HAEM5:B-lymphoblastic leukaemia/lymphoma with hypodiploidy: Difference between revisions

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|No
|No
|Approximately 50% of children with low-hypodiploid B-ALL/LBL carry germline ''TP53'' variants associated with Li–Fraumeni syndrome, an autosomal dominant disorder caused by ''TP53'' mutations. These alterations correlate with low-hypodiploid ALL (32–39 chromosomes) and poorer clinical outcomes<ref name=":2" />.
|Approximately 50% of children with low-hypodiploid B-ALL/LBL carry germline ''TP53'' variants associated with Li–Fraumeni syndrome, an autosomal dominant disorder caused by ''TP53'' mutations. These alterations correlate with low-hypodiploid ALL (32–39 chromosomes) and poorer clinical outcomes<ref name=":2" />.
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|''RB1''
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|Tumor Supressor Gene
|Common
|No established significance
|No
|Associated with low-hypodiploid B-ALL.
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|''IKZF2''
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|Transcription
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|<span class="blue-text">EXAMPLE:</span> ''TP53''; Variable LOF mutations
|<span class="blue-text">EXAMPLE:</span> ''TP53''; Variable LOF mutations
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|''NF1, NRAS, KRAS, MAPK1, FLT3 or PTPN11''; Activating mutations<ref name=":2" />
|''NF1, NRAS, KRAS, MAPK1, FLT3 or PTPN11''; Activating mutations<ref name=":2" />
|RTK or Ras signaling  
|RTK or Ras signaling
|Constitutive activation of mitogenic and anti-apoptotic pathways, driving uncontrolled cell proliferation, survival, and malignant transformation
|Constitutive activation of mitogenic and anti-apoptotic pathways, driving uncontrolled cell proliferation, survival, and malignant transformation
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