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PERSPECTIVE ARTICLE
G. Semenzato et al.
The discovery of genetic lesions and/or biological features universally recognized as robust and reliable markers that predict the patients who are or who are not at risk of a subsequent diagnosis of T-LGLL is an unmet clinical need. Studying the temporal longitudinal dynamics of T-CUS with aging, as well as the correlation with clone size, and possibly of subclones, is warranted. However, the small number of rogue cells typically creates a limitation to this approach. Furthermore, the discovery of new dependencies beyond the STAT pathways may reveal new vulnerabilities in leuke- mic cells which could be targeted by innovative strategies. Bridging these gaps would ultimately contribute to over- coming reliance on numerical cutoffs, which are currently the standard criteria to differentiate the benign condition from the T-LGLL-related malignancy. Our understanding of the matter may also be translated into an appropriate diagnostic interpretation that distinguishes T-CUS from T-cell malignancies. This translation, leveraging on specific biological or genetic markers, will bring the field closer to
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an answer empowering treating physicians with greater confidence in informing patients about their risk of pro- gression and, ultimately, in improving clinical management.
Disclosures
No conflicts of interest to disclose.
Contributions
GS led the writing of the article with input from the other authors. All the authors read and approved the final man- uscript.
Funding
GS acknowledges support from the “Associazione Italiana Ricerca contro il Cancro” (AIRC, IG-20216 to GS and IG-29058 to RZ), “Associazione Italiana contro le Leucemie-Linfomi e Mieloma” (AIL), and Italian PNRR funds “National Center for Gene Therapy and Drugs Based on RNA Technology” (Project no. CN00000041 CN3 Spoke #6 “RNA chemistry”).
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