Relationship of Programmed Death-1 (PD-1) and Programmed Death Ligand-1 (PD-L1) Polymorphisms with Overall Cancer Susceptibility: An Updated Meta-Analysis of 28 Studies with 60 612 Subjects
BACKGROUND Programmed death-1 and its ligand-1 (PD-1/PD-L1) regulate tumor immunotherapy. A large number of studies have explored the relationship between PD-1, PD-L1, and different tumor susceptibility. However, these conclusions are not always consistent. Therefore, we updated this meta-analysis....
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Published in | Medical science monitor Vol. 27; pp. e932146 - e932146-17 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
International Scientific Literature, Inc
24.05.2021
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Subjects | |
Online Access | Get full text |
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Summary: | BACKGROUND Programmed death-1 and its ligand-1 (PD-1/PD-L1) regulate tumor immunotherapy. A large number of studies have explored the relationship between PD-1, PD-L1, and different tumor susceptibility. However, these conclusions are not always consistent. Therefore, we updated this meta-analysis. MATERIAL AND METHODS MEDLINE, Web of Science, EMBASE and other databases were searched systematically to obtain related research. Then, we used STATA15.0 software to carry out the final meta-analysis. The computational advantage is better than OR to evaluate this relationship. RESULTS A total of a total of 28 related studies were involved in our meta-analysis. It was found that PD-1 rs11568821 and rs7421861 increased the overall cancer probability in the allelic genetic model, while PD-1 rs36084323 effectively reduced the risk of cancer in the dominant genetic model. In the homozygous genetic model, PD-L1 rs17718883 effectively increased the probability of tumorigenesis. PD-L1rs4143815 is associated with a reduced incidence of cancer in heterozygote, homozygote and dominant genetic patterns. Subgroup analysis showed that PD-1rs2227981 can promote the susceptibility to breast cancer, while PD-1rs2227982 can reduce the susceptibility to breast cancer. PD-L1 rs2890658 can significantly reduce the risk of lung and liver cancer. CONCLUSIONS PD-1rs11568821, rs36084323, rs7421861, pD-L1rs17718883, and rs4143815 are associated with tumor susceptibility. However, a review based on more experimental evidence is needed to verify our findings.BACKGROUND Programmed death-1 and its ligand-1 (PD-1/PD-L1) regulate tumor immunotherapy. A large number of studies have explored the relationship between PD-1, PD-L1, and different tumor susceptibility. However, these conclusions are not always consistent. Therefore, we updated this meta-analysis. MATERIAL AND METHODS MEDLINE, Web of Science, EMBASE and other databases were searched systematically to obtain related research. Then, we used STATA15.0 software to carry out the final meta-analysis. The computational advantage is better than OR to evaluate this relationship. RESULTS A total of a total of 28 related studies were involved in our meta-analysis. It was found that PD-1 rs11568821 and rs7421861 increased the overall cancer probability in the allelic genetic model, while PD-1 rs36084323 effectively reduced the risk of cancer in the dominant genetic model. In the homozygous genetic model, PD-L1 rs17718883 effectively increased the probability of tumorigenesis. PD-L1rs4143815 is associated with a reduced incidence of cancer in heterozygote, homozygote and dominant genetic patterns. Subgroup analysis showed that PD-1rs2227981 can promote the susceptibility to breast cancer, while PD-1rs2227982 can reduce the susceptibility to breast cancer. PD-L1 rs2890658 can significantly reduce the risk of lung and liver cancer. CONCLUSIONS PD-1rs11568821, rs36084323, rs7421861, pD-L1rs17718883, and rs4143815 are associated with tumor susceptibility. However, a review based on more experimental evidence is needed to verify our findings. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Funds Collection Data Interpretation Literature Search Data Collection Study Design Manuscript Preparation Statistical Analysis |
ISSN: | 1643-3750 1234-1010 1643-3750 |
DOI: | 10.12659/MSM.932146 |