Acute lymphoblastic leukemia (ALL) is the most common cancer among children. Recent advances in chemotherapy have made ALL a curable haematological malignancy. In children, there is 25% chance of disease relapse, typically in the central nervous system. While in adults, there is a higher chance of relapse. ALL may affect B-cell or T-cell lineages. Different genetic alterations characterize the two ALL forms. Deregulated Notch, either Notch1 or Notch3, and CXCR4 receptor signaling are involved in ALL disease development and progression. By analyzing their relevant roles in the pathogenesis of the two ALL forms, new molecular mechanisms able to modulate cancer cell invasion may be visualized. Notably, the partnership between Notch and CXCR4 may have considerable implications in understanding the complexity of T- and B-ALL. These two receptor pathways intersect other critical signals in the proliferative, differentiation and metabolic programs of lymphocyte transformation. Also, the identification of the crosstalks in leukemia-stroma interaction within the tumor microenvironment may unveil new targetable mechanisms in disease relapse. Further studies are required to identify new challenges and opportunities to develop more selective and safer therapeutic strategies in ALL progression, possibly contributing to improve conventional haematogical cancer therapy.

Notch/CXCR4 partnership in acute lymphoblastic leukemia progression / Tsaouli, Georgia; Ferretti, Elisabetta; Bellavia, Diana; Vacca, Alessandra; Felli, MARIA PIA. - In: JOURNAL OF IMMUNOLOGY RESEARCH. - ISSN 2314-8861. - (2019).

Notch/CXCR4 partnership in acute lymphoblastic leukemia progression

Georgia Tsaouli
Writing – Original Draft Preparation
;
Elisabetta Ferretti
Conceptualization
;
Diana Bellavia
Conceptualization
;
Alessandra Vacca
Writing – Original Draft Preparation
;
Maria Pia Felli
Writing – Review & Editing
2019

Abstract

Acute lymphoblastic leukemia (ALL) is the most common cancer among children. Recent advances in chemotherapy have made ALL a curable haematological malignancy. In children, there is 25% chance of disease relapse, typically in the central nervous system. While in adults, there is a higher chance of relapse. ALL may affect B-cell or T-cell lineages. Different genetic alterations characterize the two ALL forms. Deregulated Notch, either Notch1 or Notch3, and CXCR4 receptor signaling are involved in ALL disease development and progression. By analyzing their relevant roles in the pathogenesis of the two ALL forms, new molecular mechanisms able to modulate cancer cell invasion may be visualized. Notably, the partnership between Notch and CXCR4 may have considerable implications in understanding the complexity of T- and B-ALL. These two receptor pathways intersect other critical signals in the proliferative, differentiation and metabolic programs of lymphocyte transformation. Also, the identification of the crosstalks in leukemia-stroma interaction within the tumor microenvironment may unveil new targetable mechanisms in disease relapse. Further studies are required to identify new challenges and opportunities to develop more selective and safer therapeutic strategies in ALL progression, possibly contributing to improve conventional haematogical cancer therapy.
2019
Notch CXCR4; T-cell leukemia; B-cell leukemia; progression
01 Pubblicazione su rivista::01g Articolo di rassegna (Review)
Notch/CXCR4 partnership in acute lymphoblastic leukemia progression / Tsaouli, Georgia; Ferretti, Elisabetta; Bellavia, Diana; Vacca, Alessandra; Felli, MARIA PIA. - In: JOURNAL OF IMMUNOLOGY RESEARCH. - ISSN 2314-8861. - (2019).
File allegati a questo prodotto
File Dimensione Formato  
Ferretti_Notch/CXCR4-partnership.pdf

solo gestori archivio

Tipologia: Documento in Post-print (versione successiva alla peer review e accettata per la pubblicazione)
Licenza: Tutti i diritti riservati (All rights reserved)
Dimensione 490.18 kB
Formato Adobe PDF
490.18 kB Adobe PDF   Contatta l'autore

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1286431
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 22
  • ???jsp.display-item.citation.isi??? 20
social impact