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20 Cards in this Set
- Front
- Back
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dwarf megakaryocytes
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CML
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phases of CML
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chronic phase
accelerated phase blast phase |
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number of blasts in chronic phase CML
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<2%
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number of blasts in accelerated phase CML
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10-19%
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number of blasts in blast phase CML
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>20%
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When can you see pseudo-Gaucher cells?
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CML aspirates can have pseudo-Gaucher cells, secondary to incr cell turnover and are derived from the neoplastic clone
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Why is the spleen enlarged in CML CP?
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Splenic enlargement occurs in CML-CP due to infiltration of the red pulp cords by different stages of maturing granulocytes
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What type of CML almost always has monocytosis?
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CML with p190 BCR-ABL almost always has monocytosis, can be confused with CMML
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basophils in CML?
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increased
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eosinophils in CML?
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increased
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platelets in CML?
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increased or can be normal
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BM cellularity in CML?
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increased, with larger than nl (i.e. 5-10 cells, vs nl 2-3 cells) paratrabecular cuff of immature neutrophils
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most common breakpoint in CML?
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p210 (M-BCR: major)
others are: p230 (longer, u-BCR) p190 (shorter fusion protein, m-BCR: minor) |
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in CML with p210, which other breakpoint can commonly be seen in small amounts?
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small amounts of p190 can be detected in >90% of CML pts with p230, due to alternative splicing
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treatment of CML?
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1st gen: imatinib - competes with ATP for BCR-ABL binding so BCR-ABL can't phosphorylate tyrK on its substrates
2nd gen: nilotinib and dasatinib - use when muts arise from imatinib |
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Most important prognostic indicator in CML?
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response to PTKI (protein tyrosine kinase inhibitor) at hematologic, cytogenetic, and molecular levels
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what cells harbor BCR-ABL fusion protein in CML?
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myeloid lineage
some lymphoid cells endothelial cells (abnl pluripotent stem cell) |
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BCR gene location?
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22q11.2
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ABL gene location?
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9q34
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90-95% of CML have what genetic abnormailty?
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t(9;22)(q34;q11.2) a reciprocal translocation resulting in the Philadelphia chromosome
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