mmtv pymt breast cancer cell line py230 (ATCC)
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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
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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
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
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
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![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.](https://bio-rxiv-images-cdn.bioz.com/dois_ending_with_10/10__64898_slash_2026__03__12__711410/10__64898_slash_2026__03__12__711410___F4.large.jpg)