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Hodgkin lymphoma
Classical subtypes – Nodular Sclerosis
Mixed cellularity
Lymphocyte rich
Lymphocyte depleted
Lymphocyte predominance
Lymph node structure
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.
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.
Pathogenesis
Pathogenesis
Non hodgkin
lymphoma(NHL)
Treatment
 DLBCL are aggressive tumor that are rapidly fatal
without t/t
 Intensive chemotherapy
 Adjuvant anti- CD20
DLBCL with myc translocation have worse prognosis.
Thank you

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LYMPHOMAS.pptx

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  • 4. Hodgkin lymphoma Classical subtypes – Nodular Sclerosis Mixed cellularity Lymphocyte rich Lymphocyte depleted Lymphocyte predominance
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  • 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.
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  • 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.
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