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KMT2D抑制了Sonic刺驱动的脑髓母细胞瘤的进展和转移

Reeti Mayur Sanghrajka^1,2, Richard Koche³, Hector Medrano¹

¹Developmental Biology Program, Sloan Kettering Institute of Memorial Sloan Kettering Cancer Center, New York, NY, USA.

|October 12, 2023

概括

对KMT2D基因的损失促进了Sonic刺驱动性脑髓母细胞瘤 (SHH-MB) 的转移. 这一发现表明,KMT2D突变可以预测哪些SHH-MB患者患转移性疾病的风险更高.

科学领域:

在瘤学瘤学.
遗传学是一个遗传学.
分子生物学分子生物学

背景情况:

脑髓母细胞瘤转移是死亡的主要原因.
在Sonic刺驱动的脑髓母细胞瘤 (SHH-MB) 中转移的分子驱动因素尚不清楚.

研究的目的:

研究KMT2D (MLL2) 在SHH-MB转移中的作用.
为了确定SHH-MB患者KMT2D突变的预后价值.

主要方法:

利用了SHH-MB.的基因小鼠模型.
分析了瘤的转录和染色质景观.
检查了异质合体Kmt2d损失对瘤进展和分化的影响.

主要成果:

在SHH-MB模型中,Kmt2d的异合性损失显著增加了疾病透率,降低了存活率,并促进了后脑入侵和脊髓转移.
Kmt2d损失抑制了神经分化和改变了基因表达,有利于前转移性途径 (TGFβ,Notch,Myc).
确定了转录格局向晚期癌症和转移性基因特征的转变.

结论:

在SHH-MB中,KMT2D充当瘤抑制剂.
二次异构的KMT2D突变可以作为SHH-MB患者转移风险的预后生物标志物.

关键词:

癌症癌症癌症癌症遗传学是一个遗传学.模型生物模型生物.

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