P1/2, N=16, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Dec 2025 --> Dec 2027 | Trial primary completion date: Dec 2025 --> Dec 2027
1 day ago
Trial completion date • Trial primary completion date
Survival analyses revealed that co-high expression of SRSF1, HNRNPF, or PTBP1 and oncogenic MYC predicts poor clinical outcomes in MCL patients. Our data describe the clinical significance of aberrant SRSF1, hnRNP F, and PTBP1 in MCL and their tumor-promoting roles via the regulation of cancer hallmarks, which could be important in understanding MCL pathogenesis and therapeutic development.
6 days ago
Journal
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CASP3 (Caspase 3) • PTBP1 (Polypyrimidine Tract Binding Protein 1)
This risk-adapted approach reflects a paradigm shift in MCL management, emphasizing the need for early molecular risk assessment to guide treatment decisions. In this scenario, TP53 mutations are no longer supporting actors, but a game-changer for the prognosis and treatment of patients with MCL.
A notable feature of the HRS-like cells in this case is the gain of markers associated with CHL, such as CD30 and CD15. This immunophenotypic shift highlights the concept of lymphoma plasticity, where the tumor cells evolve in response to selective pressures, such as CAR T cell therapy.
9 days ago
Journal
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TP53 (Tumor protein P53) • CD19 (CD19 Molecule) • TNFRSF8 (TNF Receptor Superfamily Member 8) • CCND1 (Cyclin D1)
In addition, changes in cell buoyant mass within primary patient specimens ex vivo correlate with sensitivity to Bruton's tyrosine kinase inhibitors in vivo in MCL and chronic lymphocytic leukemia, another B cell malignancy. These findings highlight the value of biophysical properties as biomarkers of response in pursuit of future precision therapeutic strategies.