16. Classification (WHO)
Nodular Sclerosis Classical Hodgkin
Mixed cellularity
Lymphocyte rich
Lymphocyte depleted
Lymphocyte predominance
First 4 types – Reed- sternberg cells have similar
immunotype, Lymphocyte predominance have
distinctive B cell immunophenotype.
17. Pathogenesis
Activation of the transcription factor NF-kB is common event in
classical hodgkin.
NF-kB can be activated by –
1. EBV infection
2. EBV tumor cells LMP-1
3. Loss of function mutations in IkB or A20(alpha induced protein 3)
Activation of NF-kB by EBV or other mechanism rescues crippled
germinal centre B cells from apoptosis, further mutations turn these to
RS cells.
RS cell – aneuploid and possess diverse aclonal chromosomal
aberrations.
Most common is gain in REL protooncogene that contribute to increase
in NF-kB activity.
49. Treatment
DLBCL are aggressive tumor that are rapidly fatal
without t/t
Intensive chemotherapy
Adjuvant anti- CD20
DLBCL with myc translocation have worse prognosis.