- Home
- Search Results
- Page 1 of 1
Search for: All records
-
Total Resources1
- Resource Type
-
0000000001000000
- More
- Availability
-
10
- Author / Contributor
- Filter by Author / Creator
-
-
Alexandrescu, Sanda (1)
-
Ceol, Craig (1)
-
Das, Sanjukta (1)
-
Feng, Hui (1)
-
Floru, Alexander E (1)
-
George, Rani E (1)
-
Iorgulescu, J Bryan (1)
-
Kashy, Daniel (1)
-
Kemet, Chinyere (1)
-
Keskin, Derin B (1)
-
Kwok, Lauren (1)
-
Lam, Andrew (1)
-
Lin, Liang (1)
-
Liu, Ching-Ti (1)
-
Lloyd, Kenneth (1)
-
Meara, Grace K (1)
-
Meijers, Rob (1)
-
Nagaraju, Raghavendar T (1)
-
Ni, Hongru (1)
-
Qin, Xiaodan (1)
-
- Filter by Editor
-
-
& Spizer, S. M. (0)
-
& . Spizer, S. (0)
-
& Ahn, J. (0)
-
& Bateiha, S. (0)
-
& Bosch, N. (0)
-
& Brennan K. (0)
-
& Brennan, K. (0)
-
& Chen, B. (0)
-
& Chen, Bodong (0)
-
& Drown, S. (0)
-
& Ferretti, F. (0)
-
& Higgins, A. (0)
-
& J. Peters (0)
-
& Kali, Y. (0)
-
& Ruiz-Arias, P.M. (0)
-
& S. Spitzer (0)
-
& Sahin. I. (0)
-
& Spitzer, S. (0)
-
& Spitzer, S.M. (0)
-
(submitted - in Review for IEEE ICASSP-2024) (0)
-
-
Have feedback or suggestions for a way to improve these results?
!
Note: When clicking on a Digital Object Identifier (DOI) number, you will be taken to an external site maintained by the publisher.
Some full text articles may not yet be available without a charge during the embargo (administrative interval).
What is a DOI Number?
Some links on this page may take you to non-federal websites. Their policies may differ from this site.
-
Solid tumors, especially those with aberrant MYCN activation, often harbor an immunosuppressive microenvironment to fuel malignant growth and trigger treatment resistance. Despite this knowledge, there are no effective strategies to tackle this problem. We found that chemokine-like factor (CKLF) is highly expressed by various solid tumor cells and transcriptionally up-regulated by MYCN. Using the MYCN-driven high-risk neuroblastoma as a model system, we demonstrated that as early as the premalignant stage, tumor cells secrete CKLF to attract CCR4-expressing CD4+cells, inducing immunosuppression and tumor aggression. Genetic depletion of CD4+T regulatory cells abolishes the immunorestrictive and protumorigenic effects of CKLF. Our work supports that disrupting CKLF-mediated cross-talk between tumor and CD4+suppressor cells represents a promising immunotherapeutic approach to battling MYCN-driven tumors.more » « less
An official website of the United States government
