MDTI - Dale Frank Lectures

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Can you name the MDTI NHL buzzwords?

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marrow replacement leads to severe anemia
lipid vacuoles in cells
diagnosis (immunophenotype) of exclusion; BCL2+, CD10-, BCL6-
morphology (centroblastic/immunoblastic) not important
most common lymphoid malignancy in African Americans
most common leukemia in adults
treatment must begin IMMEDIATELY
serum hyperviscosity
osteoclast activation leads to hypercalcemia
3 cardinal features: small mature lymphos, monocytoid B cells, plasma cells
deletion 13q/11q/trisomy 12/17p
Most common NHL
50% IgG, 25% IgA
renal failure (casting) due to paraprotein
15-30% become prolymphocytic leukemia
30-50% transform to DLBCL
grading based on centroblast number/nodular vs. diffuse growth
three separate diseases: nodal, extranodal, splenic
1/3 of all NHL's
express CD56 (NCAM)
fish-flesh appearance
plasma cells account for 10% of cellularity
interstitial aggregates
60% nodal, 40% extranodal in GI (unlike indolent lymphomas)
extreme paraprotein production
most common lymphoid malignancy in childhood
BCL6+, CD10+, BCL2-
multifocal, destroys bone
mott cells
aggressive extranodal with CNS involvement
not technically a lymphoma, but does involve mature B cells
10% undergo Richter's transformation
t(8;14) cMYC translocation
abdominal (ileocecal) masses more common
extranodal involvement uncommon
Ki67 rate is low
lymphoepithelial lesions
Does dale frank hate medical students? (T/F)
flame cell
diffuse effacement/psuedofollicles
paraprotein production (sometimes)
MUM1 (IRF4), BCL6, BCL10 positive
Bence Jones protein
male to female ratio is 2:1
hypovolemia due to hypercalcemia
EBV positive is sometimes seen (not burkitt's!)
peripheral blood involvement very common
presents at single site, bring patients in early
severe immunodeficiency due to paraprotein
85% Bone Marrow involvement
Toughie: tumor inhibiting miR-15a/MiR-16-1 lost with 13q deletion
age>60, LDH levels up, multiple extranodal involvement are all bad prognostic signs
can evolve or start de novo
two main types: germinal center or activated b cell
paratrabecular aggregates
huge expansion of marginal zone
smudge cells
Observation/Rituximab/CHOP as treatment
three main types: endemic, sporadic, everyone has aids
Zap 70+ or Zap 70 -
really attacks facial bones
spectrum from monoclonal gammopathy of undetermined significance
Ki67 100%
10-15% get AIHA caused by benign cells
uncommon, less than 5 percent
arises from chronic inflammation (h.pylori, campy, burrelia, HepC?)
proliferation rate is high, Ki67+ 40-90%
t(11:18) common/ also t(1:14) and t(14:18)
spread quickly to other mucosal sites but may be treated with antibiotics early
starry sky
pleiomorphic and heterogenous, difficult to predict behavior

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