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Cancer immunotherapy is a new treatment method in recent years.
It has not only revolutionized the effect of cancer treatment, but also revolutionized the concept of cancer treatment.
However, due to the small number of killer T lymphocytes in advanced breast tumors, the effect of immunotherapy is often unsatisfactory.
Recently, researchers from the Ohio State University Comprehensive Cancer Center published a new research report titled Metabolic modulation by CDK4/6 inhibitor promotes chemokine-mediated recruitment of T cells into mammary tumors in Cell Reports, and found that cyclins Dependent kinase (CDK) inhibitors can significantly improve the immunotherapy effect of recurrent breast cancer.
DOI: https://doi.
org/10.
1016/j.
celrep.
2021.
108944 In order to explore the impact of the CDK4/6 inhibitor PALBOCICLIB on the tumor immune microenvironment, researchers used the breast cancer MMTV-PyMT transgenic small Mice (FVB mice) and female C57BL/6 mice inoculated with PYMT tumor cells were analyzed to determine whether the efficacy of CDK4/6 inhibitors in different models (spontaneous and transplanted) and genetic background are consistent.
On this basis, the researchers analyzed the effect of CDK4/6 on the composition of the tumor immune microenvironment based on flow cytometry.
At the same time, they used spectrocytometry to characterize the effect of CDK4/6 on the phenotype of tumor infiltrating T cells.
Studies have found that CDK4/6 inhibitors can increase the number and activity of tumor T cells in mouse models of breast cancer.
CDK4/6 treatment increases the number and activity of T cells in mouse models of breast cancer.
Based on the above research, researchers speculate that the ability of CDK4/6 inhibitors to activate T cell levels may be used in cancer immunotherapy.
Consistent with expectations, the study found that compared with mice treated with only CDK4/6 inhibitors, mice inoculated with PYMT cells were stimulated with OX40 agonists and 4-1BB agonists, and then treated with CDK4/6 inhibitors.
Make chemokines "attract" T cells to invade the tumor, thereby more effectively inhibiting the growth of the tumor.
CDK4/6 improves immunotherapy response and promotes chemokine-mediated homing of T-cell tumors.
Earlier studies have shown that mTOR signaling pathway induces chemokines in certain immune cell subgroups, and it is also used in CDK4/6 inhibitors.
Targeting the PI3K/mTOR pathway in the context of treatment can improve tumor growth inhibition while preventing tumors from acquiring drug resistance through internal mechanisms.
https://doi.
org/10.
1186/s13058-020-01320-8 But because previous experiments used immunodeficient mice.
Therefore, in this latest study, the researchers tested how the combined inhibition of CDK4/6 and mTOR affects tumor growth and immune infiltration in immune-normal mice.
The study found that in the combined treatment group of CDK4/6i and mTORi, tumor growth was significantly inhibited.
Next, the researchers tried to determine how exactly mTOR regulates the expression of chemokines in CDK4/6i-treated cells? As we all know, the mTOR signaling pathway is the central regulator of cell metabolism, while glucose and glutamine are key nutrients required for the growth of cancer cells, and their consumption reflects the metabolic needs of cells.
Therefore, the researchers examined the glucose uptake rate and glutamine utilization in MCF7 cells treated with CDK4/6 to further analyze whether CDK4/6-treated cells have metabolic activity.
Studies have found that the mTOR signaling pathway is required to maintain the metabolic activity of cells treated with CDK4/6.
CDK4/6-mediated chemokine induction requires mTOR-regulated metabolic activity.
In summary, the study shows that CDK4/6 inhibitors can provide a new therapeutic strategy for attracting T cells to breast tumors, thereby increasing the sensitivity of immunotherapy Sex.
It is hoped that this new research can improve the survival time of breast cancer and bring breakthrough progress to the first-line treatment of advanced breast cancer.
End reference materials: [1]https://doi.
org/10.
1016/j.
celrep.
2021.
108944
It has not only revolutionized the effect of cancer treatment, but also revolutionized the concept of cancer treatment.
However, due to the small number of killer T lymphocytes in advanced breast tumors, the effect of immunotherapy is often unsatisfactory.
Recently, researchers from the Ohio State University Comprehensive Cancer Center published a new research report titled Metabolic modulation by CDK4/6 inhibitor promotes chemokine-mediated recruitment of T cells into mammary tumors in Cell Reports, and found that cyclins Dependent kinase (CDK) inhibitors can significantly improve the immunotherapy effect of recurrent breast cancer.
DOI: https://doi.
org/10.
1016/j.
celrep.
2021.
108944 In order to explore the impact of the CDK4/6 inhibitor PALBOCICLIB on the tumor immune microenvironment, researchers used the breast cancer MMTV-PyMT transgenic small Mice (FVB mice) and female C57BL/6 mice inoculated with PYMT tumor cells were analyzed to determine whether the efficacy of CDK4/6 inhibitors in different models (spontaneous and transplanted) and genetic background are consistent.
On this basis, the researchers analyzed the effect of CDK4/6 on the composition of the tumor immune microenvironment based on flow cytometry.
At the same time, they used spectrocytometry to characterize the effect of CDK4/6 on the phenotype of tumor infiltrating T cells.
Studies have found that CDK4/6 inhibitors can increase the number and activity of tumor T cells in mouse models of breast cancer.
CDK4/6 treatment increases the number and activity of T cells in mouse models of breast cancer.
Based on the above research, researchers speculate that the ability of CDK4/6 inhibitors to activate T cell levels may be used in cancer immunotherapy.
Consistent with expectations, the study found that compared with mice treated with only CDK4/6 inhibitors, mice inoculated with PYMT cells were stimulated with OX40 agonists and 4-1BB agonists, and then treated with CDK4/6 inhibitors.
Make chemokines "attract" T cells to invade the tumor, thereby more effectively inhibiting the growth of the tumor.
CDK4/6 improves immunotherapy response and promotes chemokine-mediated homing of T-cell tumors.
Earlier studies have shown that mTOR signaling pathway induces chemokines in certain immune cell subgroups, and it is also used in CDK4/6 inhibitors.
Targeting the PI3K/mTOR pathway in the context of treatment can improve tumor growth inhibition while preventing tumors from acquiring drug resistance through internal mechanisms.
https://doi.
org/10.
1186/s13058-020-01320-8 But because previous experiments used immunodeficient mice.
Therefore, in this latest study, the researchers tested how the combined inhibition of CDK4/6 and mTOR affects tumor growth and immune infiltration in immune-normal mice.
The study found that in the combined treatment group of CDK4/6i and mTORi, tumor growth was significantly inhibited.
Next, the researchers tried to determine how exactly mTOR regulates the expression of chemokines in CDK4/6i-treated cells? As we all know, the mTOR signaling pathway is the central regulator of cell metabolism, while glucose and glutamine are key nutrients required for the growth of cancer cells, and their consumption reflects the metabolic needs of cells.
Therefore, the researchers examined the glucose uptake rate and glutamine utilization in MCF7 cells treated with CDK4/6 to further analyze whether CDK4/6-treated cells have metabolic activity.
Studies have found that the mTOR signaling pathway is required to maintain the metabolic activity of cells treated with CDK4/6.
CDK4/6-mediated chemokine induction requires mTOR-regulated metabolic activity.
In summary, the study shows that CDK4/6 inhibitors can provide a new therapeutic strategy for attracting T cells to breast tumors, thereby increasing the sensitivity of immunotherapy Sex.
It is hoped that this new research can improve the survival time of breast cancer and bring breakthrough progress to the first-line treatment of advanced breast cancer.
End reference materials: [1]https://doi.
org/10.
1016/j.
celrep.
2021.
108944
