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mmtv pymt breast cancer cell line py230  (ATCC)


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    Structured Review

    ATCC mmtv pymt breast cancer cell line py230
    (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line <t>(Py230,</t> 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.
    Mmtv Pymt Breast Cancer Cell Line Py230, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 62 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mmtv+pymt/Py230/bio_rxiv__64898__2026__03__26__714544-174-2-8
    Average 95 stars, based on 62 article reviews
    mmtv pymt breast cancer cell line py230 - by Bioz Stars, 2026-09
    95/100 stars

    Images

    1) Product Images from "Glutamine addiction is a therapeutic target to block emergency myelopoiesis"

    Article Title: Glutamine addiction is a therapeutic target to block emergency myelopoiesis

    Journal: bioRxiv

    doi: 10.64898/2026.03.26.714544

    (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line (Py230, 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.
    Figure Legend Snippet: (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line (Py230, 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.

    Techniques Used: Immunofluorescence, Imaging, Two Tailed Test

    (A-B) Regenerative response in mice treated with the glutamine metabolism inhibitor 6-Diazo-5-oxo-L-norleucine (DON) or PBS vehicle (Veh) control: (A) treatment scheme with daily DON injections of days 6 to 9 post-5FU treatment; and (B) quantification of peripheral blood neutrophils and RBCs (n=10; 3 independent experiments). (C-G) Impact of pharmacological inhibition of glutaminolysis on breast cancer development in Veh and DON-treated WT mice (n=9; 1 independent experiments): (C) breast cancer model with daily DON injections 5 weeks after orthotopic implantation of MMTV-PyMT cell line (Py230, 1×106 cells); (D) breast tumor growth over time measured by external palpation (left), with tumor volume after 14 days of DON treatment; and quantification of (E) BM, (F) peripheral blood and (G) intratumoral myeloid populations after 14 days of DON treatment. (H) Model of glutaminase targeting to impair glutamine-driven OXPHOS and redox balance in myeloid progenitors as a novel therapeutic strategy to suppress tumor-associated myelopoiesis and neutrophil overproduction in breast cancer. Data are means ± S.E.M.; circles represent individual mice; P. values were obtained by an unpaired t-test. See also Figure S1, and S11.
    Figure Legend Snippet: (A-B) Regenerative response in mice treated with the glutamine metabolism inhibitor 6-Diazo-5-oxo-L-norleucine (DON) or PBS vehicle (Veh) control: (A) treatment scheme with daily DON injections of days 6 to 9 post-5FU treatment; and (B) quantification of peripheral blood neutrophils and RBCs (n=10; 3 independent experiments). (C-G) Impact of pharmacological inhibition of glutaminolysis on breast cancer development in Veh and DON-treated WT mice (n=9; 1 independent experiments): (C) breast cancer model with daily DON injections 5 weeks after orthotopic implantation of MMTV-PyMT cell line (Py230, 1×106 cells); (D) breast tumor growth over time measured by external palpation (left), with tumor volume after 14 days of DON treatment; and quantification of (E) BM, (F) peripheral blood and (G) intratumoral myeloid populations after 14 days of DON treatment. (H) Model of glutaminase targeting to impair glutamine-driven OXPHOS and redox balance in myeloid progenitors as a novel therapeutic strategy to suppress tumor-associated myelopoiesis and neutrophil overproduction in breast cancer. Data are means ± S.E.M.; circles represent individual mice; P. values were obtained by an unpaired t-test. See also Figure S1, and S11.

    Techniques Used: Control, Inhibition

    Related Articles

    Derivative Assay:

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome
    Article Snippet: .. Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV-PyMT (mouse mammary tumor virus promoter driven Polyoma middle T-antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host. mBCSCs were purchased from ATCC (ATCC Cat# CRL-3279, RRID:CVCL_AQ08) and authenticated by Short-Tandem Repeat profiling. ..

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome.
    Article Snippet: .. MATERIALS AND METHODS Cell cultures and MTT assay Human (h) BCSCs, BCSC- 608 and BCSC- 105, were generated and provided by Professor G Stassi (University of Palermo, Italy), who characterized them as CSCs, which grew in spheres and reproduced, in immunocompromised host, the tumor of origin.20 Both cell lines were authenticated by surface staining for characteristic markers, as described.20 Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV- PyMT (mouse mammary tumor virus promoter driven Polyoma middle T- antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host.21 mBCSCs were purchased from ATCC (ATCC Cat# CRL- 3279, RRID:CVCL_AQ08) and authenticated by Short- Tandem Repeat profiling. .. Murine (m) BC cells, E0771 mammary adenocarcinoma cell line (RRID:CVCL_GR23), were derived from a spontaneous mammary tumor developed in a female C57BL/6J mouse,22 and were characterized as TripleNegative and Basal- like.23 E0771 cells were purchased from CH3BioSystems (Amherst, NY, USA) and authenticated by Short- Tandem Repeat profiling.

    Virus:

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome
    Article Snippet: .. Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV-PyMT (mouse mammary tumor virus promoter driven Polyoma middle T-antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host. mBCSCs were purchased from ATCC (ATCC Cat# CRL-3279, RRID:CVCL_AQ08) and authenticated by Short-Tandem Repeat profiling. ..

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome.
    Article Snippet: .. MATERIALS AND METHODS Cell cultures and MTT assay Human (h) BCSCs, BCSC- 608 and BCSC- 105, were generated and provided by Professor G Stassi (University of Palermo, Italy), who characterized them as CSCs, which grew in spheres and reproduced, in immunocompromised host, the tumor of origin.20 Both cell lines were authenticated by surface staining for characteristic markers, as described.20 Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV- PyMT (mouse mammary tumor virus promoter driven Polyoma middle T- antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host.21 mBCSCs were purchased from ATCC (ATCC Cat# CRL- 3279, RRID:CVCL_AQ08) and authenticated by Short- Tandem Repeat profiling. .. Murine (m) BC cells, E0771 mammary adenocarcinoma cell line (RRID:CVCL_GR23), were derived from a spontaneous mammary tumor developed in a female C57BL/6J mouse,22 and were characterized as TripleNegative and Basal- like.23 E0771 cells were purchased from CH3BioSystems (Amherst, NY, USA) and authenticated by Short- Tandem Repeat profiling.

    Transgenic Assay:

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome
    Article Snippet: .. Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV-PyMT (mouse mammary tumor virus promoter driven Polyoma middle T-antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host. mBCSCs were purchased from ATCC (ATCC Cat# CRL-3279, RRID:CVCL_AQ08) and authenticated by Short-Tandem Repeat profiling. ..

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome.
    Article Snippet: .. MATERIALS AND METHODS Cell cultures and MTT assay Human (h) BCSCs, BCSC- 608 and BCSC- 105, were generated and provided by Professor G Stassi (University of Palermo, Italy), who characterized them as CSCs, which grew in spheres and reproduced, in immunocompromised host, the tumor of origin.20 Both cell lines were authenticated by surface staining for characteristic markers, as described.20 Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV- PyMT (mouse mammary tumor virus promoter driven Polyoma middle T- antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host.21 mBCSCs were purchased from ATCC (ATCC Cat# CRL- 3279, RRID:CVCL_AQ08) and authenticated by Short- Tandem Repeat profiling. .. Murine (m) BC cells, E0771 mammary adenocarcinoma cell line (RRID:CVCL_GR23), were derived from a spontaneous mammary tumor developed in a female C57BL/6J mouse,22 and were characterized as TripleNegative and Basal- like.23 E0771 cells were purchased from CH3BioSystems (Amherst, NY, USA) and authenticated by Short- Tandem Repeat profiling.

    Single Cell:

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome
    Article Snippet: .. Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV-PyMT (mouse mammary tumor virus promoter driven Polyoma middle T-antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host. mBCSCs were purchased from ATCC (ATCC Cat# CRL-3279, RRID:CVCL_AQ08) and authenticated by Short-Tandem Repeat profiling. ..

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome.
    Article Snippet: .. MATERIALS AND METHODS Cell cultures and MTT assay Human (h) BCSCs, BCSC- 608 and BCSC- 105, were generated and provided by Professor G Stassi (University of Palermo, Italy), who characterized them as CSCs, which grew in spheres and reproduced, in immunocompromised host, the tumor of origin.20 Both cell lines were authenticated by surface staining for characteristic markers, as described.20 Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV- PyMT (mouse mammary tumor virus promoter driven Polyoma middle T- antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host.21 mBCSCs were purchased from ATCC (ATCC Cat# CRL- 3279, RRID:CVCL_AQ08) and authenticated by Short- Tandem Repeat profiling. .. Murine (m) BC cells, E0771 mammary adenocarcinoma cell line (RRID:CVCL_GR23), were derived from a spontaneous mammary tumor developed in a female C57BL/6J mouse,22 and were characterized as TripleNegative and Basal- like.23 E0771 cells were purchased from CH3BioSystems (Amherst, NY, USA) and authenticated by Short- Tandem Repeat profiling.

    MTT Assay:

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome.
    Article Snippet: .. MATERIALS AND METHODS Cell cultures and MTT assay Human (h) BCSCs, BCSC- 608 and BCSC- 105, were generated and provided by Professor G Stassi (University of Palermo, Italy), who characterized them as CSCs, which grew in spheres and reproduced, in immunocompromised host, the tumor of origin.20 Both cell lines were authenticated by surface staining for characteristic markers, as described.20 Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV- PyMT (mouse mammary tumor virus promoter driven Polyoma middle T- antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host.21 mBCSCs were purchased from ATCC (ATCC Cat# CRL- 3279, RRID:CVCL_AQ08) and authenticated by Short- Tandem Repeat profiling. .. Murine (m) BC cells, E0771 mammary adenocarcinoma cell line (RRID:CVCL_GR23), were derived from a spontaneous mammary tumor developed in a female C57BL/6J mouse,22 and were characterized as TripleNegative and Basal- like.23 E0771 cells were purchased from CH3BioSystems (Amherst, NY, USA) and authenticated by Short- Tandem Repeat profiling.

    Generated:

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome.
    Article Snippet: .. MATERIALS AND METHODS Cell cultures and MTT assay Human (h) BCSCs, BCSC- 608 and BCSC- 105, were generated and provided by Professor G Stassi (University of Palermo, Italy), who characterized them as CSCs, which grew in spheres and reproduced, in immunocompromised host, the tumor of origin.20 Both cell lines were authenticated by surface staining for characteristic markers, as described.20 Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV- PyMT (mouse mammary tumor virus promoter driven Polyoma middle T- antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host.21 mBCSCs were purchased from ATCC (ATCC Cat# CRL- 3279, RRID:CVCL_AQ08) and authenticated by Short- Tandem Repeat profiling. .. Murine (m) BC cells, E0771 mammary adenocarcinoma cell line (RRID:CVCL_GR23), were derived from a spontaneous mammary tumor developed in a female C57BL/6J mouse,22 and were characterized as TripleNegative and Basal- like.23 E0771 cells were purchased from CH3BioSystems (Amherst, NY, USA) and authenticated by Short- Tandem Repeat profiling.

    Staining:

    Article Title: Interleukin-30 feeds breast cancer stem cells via CXCL10 and IL23 autocrine loops and shapes immune contexture and host outcome.
    Article Snippet: .. MATERIALS AND METHODS Cell cultures and MTT assay Human (h) BCSCs, BCSC- 608 and BCSC- 105, were generated and provided by Professor G Stassi (University of Palermo, Italy), who characterized them as CSCs, which grew in spheres and reproduced, in immunocompromised host, the tumor of origin.20 Both cell lines were authenticated by surface staining for characteristic markers, as described.20 Murine (m) BCSCs, Py230 cells, were derived from a mammary tumor spontaneously arisen in a MMTV- PyMT (mouse mammary tumor virus promoter driven Polyoma middle T- antigen) transgenic female C57BL/6J mouse, and were identified as CSCs, which grew in spheres and reproduced the parental tumor, when implanted as a single cell into syngeneic host.21 mBCSCs were purchased from ATCC (ATCC Cat# CRL- 3279, RRID:CVCL_AQ08) and authenticated by Short- Tandem Repeat profiling. .. Murine (m) BC cells, E0771 mammary adenocarcinoma cell line (RRID:CVCL_GR23), were derived from a spontaneous mammary tumor developed in a female C57BL/6J mouse,22 and were characterized as TripleNegative and Basal- like.23 E0771 cells were purchased from CH3BioSystems (Amherst, NY, USA) and authenticated by Short- Tandem Repeat profiling.

    Cell Culture:

    Article Title: Pharmacological CDK4/6 inhibition reveals a p53-dependent senescent state with restricted toxicity.
    Article Snippet: .. Cell culture and drug administration BJ (CRL-2522), WI38 (CRL-7728), MMTV-PyMT (CRL-3278), A549 (CCL-185), HCC827 (CRL-2868), MCF7 (HTB-22), and hTERT-RPE1 (CRL-4000) cells were purchased from ATCC. ..



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    (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line <t>(Py230,</t> 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.
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    Galectin Therapeutics mmtv pymt cells
    (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line <t>(Py230,</t> 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.
    Mmtv Pymt Cells, supplied by Galectin Therapeutics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Jackson Laboratory mmtv pymt mice
    (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation <t>of</t> <t>MMTV-PyMT</t> cell line (Py230, 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.
    Mmtv Pymt Mice, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Jackson Laboratory mmtv pymt tumor organoid cells
    CreER/tamoxifen-induced LSD1-loss in the PyMT model led to increased lung metastasis and reprogrammed tumor immune microenvironment. (A ) Schematic diagram showing disruption of Lsd1 and activation of the YFP reporter in <t>MMTV-PyMT;K8-CreER;Lsd1</t> L/L ;R26Y female mice induced by tamoxifen injection (TAM). (B ) Left: H&E images showing representative lung metastatic lesions (arrows) of mice with the indicated genotypes; right: numbers and sizes of lung metastatic lesions as indicated in the left panel. mets: metastases. Scale bar: 500 µm. (C) Quantification of % of cells positive for MHC-I molecules (Qa-1, H2-K, and H2-D) in CD45⁻YFP + PyMT tumor cells with or without TAM-induced LSD1-loss. (D) Alteration of CD45 + cells in PyMT tumors with TAM-induced LSD1-loss. (E) Pie charts summarizing the mean abundance [shown as % within CD45 + cells (=100%, inner cycle); the statistical significance was calculated based on this %] of immune cell subsets in PyMT tumors with or without TAM-induced LSD1-loss; mean % of each immune cell population within live cells (100%, outer circle) is provided in the parentheses in red font. (F) Alteration of the immature NK cell subset and activated CD107a + NK cells in PyMT tumors with TAM-induced LSD1-loss. (G) Decreased % of NK cells in peripheral blood of PyMT female mice with TAM-induced LSD1-loss. Sample legends in (D) and (G) are the same as in (C). P value: *p<0.05, **p<0.01, ***p<0.005, NS = not significant, two-tailed Student’s t -test. Data represent mean ± SEM.
    Mmtv Pymt Tumor Organoid Cells, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Jackson Laboratory mmtv pymt fvb transgenic mouse breast cancer model
    CreER/tamoxifen-induced LSD1-loss in the PyMT model led to increased lung metastasis and reprogrammed tumor immune microenvironment. (A ) Schematic diagram showing disruption of Lsd1 and activation of the YFP reporter in <t>MMTV-PyMT;K8-CreER;Lsd1</t> L/L ;R26Y female mice induced by tamoxifen injection (TAM). (B ) Left: H&E images showing representative lung metastatic lesions (arrows) of mice with the indicated genotypes; right: numbers and sizes of lung metastatic lesions as indicated in the left panel. mets: metastases. Scale bar: 500 µm. (C) Quantification of % of cells positive for MHC-I molecules (Qa-1, H2-K, and H2-D) in CD45⁻YFP + PyMT tumor cells with or without TAM-induced LSD1-loss. (D) Alteration of CD45 + cells in PyMT tumors with TAM-induced LSD1-loss. (E) Pie charts summarizing the mean abundance [shown as % within CD45 + cells (=100%, inner cycle); the statistical significance was calculated based on this %] of immune cell subsets in PyMT tumors with or without TAM-induced LSD1-loss; mean % of each immune cell population within live cells (100%, outer circle) is provided in the parentheses in red font. (F) Alteration of the immature NK cell subset and activated CD107a + NK cells in PyMT tumors with TAM-induced LSD1-loss. (G) Decreased % of NK cells in peripheral blood of PyMT female mice with TAM-induced LSD1-loss. Sample legends in (D) and (G) are the same as in (C). P value: *p<0.05, **p<0.01, ***p<0.005, NS = not significant, two-tailed Student’s t -test. Data represent mean ± SEM.
    Mmtv Pymt Fvb Transgenic Mouse Breast Cancer Model, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Jackson Laboratory mmtv pymt mice83
    CreER/tamoxifen-induced LSD1-loss in the PyMT model led to increased lung metastasis and reprogrammed tumor immune microenvironment. (A ) Schematic diagram showing disruption of Lsd1 and activation of the YFP reporter in <t>MMTV-PyMT;K8-CreER;Lsd1</t> L/L ;R26Y female mice induced by tamoxifen injection (TAM). (B ) Left: H&E images showing representative lung metastatic lesions (arrows) of mice with the indicated genotypes; right: numbers and sizes of lung metastatic lesions as indicated in the left panel. mets: metastases. Scale bar: 500 µm. (C) Quantification of % of cells positive for MHC-I molecules (Qa-1, H2-K, and H2-D) in CD45⁻YFP + PyMT tumor cells with or without TAM-induced LSD1-loss. (D) Alteration of CD45 + cells in PyMT tumors with TAM-induced LSD1-loss. (E) Pie charts summarizing the mean abundance [shown as % within CD45 + cells (=100%, inner cycle); the statistical significance was calculated based on this %] of immune cell subsets in PyMT tumors with or without TAM-induced LSD1-loss; mean % of each immune cell population within live cells (100%, outer circle) is provided in the parentheses in red font. (F) Alteration of the immature NK cell subset and activated CD107a + NK cells in PyMT tumors with TAM-induced LSD1-loss. (G) Decreased % of NK cells in peripheral blood of PyMT female mice with TAM-induced LSD1-loss. Sample legends in (D) and (G) are the same as in (C). P value: *p<0.05, **p<0.01, ***p<0.005, NS = not significant, two-tailed Student’s t -test. Data represent mean ± SEM.
    Mmtv Pymt Mice83, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line (Py230, 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.

    Journal: bioRxiv

    Article Title: Glutamine addiction is a therapeutic target to block emergency myelopoiesis

    doi: 10.64898/2026.03.26.714544

    Figure Lengend Snippet: (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line (Py230, 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.

    Article Snippet: The syngeneic MMTV-PyMT breast cancer cell line Py230 (ATCC CRL-3279) was used for orthotopic tumor implantation experiments.

    Techniques: Immunofluorescence, Imaging, Two Tailed Test

    (A-B) Regenerative response in mice treated with the glutamine metabolism inhibitor 6-Diazo-5-oxo-L-norleucine (DON) or PBS vehicle (Veh) control: (A) treatment scheme with daily DON injections of days 6 to 9 post-5FU treatment; and (B) quantification of peripheral blood neutrophils and RBCs (n=10; 3 independent experiments). (C-G) Impact of pharmacological inhibition of glutaminolysis on breast cancer development in Veh and DON-treated WT mice (n=9; 1 independent experiments): (C) breast cancer model with daily DON injections 5 weeks after orthotopic implantation of MMTV-PyMT cell line (Py230, 1×106 cells); (D) breast tumor growth over time measured by external palpation (left), with tumor volume after 14 days of DON treatment; and quantification of (E) BM, (F) peripheral blood and (G) intratumoral myeloid populations after 14 days of DON treatment. (H) Model of glutaminase targeting to impair glutamine-driven OXPHOS and redox balance in myeloid progenitors as a novel therapeutic strategy to suppress tumor-associated myelopoiesis and neutrophil overproduction in breast cancer. Data are means ± S.E.M.; circles represent individual mice; P. values were obtained by an unpaired t-test. See also Figure S1, and S11.

    Journal: bioRxiv

    Article Title: Glutamine addiction is a therapeutic target to block emergency myelopoiesis

    doi: 10.64898/2026.03.26.714544

    Figure Lengend Snippet: (A-B) Regenerative response in mice treated with the glutamine metabolism inhibitor 6-Diazo-5-oxo-L-norleucine (DON) or PBS vehicle (Veh) control: (A) treatment scheme with daily DON injections of days 6 to 9 post-5FU treatment; and (B) quantification of peripheral blood neutrophils and RBCs (n=10; 3 independent experiments). (C-G) Impact of pharmacological inhibition of glutaminolysis on breast cancer development in Veh and DON-treated WT mice (n=9; 1 independent experiments): (C) breast cancer model with daily DON injections 5 weeks after orthotopic implantation of MMTV-PyMT cell line (Py230, 1×106 cells); (D) breast tumor growth over time measured by external palpation (left), with tumor volume after 14 days of DON treatment; and quantification of (E) BM, (F) peripheral blood and (G) intratumoral myeloid populations after 14 days of DON treatment. (H) Model of glutaminase targeting to impair glutamine-driven OXPHOS and redox balance in myeloid progenitors as a novel therapeutic strategy to suppress tumor-associated myelopoiesis and neutrophil overproduction in breast cancer. Data are means ± S.E.M.; circles represent individual mice; P. values were obtained by an unpaired t-test. See also Figure S1, and S11.

    Article Snippet: The syngeneic MMTV-PyMT breast cancer cell line Py230 (ATCC CRL-3279) was used for orthotopic tumor implantation experiments.

    Techniques: Control, Inhibition

    (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line (Py230, 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.

    Journal: bioRxiv

    Article Title: Glutamine addiction is a therapeutic target to block emergency myelopoiesis

    doi: 10.64898/2026.03.26.714544

    Figure Lengend Snippet: (A-B) Targeting hematopoietic-specific glutaminolysis during breast cancer development in Ctrl and Gls Δ/Δ mice: (A) breast cancer model with orthotopic implantation of MMTV-PyMT cell line (Py230, 1×10 6 cells); and (B) breast tumor growth over time measured by external palpation (n=16-18; 4 independent experiments; left), with tumor volume at 8 weeks (8-wks) post-orthotopic implantation (n=8-9; 2 independent experiments; right). (C-H) Characterization of non-implanted (NI) and tumor-bearing (PyMT) Ctrl and Gls Δ/Δ mice at 8-wks post-orthotopic implantation: (C) quantification of BM neutrophils (Neu) and granulocyte progenitors (GP) (n=8-9; 2 independent experiments); (D) immunofluorescence imaging of BM GMP patches (stars) and GMP clusters (dotted line) (representative images from 2 independent experiments); (E) transcriptional regulation of HSPCs analyzed by scRNA-seq, with contour density plots of BM LK cells showing tumor-induced loss of granulopoiesis in tumor-bearing Gls Δ/Δ mice; (F) OXPHOS measurement by extracellular flux analysis of LSK, with OCR levels (left) and detailed maximal respiration levels (right) (n=6-9; 6 independent experiments); (G) circulating WBC and Neu plotted as a function of PyMT tumor volume (n=16-18; 3 independent experiments), with simple linear regression reporting slope (S) and goodness of fit (R2); and (H) quantification of intratumoral pro-tumorigenic neutrophil subsets (n=8; 3 independent experiments). O, Oligomycin A; F, FCCP; R/A, Rotenone/Antimycin A; T1, DcTrailR1 - /CD101 - ; T2, DcTrailR1 - /CD101 + ; T3, DcTrailR1 + /CD101 +/- . (I) Targeting myeloid-specific glutaminolysis during breast cancer development in Ctrl and Gls mΔ/Δ mice (n=6-11; 3 independent experiments) with tumor growth over time measured by external palpation (left), and tumor volume at 8 weeks (8-wks) post-orthotopic implantation (right). Data are means ± S.E.M. (B, C, F, H, I) or linear regression with 95% C.I. (G); dots represent individual measurements (G) and circles individual mice (B, C, F, H, I); P. values were obtained by an unpaired t-test (B, C, F, H, I) or a two-tailed test (G). See also Figures S1, S8, S9, and S10.

    Article Snippet: MMTV-PyMT mice (FVB/N-Tg(MMTV-PyVT)634Mul/J), Myc-eGfp mice (Myctm1.1Dlev/J), and MRP8-Cre-ires-Gfp mice (B6.Cg-Tg(S100A8-cre,-EGFP)1Ilw/J) were purchased from the Jackson Laboratory.

    Techniques: Immunofluorescence, Imaging, Two Tailed Test

    (A-B) Regenerative response in mice treated with the glutamine metabolism inhibitor 6-Diazo-5-oxo-L-norleucine (DON) or PBS vehicle (Veh) control: (A) treatment scheme with daily DON injections of days 6 to 9 post-5FU treatment; and (B) quantification of peripheral blood neutrophils and RBCs (n=10; 3 independent experiments). (C-G) Impact of pharmacological inhibition of glutaminolysis on breast cancer development in Veh and DON-treated WT mice (n=9; 1 independent experiments): (C) breast cancer model with daily DON injections 5 weeks after orthotopic implantation of MMTV-PyMT cell line (Py230, 1×106 cells); (D) breast tumor growth over time measured by external palpation (left), with tumor volume after 14 days of DON treatment; and quantification of (E) BM, (F) peripheral blood and (G) intratumoral myeloid populations after 14 days of DON treatment. (H) Model of glutaminase targeting to impair glutamine-driven OXPHOS and redox balance in myeloid progenitors as a novel therapeutic strategy to suppress tumor-associated myelopoiesis and neutrophil overproduction in breast cancer. Data are means ± S.E.M.; circles represent individual mice; P. values were obtained by an unpaired t-test. See also Figure S1, and S11.

    Journal: bioRxiv

    Article Title: Glutamine addiction is a therapeutic target to block emergency myelopoiesis

    doi: 10.64898/2026.03.26.714544

    Figure Lengend Snippet: (A-B) Regenerative response in mice treated with the glutamine metabolism inhibitor 6-Diazo-5-oxo-L-norleucine (DON) or PBS vehicle (Veh) control: (A) treatment scheme with daily DON injections of days 6 to 9 post-5FU treatment; and (B) quantification of peripheral blood neutrophils and RBCs (n=10; 3 independent experiments). (C-G) Impact of pharmacological inhibition of glutaminolysis on breast cancer development in Veh and DON-treated WT mice (n=9; 1 independent experiments): (C) breast cancer model with daily DON injections 5 weeks after orthotopic implantation of MMTV-PyMT cell line (Py230, 1×106 cells); (D) breast tumor growth over time measured by external palpation (left), with tumor volume after 14 days of DON treatment; and quantification of (E) BM, (F) peripheral blood and (G) intratumoral myeloid populations after 14 days of DON treatment. (H) Model of glutaminase targeting to impair glutamine-driven OXPHOS and redox balance in myeloid progenitors as a novel therapeutic strategy to suppress tumor-associated myelopoiesis and neutrophil overproduction in breast cancer. Data are means ± S.E.M.; circles represent individual mice; P. values were obtained by an unpaired t-test. See also Figure S1, and S11.

    Article Snippet: MMTV-PyMT mice (FVB/N-Tg(MMTV-PyVT)634Mul/J), Myc-eGfp mice (Myctm1.1Dlev/J), and MRP8-Cre-ires-Gfp mice (B6.Cg-Tg(S100A8-cre,-EGFP)1Ilw/J) were purchased from the Jackson Laboratory.

    Techniques: Control, Inhibition

    CreER/tamoxifen-induced LSD1-loss in the PyMT model led to increased lung metastasis and reprogrammed tumor immune microenvironment. (A ) Schematic diagram showing disruption of Lsd1 and activation of the YFP reporter in MMTV-PyMT;K8-CreER;Lsd1 L/L ;R26Y female mice induced by tamoxifen injection (TAM). (B ) Left: H&E images showing representative lung metastatic lesions (arrows) of mice with the indicated genotypes; right: numbers and sizes of lung metastatic lesions as indicated in the left panel. mets: metastases. Scale bar: 500 µm. (C) Quantification of % of cells positive for MHC-I molecules (Qa-1, H2-K, and H2-D) in CD45⁻YFP + PyMT tumor cells with or without TAM-induced LSD1-loss. (D) Alteration of CD45 + cells in PyMT tumors with TAM-induced LSD1-loss. (E) Pie charts summarizing the mean abundance [shown as % within CD45 + cells (=100%, inner cycle); the statistical significance was calculated based on this %] of immune cell subsets in PyMT tumors with or without TAM-induced LSD1-loss; mean % of each immune cell population within live cells (100%, outer circle) is provided in the parentheses in red font. (F) Alteration of the immature NK cell subset and activated CD107a + NK cells in PyMT tumors with TAM-induced LSD1-loss. (G) Decreased % of NK cells in peripheral blood of PyMT female mice with TAM-induced LSD1-loss. Sample legends in (D) and (G) are the same as in (C). P value: *p<0.05, **p<0.01, ***p<0.005, NS = not significant, two-tailed Student’s t -test. Data represent mean ± SEM.

    Journal: bioRxiv

    Article Title: LSD1 ablation promotes mammary tumor metastasis by attenuating NK cell-mediated anti-tumor immunity

    doi: 10.64898/2026.03.12.711410

    Figure Lengend Snippet: CreER/tamoxifen-induced LSD1-loss in the PyMT model led to increased lung metastasis and reprogrammed tumor immune microenvironment. (A ) Schematic diagram showing disruption of Lsd1 and activation of the YFP reporter in MMTV-PyMT;K8-CreER;Lsd1 L/L ;R26Y female mice induced by tamoxifen injection (TAM). (B ) Left: H&E images showing representative lung metastatic lesions (arrows) of mice with the indicated genotypes; right: numbers and sizes of lung metastatic lesions as indicated in the left panel. mets: metastases. Scale bar: 500 µm. (C) Quantification of % of cells positive for MHC-I molecules (Qa-1, H2-K, and H2-D) in CD45⁻YFP + PyMT tumor cells with or without TAM-induced LSD1-loss. (D) Alteration of CD45 + cells in PyMT tumors with TAM-induced LSD1-loss. (E) Pie charts summarizing the mean abundance [shown as % within CD45 + cells (=100%, inner cycle); the statistical significance was calculated based on this %] of immune cell subsets in PyMT tumors with or without TAM-induced LSD1-loss; mean % of each immune cell population within live cells (100%, outer circle) is provided in the parentheses in red font. (F) Alteration of the immature NK cell subset and activated CD107a + NK cells in PyMT tumors with TAM-induced LSD1-loss. (G) Decreased % of NK cells in peripheral blood of PyMT female mice with TAM-induced LSD1-loss. Sample legends in (D) and (G) are the same as in (C). P value: *p<0.05, **p<0.01, ***p<0.005, NS = not significant, two-tailed Student’s t -test. Data represent mean ± SEM.

    Article Snippet: For transplantation, MMTV-PyMT tumor organoid cells (mixed background of C57BL/6 and FVB) with or without LSD-loss (20,000 cells) were injected into each #4 inguinal glands of NSG (JAX) or SCID (CRL) mice at ∼5 weeks of age via intraductal injection (n=6) , .

    Techniques: Disruption, Activation Assay, Injection, Two Tailed Test