Skip to main content
. Author manuscript; available in PMC: 2018 Jul 11.
Published in final edited form as: Semin Oncol. 2017 Jul 11;44(2):101–112. doi: 10.1053/j.seminoncol.2017.06.005

Table 3.

Integrins implicated in chemoresistance in ALL

Integrin Target Expression Function in malignant cells Reference/s
Integrin α4β1 or VLA-4 (very late antigen-4) Binds to VCAM-1 (vascular cell adhesion molecule-1) expressed on bone marrow stromal cells and osteoblasts

  • VLA-4/VCAM-1 interactions required for engraftment of human B-ALL in immunocompromised mice

  • VLA-4/VCAM-1 interaction protected B-ALL cells from apoptotic cell death induced by variety of chemotherapy agents

  • These interactions activate pro-survival pathways such as PI3K/Akt

  • VLA-4/VCAM-1 interaction activated reciprocal NF-κb signaling in contacting ALL/AML cells and stromal cells

  • VLA4/VCAM-1 mediated adhesion to bone marrow stromal cells induced resistance to vincristine in lymphoma cells

  • VLA-4 played a critical role in CAM-DR in multiple myeloma cells
Integrin α5β1 or VLA-5 (very late antigen-5) Also binds to VCAM-1 (vascular cell adhesion molecule-1)

  • Bcr/Abl tyrosine kinase expressed by patients presenting with the Philadelphia chromosome stimulates VLA-5 function.

  • VLA-5 mediated adhesion to bone marrow stromal cells protected Ph+ ALL cells from imatinib-induced apoptosis

  • VLA-4/VCAM-1 interactions required for engraftment of Ph+ ALL in immunocompromised mice
Integrin αLβ2 or LFA-1 (leukocyte function- associated antigen-1) Binds to ICAM-1 (intercellular cell adhesion molecule-1) on bone marrow stromal cells

  • LFA-1/ICAM-1 interaction enhanced the survival of T-ALL cells by decreasing the rate of apoptosis