of Laboratory Medicine and Pathology, National Center for Cancer Care
and Research, Hamad Medical Corporation, Doha, Qatar.
2 Department of Laboratory Medicine and Pathology, Hamad Medical Corporation, Doha, Qatar.
3 Weill Cornell Medicine-Qatar, Doha, Qatar.
4 Department of Clinical Pathology, National Cancer Institute, Cairo, Egypt.
5 Department of Hematology and Medical Oncology, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
6 PET/CT Center, Clinical Imaging, National Center for Cancer Care and Research, Hamad Medical Corporation, Doha, Qatar.
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Plasma cell neoplasms can show aberrant expression of different
lineage-related antigens; however, co-expression of T-cell-associated
markers on malignant plasma cells is extremely rare.
1. Clinical, morphologic, immunophenotypic and cytogenetics features of
cases of plasma cell neoplasm with aberrant expression of T-cell
|Figure 1. Case (1): BM
aspirate at relapse (100x) revealed extensive infiltration with many
myeloma cells showing marked pleomorphism including many forms with
plasmablastic and anaplastic morphology (with marked nuclear
irregularities) (A and B) and increased mitotic figures (B, black
|Figure 2. Case (1): Flow cytometry on BM aspirate showing a large population of monotypic plasma cells showing variation in forward scatter (cell size) and side scatter (cytoplasm complexity), and are positive for: CD45, CD38, CD138 and dim CD10 (majority) with cytoplasmic lambda light chain expression and aberrant expression of CD33 and CD4 (majority). A subpopulation of plasma cells (~ 10%) shows aberrant expression of CD7. Plasma cells are negative for CD19, CD20, CD117 or CD56.|
|Figure 3. Case (1): BM biopsy (H&E; 50x) (A): showing extensive infiltration by myeloma cells of plasmablastic morphology with prominent nucleoli. By IHC: The PCs were Lambda restricted (B), negative for Kappa (C) with aberrant expression of CD4 (D) and partial expression of CD7 (E) and CD3 (weak positive cells) (F). The myeloma cells showed a very high mitotic index reflected by KI-67 >90% (G).|
|Figure 4. Case (1): FDG PET/CT showing intramedullary and extramedullary involvement: MIP image (A), sagittal CT (B), sagittal fused (C), transaxial CT (D, F) and transaxial fused (E, G)
images showing multiple intramedullary lesions in bilateral humerus and
femur (red arrowheads), multiple newly developed FDG-avid subcutaneous
nodules in the right upper chest wall (green arrowhead) and right lower
renal pole lesion (blue arrowhead).
|Figure 5. Case (3): FDG PET/CT showing extramedullary involvement: maximum intensity projection (MIP) image (A), coronal CT (B), coronal fused (C) and transaxial fused images (D-G)
showing multiple enlarged left axillary and supracalvicular lymph nodes
(red arrowheads), left humeral head and neck lesion (green arrowhead),
intramuscular involvements (blue arrowheads), FDG-avid peripancreatic
lymph node (yellow arrowhead) and paracardiac lymph node (orange
|Figure 6. Case (3): Lymph node biopsy showed diffuse sheets of PCs with many plasmablasts, scattered anaplastic forms and significantly increased mitotic figures (H & E 20x) (A). The neoplastic PCs are positive for CD138 immunostain (B) and CD3 (weak) (C)|