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ll  (ATCC)
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The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled <t>LL/2)</t> into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.
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The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled <t>LL/2)</t> into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.
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murine lewis lung carcinoma llc1 ll 2 cells  (ATCC)
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The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled <t>LL/2)</t> into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.
Murine Lewis Lung Carcinoma Llc1 Ll 2 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled <t>LL/2)</t> into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.
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The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled <t>LL/2)</t> into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.
Crl 2539 Murine Lewis Lung Carcinoma Llc1 Ll 2 Cells Atcc, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled <t>LL/2)</t> into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.
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The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled <t>LL/2)</t> into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.
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The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled <t>LL/2)</t> into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.
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Image Search Results


The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled LL/2) into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.

Journal: Oncoimmunology

Article Title: Steroid receptor coactivator 3-deficient regulatory T cells eradicate multiple solid tumors in syngeneic mouse models

doi: 10.1080/2162402X.2026.2640261

Figure Lengend Snippet: The loss of SRC-3 in Treg suppress lung cancer progression in mice: (A) Experimental design for the orthotopic injection of lung cancer cells (luciferase labeled LL/2) into lung of mouse, followed by tamoxifen treatment to induce SRC-3 KO Tregs. (B) In vivo imaging analysis of luciferase activity in lung cancer-bearing SRC-3 f/f ( n = 5) and SRC-3 f/f :Foxp3 ERT2Cre/Y ( n = 5) male mice treated with tamoxifen. The lung tumor luciferase signal was very weak before tamoxifen treatment. Therefore, the luciferase image was overexposed to determine whether lung cancer cells had established in the lung. (C) H&E staining of lung from #2 and #5 SRC-3 f/f :Foxp3 ERT2Cre/Y in panel B. (D) Quantification of luciferase activity in lung cancer-bearing SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice from panel B. Each line represents a single mouse. (E) Tumor luciferase activity was measured across three independent experiments. The total number of mice used for the SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y groups was 10 and 10, respectively. Luciferase activity was recorded for each mouse at the conclusion of the experiment. (F) Survival curve of SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y male mice with lung cancer. (G) Representative H&E staining of lung cancers harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice. Arrowheads indicated the lung cancer mass. (H–J) Levels of CD4⁺ T cells (H), CD8⁺ T cells (I), and NK cells, identified by CD49b staining (J), were assessed in melanomas harvested 18 d after tamoxifen treatment in SRC-3 f/f and SRC-3 f/f :Foxp3 ERT2Cre/Y mice using IHC and quantified with the QuPath software. Statistical significance was determined using an unpaired two-tailed Student’s t -test in GraphPad Prism.

Article Snippet: CT-2A (MilliporeSigma, Catalog number: SCC194), B16F10 (American Type Culture Collection, Catalog number: CRL-6475), and LL/2 cells (American Type Culture Collection, Catalog number: CRL-1642) were used to generate syngeneic mouse models of glioblastoma, melanoma, and lung cancer, respectively.

Techniques: Injection, Luciferase, Labeling, In Vivo Imaging, Activity Assay, Staining, Software, Two Tailed Test