MDTI - Dale Frank Lectures

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Can you name the MDTI NHL buzzwords?

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Prompt
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
13q/14q32
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
Prompt
most common lymphoid malignancy in childhood
BCL6+, CD10+, BCL2-
CD5+/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
rouleaux
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
Prompt
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
BCL2+
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 -
prolymphocytes/paraimmunoblasts
really attacks facial bones
spectrum from monoclonal gammopathy of undetermined significance
Ki67 100%
10-15% get AIHA caused by benign cells
t(14:18)
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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