4.6 Review

Latest Contributions of Genomics to T-Cell Acute Lymphoblastic Leukemia (T-ALL)

期刊

CANCERS
卷 14, 期 10, 页码 -

出版社

MDPI
DOI: 10.3390/cancers14102474

关键词

T-cell acute lymphoblastic leukemia; genomics; non-coding; germline; aging; relapse

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资金

  1. AECC [GC16173697BIGA]
  2. ISCIII [PI19/01828]
  3. ERDF/ESF, A way to make Europe/Investing in your future
  4. CERCA/Generalitat de Catalunya (GRC)/La Caixa [SGR 2017 288]
  5. AGAUR [2020 FI_B2 00210]

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Thanks to high-resolution genetic techniques, we now have a clearer understanding of the genetic landscape in T-ALL and have begun to understand relapse-specific mechanisms. This review summarizes the latest advances in our knowledge of the genome in T-ALL and highlights the areas where research in this ALL subtype is progressing.
Simple Summary Thanks to the use of high-resolution genetic techniques to detect cryptic aberrations present in T-ALL, we now have a clearer view of the genetic landscape that explains the particular oncogenetic processes taking place in each T-ALL. We also have begun to understand relapse-specific mechanisms. This review aims to summarize the latest advances in our knowledge of the genome in T-ALL and highlight the areas where the research on this ALL subtype is progressing, thereby identifying the key issues that need to be addressed in the medium-to-long term to move forward in the applicability of this knowledge into clinics. As for many neoplasms, initial genetic data about T-cell acute lymphoblastic leukemia (T-ALL) came from the application of cytogenetics. This information helped identify some recurrent chromosomal alterations in T-ALL at the time of diagnosis, although it was difficult to determine their prognostic impact because of their low incidence in the specific T-ALL cohort analyzed. Genetic knowledge accumulated rapidly following the application of genomic techniques, drawing attention to the importance of using high-resolution genetic techniques to detect cryptic aberrations present in T-ALL, which are not usually detected by cytogenetics. We now have a clearer appreciation of the genetic landscape of the different T-ALL subtypes at diagnosis, explaining the particular oncogenetic processes taking place in each T-ALL, and we have begun to understand relapse-specific mechanisms. This review aims to summarize the latest advances in our knowledge of the genome in T-ALL. We highlight areas where the research in this subtype of ALL is progressing with the aim of identifying key questions that need to be answered in the medium-long term if this knowledge is to be applied in clinics.

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