Immune Netw.
2018 Aug;18(4):e29. 10.4110/in.2018.18.e29.
Chemokine Network and Overall Survival in TP53 Wild-Type and Mutant Ovarian Cancer
- Affiliations
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- 1Department of Biochemistry and Cancer Biology, Meharry Medical College, Nashville, TN 37208, USA. dson@mmc.edu
- 2Department of Pharmaceutical Sciences, College of Pharmacy, Florida A&M University, Tallahassee, FL 32301, USA.
- 3Department of Obstetrics and Gynecology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
- 4Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, TN 37203, USA.
- 5Division of Epidemiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN 37203, USA.
- 6Department of Chemistry, Tennessee State University, Nashville, TN 37209, USA.
- KMID: 2419774
- DOI: http://doi.org/10.4110/in.2018.18.e29
Abstract
- Ovarian cancer (OC) has the highest mortality rate among gynecological malignancies. Because chemokine network is involved in OC progression, we evaluated associations between chemokine expression and survival in tumor suppressor protein p53 (TP53) wild-type (TP53WT) and mutant (TP53m) OC datasets. TP53 was highly mutated in OC compared to other cancer types. Among OC subtypes, CXCL14 was predominantly expressed in clear cell OC, and CCL15 and CCL20 in mucinous OC. TP53WT endometrioid OC highly expressed CXCL14 compared to TP53m, showing better progression-free survival but no difference in overall survival (OS). TP53m serous OC highly expressed CCL8, CCL20, CXCL10 and CXCL11 compared to TP53WT. CXCL12 and CCL21 were associated with poor OS in TP53WT serous OC. CXCR2 was associated with poor OS in TP53m serous OC, while CXCL9, CCL5, CXCR4, CXCL11, and CXCL13 were associated with better OS. Taken together, specific chemokine signatures may differentially influence OS in TP53WT and TP53m OC.
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