Checkpoint inhibitors in hematological malignancies.

Journal Article (Journal Article;Review)

Inhibitory molecules such as PD-1, CTLA-4, LAG-3, or TIM-3 play a role to keep a balance in immune function. However, many cancers exploit such molecules to escape immune surveillance. Accumulating data support that their functions are dysregulated in lymphoid neoplasms, including plasma cell myeloma, myelodysplastic syndrome, and acute myeloid leukemia. In lymphoid neoplasms, aberrations in 9p24.1 (PD-L1, PD-L2, and JAK2 locus), latent Epstein-Barr virus infection, PD-L1 3'-untranslated region disruption, and constitutive JAK-STAT pathway are known mechanisms to induce PD-L1 expression in lymphoma cells. Clinical trials demonstrated that PD-1 blockade is an attractive way to restore host's immune function in hematological malignancies, particularly classical Hodgkin lymphoma. Numerous clinical trials exploring PD-1 blockade as a single therapy or in combination with other immune checkpoint inhibitors in patients with hematologic cancers are under way. Although impressive clinical response is observed with immune checkpoint inhibitors in patients with certain cancers, not all patients respond to immune checkpoint inhibitors. Therefore, to identify best candidates who would have excellent response to checkpoint inhibitors is of utmost importance. Several possible biomarkers are available, but consensus has not been made and pursuit to discover the best biomarker is ongoing.

Full Text

Duke Authors

Cited Authors

  • Ok, CY; Young, KH

Published Date

  • May 8, 2017

Published In

Volume / Issue

  • 10 / 1

Start / End Page

  • 103 -

PubMed ID

  • 28482851

Pubmed Central ID

  • PMC5422942

Electronic International Standard Serial Number (EISSN)

  • 1756-8722

Digital Object Identifier (DOI)

  • 10.1186/s13045-017-0474-3


  • eng

Conference Location

  • England