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2014 ; 15
(9
): 1153-62
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gab.com Text
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English Wikipedia
Inhibition of STAT3 activity re-activates anti-tumor immunity but fails to
restore the immunogenicity of tumor cells in a B-cell lymphoma model
#MMPMID24915165
Cao Y
; Zhou X
; Zhou M
; Xu D
; Ma Q
; Zhang P
; Huang X
; Li Q
; Ma D
; Zhou J
Cancer Biol Ther
2014[Sep]; 15
(9
): 1153-62
PMID24915165
show ga
A large number of patients with advanced lymphoma become refractory or relapse
after initial treatment due to the persistence of minimal residual disease. Ideal
immunotherapy strategy for eradicating the minimal residual disease of lymphoma
and preventing the tendency to relapse need to be developed. Here, we use a mice
model mimicked the disease entities of aggressive B-cell lymphoma dynamically to
analyze the host anti-lymphoma immunity during the progression of lymphoma. We
have shown that STAT3 activity was gradually enhanced in host immune effector
cells with the progression of lymphoma. Inhibition of the STAT3 activity with a
small molecule inhibitor was able to effectively enhance the function of both
host innate and adaptive immunity, and thereby delayed the progression of
lymphoma. Despite the therapeutic benefits were achieved by using of the STAT3
inhibitor, disrupting of STAT3 pathway did not prevent the eventual development
of lymphoma due to the presence of point mutation of ?2M, which controls immune
recognition by T cells. Our findings highlight the complexity of the mechanism of
immune evasion; therefore a detailed analysis of genes involved in the immune
recognition process should be essential before an elegant immunotherapy strategy
could be conducted.