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Checkpoint inhibitors in hematological malignancies
#MMPMID28482851
Ok CY
; Young KH
J Hematol Oncol
2017[May]; 10
(1
): 103
PMID28482851
show ga
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.
|*Molecular Targeted Therapy
[MESH]
|Antigen-Presenting Cells/immunology
[MESH]
|Antigens, CD/*drug effects/physiology
[MESH]
|Antineoplastic Agents, Immunological/adverse effects/*therapeutic use
[MESH]
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