Match each patient's clinical and histopathologic presentation with the primary molecular mechanism driving their underlying neoplastic process.
- A 65-year-old man presents with generalized lymphadenopathy. Biopsy shows an aggressive proliferation of small to medium-sized CD5-positive, CD23-negative B cells.Overexpression of a regulatory protein that promotes cell cycle progression from the G1 phase to the S phase.
- A 58-year-old woman with a history of painless, waxing and waning lymphadenopathy undergoes a biopsy showing nodular aggregates of neoplastic cells lacking tingible body macrophages.Overexpression of a mitochondrial protein that inhibits the release of cytochrome c.
- A 48-year-old man presents with early satiety and massive splenomegaly. Labs show a leukocyte count of with a full spectrum of granulocytic differentiation and low leukocyte alkaline phosphatase.Constitutive activation of a non-receptor tyrosine kinase signaling pathway.
- A 25-year-old man presents with a rapidly expanding neck mass. Biopsy reveals uniform, medium-sized lymphoid cells with numerous mitotic figures and interspersed macrophages containing apoptotic debris.Overexpression of a nuclear transcription factor that functions as a master regulator of cellular proliferation.
Answer
The correct pairings match Mantle cell lymphoma with cell cycle progression (Cyclin D1); Follicular lymphoma with inhibition of apoptosis (BCL-2); Chronic myeloid leukemia with activated tyrosine kinase signaling (BCR-ABL); and Burkitt lymphoma with transcription factor overexpression (c-Myc).
Each correct pairing accurately links the diagnostic clinical/pathologic features of a hematologic malignancy to the precise intracellular mechanism of its primary oncogenic driver (Cyclin D1 for Mantle Cell, BCL-2 for Follicular, BCR-ABL for CML, and c-Myc for Burkitt).
Step-by-Step Solution
Key Concept
Molecular pathogenesis of hematologic malignancies via specific chromosomal translocations.