Compendium of Cancer Genome Aberrations

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

← Older editNewer edit →
VisualWikitext
Ian.King (talk | contribs)
12 edits
Ian.King (talk | contribs)
12 edits
mNo edit summary
Line 107: Line 107:
!Clinical Relevance Details/Other Notes
!Clinical Relevance Details/Other Notes
|-
|-
|<span class="blue-text">EXAMPLE:</span>''EGFR''
|JAK3
 
<br />
|<span class="blue-text">EXAMPLE:</span> Exon 18-21 activating mutations
|<span class="blue-text">EXAMPLE:</span> Exon 18-21 activating mutations
|<span class="blue-text">EXAMPLE:</span> Oncogene
|Oncogene
|<span class="blue-text">EXAMPLE:</span> Common (lung cancer)
|Common
|<span class="blue-text">EXAMPLE:</span> T
|T
|<span class="blue-text">EXAMPLE:</span> Yes (NCCN)
|No
|<span class="blue-text">EXAMPLE:</span> Exons 18, 19, and 21 mutations are targetable for therapy. Exon 20 T790M variants cause resistance to first generation TKI therapy and are targetable by second and third generation TKIs (add references).
|Pan-JAK and selective JAK3 inhibitors have been suggested as potential therapeutic options<ref name=":10" /><ref name=":33" />. [https://clinicaltrials.gov/study/NCT02974647 Clinical trials evaluating JAK inhibitors] are in progress.
|-
|-
|<span class="blue-text">EXAMPLE:</span> ''TP53''; Variable LOF mutations
|<span class="blue-text">EXAMPLE:</span> ''TP53''; Variable LOF mutations
Line 157: Line 155:
|Unknown
|Unknown
|Unknown
|Unknown
|Pan-JAK and selective JAK3 inhibitors have been suggested as potential therapeutic options<ref name=":10" /><ref>{{Cite journal|last=Nairismägi|first=M.-L.|last2=Gerritsen|first2=M. E.|last3=Li|first3=Z. M.|last4=Wijaya|first4=G. C.|last5=Chia|first5=B. K. H.|last6=Laurensia|first6=Y.|last7=Lim|first7=J. Q.|last8=Yeoh|first8=K. W.|last9=Yao|first9=X. S.|date=2018-05|title=Oncogenic activation of JAK3-STAT signaling confers clinical sensitivity to PRN371, a novel selective and potent JAK3 inhibitor, in natural killer/T-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/29434279|journal=Leukemia|volume=32|issue=5|pages=1147–1156|doi=10.1038/s41375-017-0004-x|issn=1476-5551|pmc=5940653|pmid=29434279}}</ref>. [https://clinicaltrials.gov/study/NCT02974647 Clinical trials evaluating JAK inhibitors] are in progress.
|Pan-JAK and selective JAK3 inhibitors have been suggested as potential therapeutic options<ref name=":10" /><ref name=":33">{{Cite journal|last=Nairismägi|first=M.-L.|last2=Gerritsen|first2=M. E.|last3=Li|first3=Z. M.|last4=Wijaya|first4=G. C.|last5=Chia|first5=B. K. H.|last6=Laurensia|first6=Y.|last7=Lim|first7=J. Q.|last8=Yeoh|first8=K. W.|last9=Yao|first9=X. S.|date=2018-05|title=Oncogenic activation of JAK3-STAT signaling confers clinical sensitivity to PRN371, a novel selective and potent JAK3 inhibitor, in natural killer/T-cell lymphoma|url=https://pubmed.ncbi.nlm.nih.gov/29434279|journal=Leukemia|volume=32|issue=5|pages=1147–1156|doi=10.1038/s41375-017-0004-x|issn=1476-5551|pmc=5940653|pmid=29434279}}</ref>. [https://clinicaltrials.gov/study/NCT02974647 Clinical trials evaluating JAK inhibitors] are in progress.
|
|
|-
|-
Retrieved from "https://content.ccga.io/index.php/HAEM5:Extranodal_NK/T-cell_lymphoma"