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

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|No established significance
|No established significance
|No (NCCN)
|No (NCCN)
|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. Accordingly, genetic counseling is recommended for children with low-hypodiploid B-ALL carrying ''TP53'' mutations, and their relatives<ref name=":17" />.  
|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. Accordingly, genetic counseling is recommended for children with low-hypodiploid B-ALL carrying ''TP53'' mutations, and their relatives<ref name=":17" />. In contrast to childhood cases, ''TP53'' mutations in low-hypodiploid adult B-ALL are somatic, are not found in healthy hematopoietic cells, and not detectable in remission samples<ref name=":2" /><ref name=":6" />.  
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|''RB1''
|''RB1''
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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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|''IKZF1, IKZF2, IKZF3, PAX5, EBF1, VPREB1''
|''IKZF1, IKZF2, IKZF3, PAX5, EBF1, VPREB1''