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Nod cg prkdcscid il2rgtm1sug jictac mice

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The NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac mice are a genetically engineered mouse model developed by Taconic Biosciences. The model features a severe combined immunodeficiency (SCID) mutation and a targeted mutation in the interleukin-2 receptor gamma chain gene, resulting in the absence of T cells, B cells, and functional natural killer cells.

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Lab products found in correlation

Crtac ncr foxn1nu, by Taconic Biosciences (2 mentions) Matrigel, by BD (2 mentions)

6 protocols using nod cg prkdcscid il2rgtm1sug jictac mice

1

Xenograft Mouse Model Study

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Female NOG (NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac) mice (Taconic Biosciences) were housed in a specific
pathogen-free environment at the animal facility. All experiments were performed under the protocol approved by the Mayo Clinic
and Baylor Health Care System Institutional Animal Care and Use Committee. All mice received daily monitoring and care from the
animal facility staff under the supervision of a veterinarian.
Tripathi T., Yin W., Xue Y., Zurawski S., Fujita H., Hanabuchi S., Liu Y.J., Oh S, & Joo H. (2019). Central Roles of OX40L-OX40 Interaction in the Induction and Progression of Human T Cell-Driven Acute Graft-versus-Host Disease. ImmunoHorizons, 3(3), 110-120.
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2

Inducible HMGA2 knockdown inhibits xenograft tumor growth

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Cal-51 cells (2 × 106) stably transduced with doxycycline (dox)-inducible scramble or HMGA2 shRNA encoding plasmids were injected subcutaneously in 8-week-old female NOG CIEA (NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac) mice (Taconic). Drinking water supplemented with 50 mg/mL doxycycline and 5% sucrose was supplied to mice to induce shRNA expression in tumor cells. Tumor volumes were measured at the indicated time points using a vernier caliper. The mice were sacrificed five weeks after tumor initiation and the weight and size of excised tumors were evaluated. Lungs and livers were fixed in formalin and paraffin-embedded and stained for pan-cytokeratin (anti-CKKL1; 1:30) to identify metastasis. Animal experiments were approved by the Experimental Animal Committee of The Danish Ministry of Justice and were performed at the animal core facility at the University of Southern Denmark (ethical code number 2021-15-0201-00843). Animals were euthanized if they showed any adverse signs of disease, including weight loss, paralysis, thymus dysfunction or general discomfort. Mice were housed under pathogen-free conditions with ad libitum food and water.
Mansoori B., Terp M.G., Mohammadi A., Pedersen C.B., Ditzel H.J., Baradaran B, & Gjerstorff M.F. (2021). HMGA2 Supports Cancer Hallmarks in Triple-Negative Breast Cancer. Cancers, 13(20), 5197.
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3

Xenograft Assays and JQ1 Treatment

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For xenograft assays 5-6-weeks old female CrTac:NCr-Foxn1nu and NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac mice were purchased from Taconic. Tumors were induced by bilateral orthotopic mammary fat pad injection of 1×106 cells in 50% Matrigel (BD Biosciences) in DMEM/F12 or Medium 171 (except for IDC50-X cells, which were injected with 3% FBS and 4 mg/ml collagen gel in Medium 171). Animal experiments were conducted following protocol 11-023 approved by the Dana-Farber Cancer Institute Animal Care and Use Committee. For all the xenograft studies, the sample size of each group (5-10 mice) is indicated in the figures. We performed pilot experiments using a few (5-10) mice/group followed by larger studies if needed to reach statistical significance and repeated experiments to ensure reproducibility. Due to the nature of the performed experiments, no randomization and no blinding was used as it was deemed unfeasible. However, the resulting tumors were analyzed in a blinded manner. Mice were administered JQ1 (50mg/kg, daily), vehicle only (control) for 14 days beginning at day 14 (SUM159), or doxycycline at day 21 (SUM159-shBRD4) after injection. Mice were euthanized and tumors evaluated 28 and 60 days after injection of parental and TET-inducible shBRD4-expressing SUM159 cells into mammary fat pads.
Shu S., Lin C.Y., He H.H., Witwicki R.M., Tabassum D.P., Roberts J.M., Janiszewska M., Huh S.J., Liang Y., Ryan J., Doherty E., Mohammed H., Guo H., Stover D.G., Ekram M.B., Brown J., D'Santos C., Krop I.E., Dillon D., McKeown M., Ott C., Qi J., Ni M., Rao P.K., Duarte M., Wu S.Y., Chiang C.M., Anders L., Young R.A., Winer E., Letai A., Barry W.T., Carroll J.S., Long H., Brown M., Liu X.S., Meyer C.A., Bradner J.E, & Polyak K. (2016). Response and resistance to BET bromodomain inhibitors in triple negative breast cancer. Nature, 529(7586), 413-417.
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4

Patient-Derived Xenograft Model for Neuroblastoma

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All experiments were conducted according to the institutional animal protocols and the national laws and regulations. The experiments were conducted as previously described in four replicates [35 ]. In short, NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac mice (Taconic) were used to perform all patient-derived xenograft experiments. Two neuroblastomas from two independent patients with MYCN-amplified neuroblastoma were serially transplanted in mice at least three times prior to the experiments. Caliper measurement was used to monitor tumor growth. Tumor volume was calculated with the formula length x width 2/2. Mice were sacrificed with cervical dislocation when tumor size exceeded 2000 mm³. Drugs were dissolved in DMSO/Tween/0.9%NaCl and administered intraperitoneally at 20 mg/kg body weight per day.
Timme N., Han Y., Liu S., Yosief H.O., García H.D., Bei Y., Klironomos F., MacArthur I.C., Szymansky A., von Stebut J., Bardinet V., Dohna C., Künkele A., Rolff J., Hundsdörfer P., Lissat A., Seifert G., Eggert A., Schulte J.H., Zhang W, & Henssen A.G. (2019). Small-Molecule Dual PLK1 and BRD4 Inhibitors are Active Against Preclinical Models of Pediatric Solid Tumors. Translational Oncology, 13(2), 221-232.
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5

Xenograft Tumor Model for Viscum and TT Treatment

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Eight-week-old female NOD.Cg-PrkdcscidIl2rgtm1Sug/JicTac mice were obtained from Taconic Biosciences GmbH, Cologne, Germany. The mice were housed in a pathogen-free facility under pathogen-free conditions and fed autoclaved standard diet (Sniff, Soest, Germany) with acidified drinking water ad libitum. Saos-2 cells (1 × 107) were subcutaneously injected into the left flank and treatment started after day 21, when tumor was palpable. Viscum (0.75/1.25/1.75 μg/kg ML I), TT (50/70/90 mg/kg OA) and the combination thereof viscumTT were administered intratumorally twice a week. Each concentration was given twice. Control mice were treated with CD. Mice were monitored daily for health and symptoms of toxicity, and tumor volume was measured twice weekly. On day 43 the mice were sacrificed by cervical dislocation or sacrificed earlier if considered moribund (tumor volume >1.2 cm3 or >10% body weight lost). The experiments were performed in accordance with German legislation on the care and use of laboratory animals and with the United Kingdom Coordinating Committee on Cancer Research Guidelines for the Welfare of Animals in Experimental Neoplasia so as to minimize suffering. Approval for the study was obtained from the Regional Office for Health and Social Affairs (LaGeSo, approval A0452/08).
Kleinsimon S., Longmuss E., Rolff J., Jäger S., Eggert A., Delebinski C, & Seifert G. (2018). GADD45A and CDKN1A are involved in apoptosis and cell cycle modulatory effects of viscumTT with further inactivation of the STAT3 pathway. Scientific Reports, 8, 5750.
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6

Xenograft Assays and JQ1 Treatment

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For xenograft assays 5-6-weeks old female CrTac:NCr-Foxn1nu and NOD.Cg-Prkdcscid Il2rgtm1Sug/JicTac mice were purchased from Taconic. Tumors were induced by bilateral orthotopic mammary fat pad injection of 1×106 cells in 50% Matrigel (BD Biosciences) in DMEM/F12 or Medium 171 (except for IDC50-X cells, which were injected with 3% FBS and 4 mg/ml collagen gel in Medium 171). Animal experiments were conducted following protocol 11-023 approved by the Dana-Farber Cancer Institute Animal Care and Use Committee. For all the xenograft studies, the sample size of each group (5-10 mice) is indicated in the figures. We performed pilot experiments using a few (5-10) mice/group followed by larger studies if needed to reach statistical significance and repeated experiments to ensure reproducibility. Due to the nature of the performed experiments, no randomization and no blinding was used as it was deemed unfeasible. However, the resulting tumors were analyzed in a blinded manner. Mice were administered JQ1 (50mg/kg, daily), vehicle only (control) for 14 days beginning at day 14 (SUM159), or doxycycline at day 21 (SUM159-shBRD4) after injection. Mice were euthanized and tumors evaluated 28 and 60 days after injection of parental and TET-inducible shBRD4-expressing SUM159 cells into mammary fat pads.
Shu S., Lin C.Y., He H.H., Witwicki R.M., Tabassum D.P., Roberts J.M., Janiszewska M., Huh S.J., Liang Y., Ryan J., Doherty E., Mohammed H., Guo H., Stover D.G., Ekram M.B., Brown J., D'Santos C., Krop I.E., Dillon D., McKeown M., Ott C., Qi J., Ni M., Rao P.K., Duarte M., Wu S.Y., Chiang C.M., Anders L., Young R.A., Winer E., Letai A., Barry W.T., Carroll J.S., Long H., Brown M., Liu X.S., Meyer C.A., Bradner J.E, & Polyak K. (2016). Response and resistance to BET bromodomain inhibitors in triple negative breast cancer. Nature, 529(7586), 413-417.
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