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Abstract 755: Antagonistic effect of M-MDSC and N-MDSC during astrocytoma progression

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Abstract The traditional dogma holds that tumor size has a positive correlation with tumor progression. However, on murine orthotopical astrocytoma model ALTS1C1, we found that the tumor growth is not a linear function instead a shrinkage and regrowth wave was noticed. To examine the un-characteristic tumor growth behavior, the relative relationship among tumor cells, brain resident cells, such as astrocytes and microglia, and infiltrating cells, such as monocytic (CD45+CD11b+) or lymphocytic (CD45+CD11b-) lineage cells, was analyzed by flow cytometry and immunohistochemistry (IHC). Not only tumor area, peripheral organs, including spleen, blood, and lymph nodes were also examined. The preliminary data showed that in tumor shrinkage stage, CD3+ lymphocytes increased dramatically, while CD11b+CD45low microglia decreased. Furthermore, we found that the change of two subtypes of myeloid derived suppressor cells (MDSCs), Ly6G+ neutrophilic MDSC (N-MDSC) and Ly6G- monocytic MDSC (M-MDSC), was in opposite direction during tumor progression. The increase of M-MDSCs is associated with the increase of tumor size while the N-MDSC is decreased. More interestingly, the flow cytometry data shows that the total amount of CD11b+ macrophages was constant during tumor growth phase, but IHC shows the different distribution pattern of macrophage subsets within different tumor regions (invasion tumor front vs tumor core). Currently, we are examining the dynamic change of these cells following irradiation to identify the cells that are responsive for tumor shrinkage and re-growth following radiation therapy for brain tumor. These results will be presented in the meeting. Citation Format: Chin-NIng Huang. Antagonistic effect of M-MDSC and N-MDSC during astrocytoma progression. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 755.
American Association for Cancer Research (AACR)
Title: Abstract 755: Antagonistic effect of M-MDSC and N-MDSC during astrocytoma progression
Description:
Abstract The traditional dogma holds that tumor size has a positive correlation with tumor progression.
However, on murine orthotopical astrocytoma model ALTS1C1, we found that the tumor growth is not a linear function instead a shrinkage and regrowth wave was noticed.
To examine the un-characteristic tumor growth behavior, the relative relationship among tumor cells, brain resident cells, such as astrocytes and microglia, and infiltrating cells, such as monocytic (CD45+CD11b+) or lymphocytic (CD45+CD11b-) lineage cells, was analyzed by flow cytometry and immunohistochemistry (IHC).
Not only tumor area, peripheral organs, including spleen, blood, and lymph nodes were also examined.
The preliminary data showed that in tumor shrinkage stage, CD3+ lymphocytes increased dramatically, while CD11b+CD45low microglia decreased.
Furthermore, we found that the change of two subtypes of myeloid derived suppressor cells (MDSCs), Ly6G+ neutrophilic MDSC (N-MDSC) and Ly6G- monocytic MDSC (M-MDSC), was in opposite direction during tumor progression.
The increase of M-MDSCs is associated with the increase of tumor size while the N-MDSC is decreased.
More interestingly, the flow cytometry data shows that the total amount of CD11b+ macrophages was constant during tumor growth phase, but IHC shows the different distribution pattern of macrophage subsets within different tumor regions (invasion tumor front vs tumor core).
Currently, we are examining the dynamic change of these cells following irradiation to identify the cells that are responsive for tumor shrinkage and re-growth following radiation therapy for brain tumor.
These results will be presented in the meeting.
Citation Format: Chin-NIng Huang.
Antagonistic effect of M-MDSC and N-MDSC during astrocytoma progression.
[abstract].
In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA.
Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 755.

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