Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2023 Apr 7;142(1):73–89. doi: 10.1182/blood.2022016896

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2023 by The American Society of Hematology. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved.

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

Figure 5. — CXCL14 treatment in vivo suppresses CML cell engraftment in a patient-derived xenograft NSG-SGM3 mouse model. (A) Experimental design for assessing the in vivo effect of CXCL14 and IM on CML cell growth by xenograft transplantation into NSG-SGM3 mice. Primary BM MNCs from patients with CML were transplanted via tail vein into the NSG-SGM3 mice. Peripheral blood was collected at 3 weeks after transplantation to examine CML engraftment before treatment. The mice with similar CML engraftment were subjected to daily intraperitoneal injections of saline (NS), CXCL14, IM, or the combination for 7 to 12 days at the indicated doses. From 1 day to 19 weeks after the last injection, CML engraftment in the BM, spleen, and PB of the recipient mice were analyzed by FACS. (B-D) The relative frequencies of the CML cells in the recipient PB (B) at 1 day and 1 week after 7 to 12 days of treatment, and in the spleen (C) and BM (D) at the end points (1-8 days after treatment). The numbers in the panels are P values determined by unpaired t test; or ∗P < .05, ∗∗P < .01, by one-way analysis of variance Kruskal-Wallis test. (E) The CML engraftment derived from patients with CML with suboptimal response to TKI. The BM, spleen, and blood in the recipient mice were analyzed at the end point (when 1 of the mice showed symptoms) after 10- to 12-day treatments. The CML cell numbers were calculated based on the percentage of human CD45⁺ cells in each tissue type. The numbers in the lower right panel are frequencies of the mice with detectable CML cells (>0.01% of hCD45⁺ cells), defined based on the background staining in the mice that did not undergo transplantation. TKI suboptimal response: the patients who failed to reach <1% in BCR-ABL1 expression by polymerase chain reaction in blood by 6 months after TKI treatment initiation. The P values in the panels were determined by unpaired t test. Data were from 3 independent experiments on 3 patients with CML. Each dot represents CML engraftment in a single recipient mouse. Horizontal bars indicate median values. See also supplemental Figures 7-8.

Figure 5. — CXCL14 treatment in vivo suppresses CML cell engraftment in a patient-derived xenograft NSG-SGM3 mouse model. (A) Experimental design for assessing the in vivo effect of CXCL14 and IM on CML cell growth by xenograft transplantation into NSG-SGM3 mice. Primary BM MNCs from patients with CML were transplanted via tail vein into the NSG-SGM3 mice. Peripheral blood was collected at 3 weeks after transplantation to examine CML engraftment before treatment. The mice with similar CML engraftment were subjected to daily intraperitoneal injections of saline (NS), CXCL14, IM, or the combination for 7 to 12 days at the indicated doses. From 1 day to 19 weeks after the last injection, CML engraftment in the BM, spleen, and PB of the recipient mice were analyzed by FACS. (B-D) The relative frequencies of the CML cells in the recipient PB (B) at 1 day and 1 week after 7 to 12 days of treatment, and in the spleen (C) and BM (D) at the end points (1-8 days after treatment). The numbers in the panels are P values determined by unpaired t test; or ∗P < .05, ∗∗P < .01, by one-way analysis of variance Kruskal-Wallis test. (E) The CML engraftment derived from patients with CML with suboptimal response to TKI. The BM, spleen, and blood in the recipient mice were analyzed at the end point (when 1 of the mice showed symptoms) after 10- to 12-day treatments. The CML cell numbers were calculated based on the percentage of human CD45⁺ cells in each tissue type. The numbers in the lower right panel are frequencies of the mice with detectable CML cells (>0.01% of hCD45⁺ cells), defined based on the background staining in the mice that did not undergo transplantation. TKI suboptimal response: the patients who failed to reach <1% in BCR-ABL1 expression by polymerase chain reaction in blood by 6 months after TKI treatment initiation. The P values in the panels were determined by unpaired t test. Data were from 3 independent experiments on 3 patients with CML. Each dot represents CML engraftment in a single recipient mouse. Horizontal bars indicate median values. See also supplemental Figures 7-8.