mt4 pancreatic cell line Search Results


tumor models mt4 pancreatic cell line  (Cold Spring Harbor Laboratory Meetings)
86
Cold Spring Harbor Laboratory Meetings tumor models mt4 pancreatic cell line
Tumor Models Mt4 Pancreatic Cell Line, supplied by Cold Spring Harbor Laboratory Meetings, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mt4+pancreatic+cell+line/bl6+c57+cancer+cell+derived+derivedtb32048+from+kpc+line+murine+pancreatic+pdxcretg+%C3%BE/pm41106379-251-3-18
Average 86 stars, based on 1 article reviews
tumor models mt4 pancreatic cell line - by Bioz Stars, 2026-09
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mt4 pancreatic cancer cells  (Jackson Laboratory)
86
Jackson Laboratory mt4 pancreatic cancer cells
( A ) Schematic showing schedules of the DNA-PK inhibitor, M3814, and radiation. M3814 (25 mg/kg) was administered approximately 1 hour before IR on day 0 (8 Gy×1) and alone on day 1–4. ( B, C ) <t>mT4</t> tumor size (B) and tumor volume doubling time (C) implanted in C57BL/6 mice treated with M3814 1-hour pre-RT on day 0, followed by M3814 treatment from day 1–4, n= 12–18 tumors per treatment group. ( D, E ) mT4 tumor size (D) and tumor volume doubling time (E) implanted in athymic nude mice (n=5 per group). Statistical significance was determined using Student’s two-tailed t-test or log-rank test. **P<0.01.
Mt4 Pancreatic Cancer 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
https://www.bioz.com/product/mt4+pancreatic+cell+line/4x106+cells+murine+pan02+pancreatic/pmc09262824-104-14-11
Average 86 stars, based on 1 article reviews
mt4 pancreatic cancer cells - by Bioz Stars, 2026-09
86/100 stars
  Buy from Supplier

Image Search Results


( A ) Schematic showing schedules of the DNA-PK inhibitor, M3814, and radiation. M3814 (25 mg/kg) was administered approximately 1 hour before IR on day 0 (8 Gy×1) and alone on day 1–4. ( B, C ) mT4 tumor size (B) and tumor volume doubling time (C) implanted in C57BL/6 mice treated with M3814 1-hour pre-RT on day 0, followed by M3814 treatment from day 1–4, n= 12–18 tumors per treatment group. ( D, E ) mT4 tumor size (D) and tumor volume doubling time (E) implanted in athymic nude mice (n=5 per group). Statistical significance was determined using Student’s two-tailed t-test or log-rank test. **P<0.01.

Journal: Molecular cancer research : MCR

Article Title: DNA-PK inhibition and radiation promote anti-tumoral immunity through RNA Polymerase III in pancreatic cancer

doi: 10.1158/1541-7786.MCR-21-0725

Figure Lengend Snippet: ( A ) Schematic showing schedules of the DNA-PK inhibitor, M3814, and radiation. M3814 (25 mg/kg) was administered approximately 1 hour before IR on day 0 (8 Gy×1) and alone on day 1–4. ( B, C ) mT4 tumor size (B) and tumor volume doubling time (C) implanted in C57BL/6 mice treated with M3814 1-hour pre-RT on day 0, followed by M3814 treatment from day 1–4, n= 12–18 tumors per treatment group. ( D, E ) mT4 tumor size (D) and tumor volume doubling time (E) implanted in athymic nude mice (n=5 per group). Statistical significance was determined using Student’s two-tailed t-test or log-rank test. **P<0.01.

Article Snippet: Eight- to ten-week-old athymic (NU/J), wild-type C57BL/6 mice were obtained from the Jackson Laboratory. mT4 pancreatic cancer cells (10 6 ) were subcutaneously injected to the left and right flanks of female C57BL/6 or athymic mice.

Techniques: Inhibition, Two Tailed Test

( A ) GFP MFI of control (sgCtrl) or TBK1-deleted (sgTBK1) Panc1- IFNβ1 cells at 3 days after radiation (8 Gy) and/or treatment with M3814 (1 μM). ( B, C ) qPCR of CXCL9 (B), CXCL10 (C) in control or TBK1-deleted Panc1 cells 3 days after treatment with radiation (8 Gy) and/or M3814 (1 μM). ( D, E ) Cell surface PD-L1 of control or TBK1-deleted Panc1 cells (D) and mT4 cells (E) at 3 days following treatment with M3814 (1 μM) and/or radiation (8 Gy). ( F ) GFP MFI in indicated (sgCtrl, sgSTING, or sgcGAS) Panc1- IFNβ1 promotor reporter cells at 3 days following radiation (8 Gy) and/or M3814 (1 μM). ( G-I ) qPCR for IFNα2 (G) , CXCL9 (H) , CXCL10 (I) in indicated (sgCtrl, sgSTING, or sgcGAS) Panc1 cells 3 days after treatment with radiation (8 Gy) and/or M3814 (1 μM). ( J ) Cell surface PD-L1 in Panc1 cells (sgCtrl, sgSTING, or sgcGAS) at 3 days following treatment with M3814 (1 μM) and/or radiation (8 Gy). Data represent 3 independent experiments. Mean ± SD bars shown. Statistical significance was determined using two-tailed, unpaired t tests. *P<0.05, **P<0.01, ***P<0.001.

Journal: Molecular cancer research : MCR

Article Title: DNA-PK inhibition and radiation promote anti-tumoral immunity through RNA Polymerase III in pancreatic cancer

doi: 10.1158/1541-7786.MCR-21-0725

Figure Lengend Snippet: ( A ) GFP MFI of control (sgCtrl) or TBK1-deleted (sgTBK1) Panc1- IFNβ1 cells at 3 days after radiation (8 Gy) and/or treatment with M3814 (1 μM). ( B, C ) qPCR of CXCL9 (B), CXCL10 (C) in control or TBK1-deleted Panc1 cells 3 days after treatment with radiation (8 Gy) and/or M3814 (1 μM). ( D, E ) Cell surface PD-L1 of control or TBK1-deleted Panc1 cells (D) and mT4 cells (E) at 3 days following treatment with M3814 (1 μM) and/or radiation (8 Gy). ( F ) GFP MFI in indicated (sgCtrl, sgSTING, or sgcGAS) Panc1- IFNβ1 promotor reporter cells at 3 days following radiation (8 Gy) and/or M3814 (1 μM). ( G-I ) qPCR for IFNα2 (G) , CXCL9 (H) , CXCL10 (I) in indicated (sgCtrl, sgSTING, or sgcGAS) Panc1 cells 3 days after treatment with radiation (8 Gy) and/or M3814 (1 μM). ( J ) Cell surface PD-L1 in Panc1 cells (sgCtrl, sgSTING, or sgcGAS) at 3 days following treatment with M3814 (1 μM) and/or radiation (8 Gy). Data represent 3 independent experiments. Mean ± SD bars shown. Statistical significance was determined using two-tailed, unpaired t tests. *P<0.05, **P<0.01, ***P<0.001.

Article Snippet: Eight- to ten-week-old athymic (NU/J), wild-type C57BL/6 mice were obtained from the Jackson Laboratory. mT4 pancreatic cancer cells (10 6 ) were subcutaneously injected to the left and right flanks of female C57BL/6 or athymic mice.

Techniques: Inhibition, Control, Two Tailed Test

( A ) Schematic showing schedules of the DNA-PK inhibitor M3814, radiation and αPD-L1 antibody treatment. M3814 (100 mg/kg) was orally administered approximately 1 hour before radiation (5 Gy) on day 0 as well as on days 1–4 and 7–11. Mouse αPD-L1 antibody (100 μg/ml) was intraperitoneally injected every 3 days. ( B, C, D ) mT4 tumor growth following treatment with M3814, radiation, and/or αPD-L1. Data represent mean tumor volumes ± SD (B) Individual tumor volumes with insets (n/n) providing the number of tumors with durable control/the number of total tumors (C), or tumor volume doubling time (D). n per arm (mice) = 12 (ctrl), 16 (M3814), 14 (RT), 18 (M3814+RT), 14 (αPD-L1), 16 (αPD-L1+M3814), 14 (αPD-L1+RT), and 20 (αPD-L1+ M3814+RT). ****P < 0.0001 (αPD-L1+M3814+RT vs. M3814+RT), unpaired, 2-way ANOVA. ( E ) Model for POL III/RIG-I/MAVS/TBK1 pathway activation in response to radiation plus DNA-PK inhibition in pancreatic cancer cells. Inhibition of DNA-PK with the small-molecule inhibitor M3814 leads to increased cytosolic dsDNA in pancreatic cells which is recognized by POL III rather than cGAS, leading to activation of the RIG-I/MAVS/TBK1 pathway and subsequent expression of IFNβ and interferon stimulated genes such as CXCL9 and CXCL10 chemokines. IFNβ expression also promotes adaptive upregulation of PD-L1 which is therapeutically targeted with αPD-L1 antibody leading to enhanced antitumor immunity in pancreatic cancer models.

Journal: Molecular cancer research : MCR

Article Title: DNA-PK inhibition and radiation promote anti-tumoral immunity through RNA Polymerase III in pancreatic cancer

doi: 10.1158/1541-7786.MCR-21-0725

Figure Lengend Snippet: ( A ) Schematic showing schedules of the DNA-PK inhibitor M3814, radiation and αPD-L1 antibody treatment. M3814 (100 mg/kg) was orally administered approximately 1 hour before radiation (5 Gy) on day 0 as well as on days 1–4 and 7–11. Mouse αPD-L1 antibody (100 μg/ml) was intraperitoneally injected every 3 days. ( B, C, D ) mT4 tumor growth following treatment with M3814, radiation, and/or αPD-L1. Data represent mean tumor volumes ± SD (B) Individual tumor volumes with insets (n/n) providing the number of tumors with durable control/the number of total tumors (C), or tumor volume doubling time (D). n per arm (mice) = 12 (ctrl), 16 (M3814), 14 (RT), 18 (M3814+RT), 14 (αPD-L1), 16 (αPD-L1+M3814), 14 (αPD-L1+RT), and 20 (αPD-L1+ M3814+RT). ****P < 0.0001 (αPD-L1+M3814+RT vs. M3814+RT), unpaired, 2-way ANOVA. ( E ) Model for POL III/RIG-I/MAVS/TBK1 pathway activation in response to radiation plus DNA-PK inhibition in pancreatic cancer cells. Inhibition of DNA-PK with the small-molecule inhibitor M3814 leads to increased cytosolic dsDNA in pancreatic cells which is recognized by POL III rather than cGAS, leading to activation of the RIG-I/MAVS/TBK1 pathway and subsequent expression of IFNβ and interferon stimulated genes such as CXCL9 and CXCL10 chemokines. IFNβ expression also promotes adaptive upregulation of PD-L1 which is therapeutically targeted with αPD-L1 antibody leading to enhanced antitumor immunity in pancreatic cancer models.

Article Snippet: Eight- to ten-week-old athymic (NU/J), wild-type C57BL/6 mice were obtained from the Jackson Laboratory. mT4 pancreatic cancer cells (10 6 ) were subcutaneously injected to the left and right flanks of female C57BL/6 or athymic mice.

Techniques: Inhibition, Injection, Control, Activation Assay, Expressing