first5=Anand D.|last6=Chng|first6=Wee-Joo|last7=Ng|first7=Siok-Bian|date=2018-06-30|title=The Genomics and Molecular Biology of Natural Killer/T-Cell Lymphoma: Opportunities for Translation|url=https://doi.org/10.3390/ijms19071931|journal=International Journal of Molecular Sciences|volume=19|issue=7|pages=1931|doi=10.3390/ijms19071931|issn=1422-0067}}</ref>
 |This locus harbors multiple candidate genes including ATG5, AIM1, PRDM1, PTPRK, HACE1 and FOXO3<ref name=":32">{{Cite journal|last=Iqbal|first=J.|last2=Kucuk|first2=C.|last3=Deleeuw|first3=R. J.|last4=Srivastava|first4=G.|last5=Tam|first5=W.|last6=Geng|first6=H.|last7=Klinkebiel|first7=D.|last8=Christman|first8=J. K.|last9=Patel|first9=K.|date=2009-06|title=Genomic analyses reveal global functional alterations that promote tumor growth and novel tumor suppressor genes in natural killer-cell malignancies|url=https://pubmed.ncbi.nlm.nih.gov/19194464|journal=Leukemia|volume=23|issue=6|pages=1139–1151|doi=10.1038/leu.2009.3|issn=1476-5551|pmid=19194464}}</ref><ref name=":7">{{Cite journal|last=Karube|first=Kennosuke|last2=Nakagawa|first2=Masao|last3=Tsuzuki|first3=Shinobu|last4=Takeuchi|first4=Ichiro|last5=Honma|first5=Keiichiro|last6=Nakashima|first6=Yasuhiro|last7=Shimizu|first7=Norio|last8=Ko|first8=Young-Hyeh|last9=Morishima|first9=Yasuo|date=2011-09-22|title=Identification of FOXO3 and PRDM1 as tumor-suppressor gene candidates in NK-cell neoplasms by genomic and functional analyses|url=https://pubmed.ncbi.nlm.nih.gov/21690554|journal=Blood|volume=118|issue=12|pages=3195–3204|doi=10.1182/blood-2011-04-346890|issn=1528-0020|pmid=21690554}}</ref><ref name=":1">{{Cite journal|last=Chen|first=Yun-Wen|last2=Guo|first2=Tianhuan|last3=Shen|first3=Lijun|last4=Wong|first4=Kai-Yau|last5=Tao|first5=Qian|last6=Choi|first6=William W. L.|last7=Au-Yeung|first7=Rex K. H.|last8=Chan|first8=Yuen-Piu|last9=Wong|first9=Michelle L. Y.|date=2015-03-05|title=Receptor-type tyrosine-protein phosphatase κ directly targets STAT3 activation for tumor suppression in nasal NK/T-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/25612622|journal=Blood|volume=125|issue=10|pages=1589–1600|doi=10.1182/blood-2014-07-588970|issn=1528-0020|pmid=25612622}}</ref>
 |D: Chromosome 6q loss is a recurrent abnormality in ENKTL that provides supportive molecular evidence of neoplasia and helps distinguish ENKTL from other T/NK-cell proliferations, but it is not sufficient for a standalone diagnosis.<ref>{{Cite journal|last=Liang|first=Li|last2=Zhang|first2=Zhang|last3=Wang|first3=Ying|last4=Nong|first4=Lin|last5=Zheng|first5=Yalin|last6=Qu|first6=Linlin|last7=Zhang|first7=Bo|last8=Li|first8=Ting|date=2015|title=The Genetic Deletion of 6q21 and PRDM1 and Clinical Implications in Extranodal NK/T Cell Lymphoma, Nasal Type|url=https://pubmed.ncbi.nlm.nih.gov/26221594|journal=BioMed Research International|volume=2015|pages=435423|doi=10.1155/2015/435423|issn=2314-6141|pmc=4499638|pmid=26221594}}</ref>
@@ Line 87: / Line 87: @@
 |Isochromosome 6p<ref>{{Cite journal|last=Tien|first=H. F.|last2=Su|first2=I. J.|last3=Tang|first3=J. L.|last4=Liu|first4=M. C.|last5=Lee|first5=F. Y.|last6=Chen|first6=Y. C.|last7=Chuang|first7=S. M.|date=1997-06|title=Clonal chromosomal abnormalities as direct evidence for clonality in nasal T/natural killer cell lymphomas|url=https://pubmed.ncbi.nlm.nih.gov/9207410|journal=British Journal of Haematology|volume=97|issue=3|pages=621–625|doi=10.1046/j.1365-2141.1997.752711.x|issn=0007-1048|pmid=9207410}}</ref>
 |Unknown
-|Unknown
+|Yes, isochromosome (6p) leads to '''loss of 6q tumor suppressor genes''' (''PRDM1, FOXO3, HACE1'') and '''gain of 6p genes''', which may enhance proliferation.This dual effect is thought to contribute to '''more aggressive tumor biology''' compared with simple 6q deletions.<ref>{{Cite journal|last=Tse|first=Eric|last2=Kwong|first2=Yok-Lam|date=2017-12|title=The diagnosis and management of NK/T-cell lymphomas|url=http://jhoonline.biomedcentral.com/articles/10.1186/s13045-017-0452-9|journal=Journal of Hematology & Oncology|language=en|volume=10|issue=1|doi=10.1186/s13045-017-0452-9|issn=1756-8722}}</ref><ref>{{Cite journal|last=De Mel|first=Sanjay|last2=Soon|first2=Gwyneth Shook-Ting|last3=Mok|first3=Yingting|last4=Chung|first4=Tae-Hoon|last5=Jeyasekharan|first5=Anand D.|last6=Chng|first6=Wee-Joo|last7=Ng|first7=Siok-Bian|date=2018-06-30|title=The Genomics and Molecular Biology of Natural Killer/T-Cell Lymphoma: Opportunities for Translation|url=https://www.mdpi.com/1422-0067/19/7/1931|journal=International Journal of Molecular Sciences|language=en|volume=19|issue=7|pages=1931|doi=10.3390/ijms19071931|issn=1422-0067}}</ref>
 |Unknown
 |N/A