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Title: Phenotype and functional characteristics of myeloid-derived suppressor cells in solid tumors based on the example of colorectal and prostate cancer : implications for cancer immunotherapy
Abstract:
Prostate cancer (PC) and colorectal cancer (CRC) remain the most diagnosed malignancies worldwide. Myeloid-derived suppressor cells (MDSC) have pivotal role in their development due to caused immunosuppression. Hence, this study was focused on the characterization of MDSC in PC and CRC patients, and their relation to the cancer stage and the used treatment. The obtained results showed that in both cancers the Mo-MDSC seem to be most relevant. In CRC, the blood level of Mo-MDSC positively correlated with regulatory T cells, and negatively with the level of tumor antigen - Her2/neu, specific CD8+ T cells. Considering the effect of the treatment in PC patients, the study revealed that surgery or hormonal therapy alone did not affect the level of Mo-MDSC. In this case, only a combined therapy caused significant decrease in their level. In respect to Gr-MDSC, the level of this subset was comparable to the control group, regardless of the treatment the patients received. These results were independent of the PSA level, tumor grading and the clinical stage of the patients. In the case of CRC patients, after surgery it comes to increase of Mo-MDSC blood level, and its significant increase may be associated with tumor recurrence during a 5-year follow-up. In conclusion, Mo-MDSC seem to be pivotal players in CRC related immunosuppression and may be a ; ssociated with the risk of tumor recurrence after surgery. Whereas in PC, Mo-MDSC are resistant to a single form of therapy, such as surgery or hormone therapy. Thus Mo-MDSC should be considered as a potential therapy target in the treatment of PC and CRC to enhance its anti-tumor effectiveness.
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Rada Dyscypliny Nauki medyczne
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Last modified:
May 28, 2024
In our library since:
Feb 6, 2024
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71
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24
All available object's versions:
http://dl.cm-uj.krakow.pl:8080/publication/5022
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| Edition name | Date |
|---|---|
| ZB-136751 | May 28, 2024 |
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