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Nod scid il2rgammanull mice

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The NOD-scid IL2Rgammanull (NSG) mice are a strain of immunodeficient mice. They lack mature T cells, B cells, and natural killer (NK) cells, making them useful for the engraftment of human cells and tissues.

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Lab products found in correlation

Balb c mice, by Taconic Biosciences (2 mentions) Male athymic ncr nude, by Taconic Biosciences (2 mentions) Nod scid gamma mouse, by Jackson ImmunoResearch (2 mentions) Swiss webster, by Taconic Biosciences (2 mentions) Vi cell xr, by Beckman Coulter (2 mentions) Ivis lumina, by PerkinElmer (1 mentions) Ivis spectrum, by PerkinElmer (1 mentions) Pf 477736, by AbMole (1 mentions) Cb17 scid mice, by Charles River Laboratories (1 mentions) Cd34 microbead kit, by Miltenyi Biotec (1 mentions)

Close spelling variants of this product

Male NOD-SCID IL2Rgammanull (NSG) mice NOD-scid IL2Rgammanull (NSG) female mice NOD-scid IL2Rgammanull (NSG) mice NOD-scid IL2Rgammanull NOD/SCID mice IL2Rgammanull mice NOD/SCID SCID mice NOD mice

12 protocols using nod scid il2rgammanull mice

1

Breast Cancer Cell Metastasis Model

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The University of Michigan Institutional Care and Use of Animals Committee approved all animal procedures. We used 8- to 10-week-old female NOD-scid IL2Rgammanull mice originally purchased from The Jackson Laboratory and bred in the colony maintained by the University of Michigan Lab Animal Medicine Program. Before mouse experiments, we cultured MDA-MB-231 WT and MDA-MB-231-GIV KO/WT cells in serum-free DMEM with 25 mM glucose overnight. We verified that these cells did not lose viability after overnight culture in a serum-free medium relative to a medium with 10% serum as determined by cell-based measurements of CBG bioluminescence in an IVIS Lumina (Perkin Elmer). We injected 1 × 105 breast cancer cells per mouse (n = 5 per each cell type), verifying the positioning of the 30 g needle in the left ventricle by the return of pulsatile bright red blood as described (83 (link)). We imaged bioluminescence with an IVIS spectrum (Perkin Elmer) in mice at time points shown in the figure legend and quantified data with Living Image software. For each mouse, we calculated the fold-change in bioluminescence relative to the value obtained one day after injection to normalize for variations in injected amounts of cells. We calculated area-under-the-curve (AUC) ± SEM for total bioluminescence in each group.
Sinha S., Farfel A., Luker K.E., Parker B.A., Yeung K.T., Luker G.D, & Ghosh P. (2024). Growth signaling autonomy in circulating tumor cells aids metastatic seeding. PNAS Nexus, 3(2), pgae014.
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2

Xenograft Tumor Model in Mice

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Male athymic NCr nude, Swiss-Webster and BALB/C mice between 6 and 8 wks of age were purchased from Taconic (Hudson, NY). NOD-scid IL2Rgammanull mice were purchased from the Jackson Laboratory (Bar Harbor, ME). Housing for these animals was maintained in a HEPA-filtrated environment within sterilized cages with 12 h light/12 h dark cycles. All animal procedures were conducted with approval of and in compliance with University of Kentucky Institutional Animal Care and Use Committee. The original patient CRC tumor (F0 generation) was divided and implanted into the flank of a NOD scid gamma mouse (The Jackson Laboratory; 005557) mouse. When the tumors grew to 1 cm3, each tumor (F1 generation) was resected, divided into 2-mm3 pieces and implanted into 5 mice (F2 generation).
For intravenous injection of CRC cells, athymic NCr nude or BALB/C mice were anesthetized with isoflurane (induction 4%, maintenance 2%). The viability of cells used for inoculation was > 95% as determined by Vi-CELL™ XR (Beckman Coulter). Gentle pressure was applied to the inoculation site until there was no visible sign of bleeding. Lung tissues were preserved for histological examination by fixation in 10% buffered formalin followed by paraffin embedding.
Rychahou P., Bae Y., Reichel D., Zaytseva Y.Y., Lee E.Y., Napier D., Weiss H.L., Roller N., Frohman H., Le A.T, & Evers B.M. (2018). Colorectal cancer lung metastasis treatment with polymer–drug nanoparticles. Journal of controlled release : official journal of the Controlled Release Society, 275, 85-91.
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3

Subcutaneous Tumor Xenograft Assay

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Animal handling and all experimental procedures were approved by the Institutional Animal Care and Use Committee (IACUC) of MGH. Cells (6×106 cells suspended in 0.1 mL PBS) were injected subcutaneously into the left dorsal flank of six-week-old female NSG mice (Jackson Laboratory, NOD-Scid IL2Rgammanull mice, for tumorigenesis studies using HCvECs) or athymic nude mice (Jackson Laboratory, Foxn1nu mice, for tumor regression studies using cancer cell lines). The tumor diameter was measured and documented every seven days. The tumor volume (mm3) was estimated by measuring the longest and shortest diameter of the tumor and calculating as follows: volume = (shortest diameter)2 x (longest diameter) x 3.142/6. All mice in tumor regression experiments were euthanized four weeks after tumor cell inoculation. Tumors were collected, weighed, and processed to prepare paraffin sections for immunohistochemical analyses as previously described [14 (link), 59 (link), 60 (link)].
Rotstein D.L, & Alter D.A. (2002). Addressing the challenges of queues. CMAJ: Canadian Medical Association Journal, 166(3), 299.
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4

Xenograft Tumor Model in Mice

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Male athymic NCr nude, Swiss-Webster and BALB/C mice between 6 and 8 wks of age were purchased from Taconic (Hudson, NY). NOD-scid IL2Rgammanull mice were purchased from the Jackson Laboratory (Bar Harbor, ME). Housing for these animals was maintained in a HEPA-filtrated environment within sterilized cages with 12 h light/12 h dark cycles. All animal procedures were conducted with approval of and in compliance with University of Kentucky Institutional Animal Care and Use Committee. The original patient CRC tumor (F0 generation) was divided and implanted into the flank of a NOD scid gamma mouse (The Jackson Laboratory; 005557) mouse. When the tumors grew to 1 cm3, each tumor (F1 generation) was resected, divided into 2-mm3 pieces and implanted into 5 mice (F2 generation).
For intravenous injection of CRC cells, athymic NCr nude or BALB/C mice were anesthetized with isoflurane (induction 4%, maintenance 2%). The viability of cells used for inoculation was > 95% as determined by Vi-CELL™ XR (Beckman Coulter). Gentle pressure was applied to the inoculation site until there was no visible sign of bleeding. Lung tissues were preserved for histological examination by fixation in 10% buffered formalin followed by paraffin embedding.
Rychahou P., Bae Y., Reichel D., Zaytseva Y.Y., Lee E.Y., Napier D., Weiss H.L., Roller N., Frohman H., Le A.T, & Evers B.M. (2018). Colorectal cancer lung metastasis treatment with polymer–drug nanoparticles. Journal of controlled release : official journal of the Controlled Release Society, 275, 85-91.
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5

Chk1 Inhibition Impairs Myeloma Growth

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All animal studies were IACUC approved and performed in accordance with AAALAC, USDA, and PHS guidelines. NOD-SCID IL2Rgammanull mice (Jackson Laboratories, Bar Harbor, ME) were subcutaneously injected with 5 × 106 U266 cells into the flank. The Chk1 inhibitor PF-477736 (Abmole, M1764) was prepared in a 1:1 (v/v) mixture of PBS and dimethyl sulfoxide at a concentration of 10.0 mg/ml. When tumors grew to 300 mm3, PF (15 mg/kg per day) was administrated (i.p.) for 3 days. Control animals received equal volumes of vehicle. Tumors were collected to perform immunoblotting and immunohistochemistry staining.
For additional information and methods, see Supplementary Materials and Methods, and Supplemental Table 1.
Zhou L., Pei X., Zhang Y., Ning Y., Li L., Hu X., Chalasani S.L., Sharma K., Nkwocha J., Yu J., Bandyopadhyay D., Sebti S.M, & Grant S. (2022). Chk1 inhibition potently blocks STAT3 tyrosine705 phosphorylation, DNA binding activity, and activation of downstream targets in human multiple myeloma cells. Molecular cancer research : MCR, 20(3), 456-467.
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6

Xenograft Mouse Models for Prostate Cancer

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All animal care and procedures were approved by University of Washington and FHCRC Institutional Animal Care and Use Committee (IACUC) and performed in accordance with NIH guidelines. Mice used in the study were between 6–10 weeks old when implanted. All animals were naive of any drug or procedure upon recruitment. A maximum of 5 mice were caged in a pathogen-free facility and given unlimited access to food and water on maintained on a 12-hour light/dark cycle. Surgeries were performed under isoflurane anesthesia and mice were given supplemental buprenorphine SR. All mice were given daily health checks after castrations and tumor/cell line implantations. Mice were euthanized when tumors reached 1000 mm3 in volume, if tumors started to ulcerate, or if the health of the animal was compromised. LuCaP PDX studies were carried out in male NOD-scid IL2R-gamma-null mice from Jackson Labs (cat#005557). All LNCaP and LNCaP-DKO xenograft studies were carried out in male CB-17 SCID mice from Charles River (cat#236)
Nyquist M.D., Corella A., Coleman I., De Sarkar N., Kaipainen A., Ha G., Gulati R., Ang L., Chatterjee P., Lucas J., Pritchard C., Risbridger G., Isaacs J., Montgomery B., Morrissey C., Corey E, & Nelson P.S. (2020). Combined TP53 and RB1 Loss Promotes Prostate Cancer Resistance to a Spectrum of Therapeutics and Confers Vulnerability to Replication Stress. Cell reports, 31(8), 107669.
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7

Generation of Humanized BLT Mice

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Humanized BLT mice were generated by implanting xenogenic thymus and liver tissue into 4 week-old NOD-scid IL2R gamma null mice (The Jackson Laboratory) as previously described (10 (link)). Briefly, implants consisted of minced fetal liver tissue and fetal thymus. Each implant was put into the right kidney capsule. In addition to the implants, the mice also received CD34+ hematopoietic stem cells isolated from fetal liver using CD34 Microbead Kit (Miltenyi Biotec). All humanized mice were maintained in a specific pathogen-free facility according to protocols approved by University of Minnesota (UMN) Institutional Animal Care and Use Committee. Humanization levels were determined in these mice 13–15 weeks after CD34+ cell injection. For that, peripheral blood was obtained from animals via submandibular venipuncture and collected into EDTA tubes. Whole peripheral leukocytes were stained for anti-human and anti-mouse CD45 antibodies and analyzed with flow cytometry. All animals with more than 25% human CD45+ cells among the combined CD45 population were used for further experimentation.
Meng J., Banerjee S., Zhang L., Sindberg G., Moidunny S., Li B., Robbins D.J., Girotra M., Segura B., Ramakrishnan S, & Roy S. (2020). Opioids Impair Intestinal Epithelial Repair in HIV-Infected Humanized Mice. Frontiers in Immunology, 10, 2999.
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8

Preclinical AML PDX model

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Mice were housed in IVC under SPF conditions in the animal facility of the VUmc (Amsterdam, The Netherlands). PDX mouse experiments were performed according to institutional and national guidelines and were approved by the Animal Ethics Committee of the VUmc (Amsterdam, The Netherlands). NOD/SCID/IL2r gamma null mice (Jackson Laboratory) (6 wk to 8 wk old) were i.v. injected with 0.7 × 106 primary human AML cells per mouse 24 h post 200-cGy total irradiation. PB was taken via the tail vein and analyzed by flow cytometry for human AML cells, defined by > 0.7% of hCD45+ cells. Six weeks after AML injection, mice were i.v. injected with 1.5 mg/kg of drug or saline weekly for the indicated times. Animals were monitored every other day. PB was taken from the tail vein and analyzed by flow cytometry at week 13. After killing, the hearts were collected for histopathological analysis, and BM was analyzed by flow cytometry.
Qiao X., van der Zanden S.Y., Wander D.P., Borràs D.M., Song J.Y., Li X., van Duikeren S., van Gils N., Rutten A., van Herwaarden T., van Tellingen O., Giacomelli E., Bellin M., Orlova V., Tertoolen L.G., Gerhardt S., Akkermans J.J., Bakker J.M., Zuur C.L., Pang B., Smits A.M., Mummery C.L., Smit L., Arens R., Li J., Overkleeft H.S, & Neefjes J. (2020). Uncoupling DNA damage from chromatin damage to detoxify doxorubicin. Proceedings of the National Academy of Sciences of the United States of America, 117(26), 15182-15192.
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9

Evaluating NK Cell Therapy in Xenograft Models

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Nod-SCID-IL-2Rgamma-null mice (NSG, Jackson Laboratory) were injected with 1 × 105 TC106 (sarcoma) cells subcutaneously bilaterally. Ten days following TC106 injection, when tumors were palpable, the mice (n = 5 per group) received 1 × 106 NK cells injected intravenously (IV) once a week or vehicle as well as IL-2 (75,000 U/ml). Tumor volumes were measured twice a week. Mice were sacrificed after they lost 15% of their initial weight.
The leukemia xenograft model was established by injecting 1 × 106 Jurkat cells IV into NSG mice. Seven days following injection, mice (n = 5 per group) received 5 × 106 NK cells or vehicle weekly as well as IL-2 (75,000 U/ml). Mice were sacrificed after becoming moribund or losing 15% of their initial weight in accordance with out institutional guidelines.
Ojo E.O., Sharma A.A., Liu R., Moreton S., Checkley-Luttge M.A., Gupta K., Lee G., Lee D.A., Otegbeye F., Sekaly R.P., de Lima M, & Wald D.N. (2019). Membrane bound IL-21 based NK cell feeder cells drive robust expansion and metabolic activation of NK cells. Scientific Reports, 9, 14916.
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10

Xenograft Mouse Model for ATR Inhibitor

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All animal studies were performed under protocol AD10000035, approved by our local IACUC, and regulated by VCU’s Animal Care and Use Program, in accordance with AAALAC, USDA, and PHS guidelines. NOD-SCID IL2Rgammanull mice (Jackson Laboratories, Bar Harbor, ME) were subcutaneously injected with 5 × 106 U266 cells into the flank. The ATR inhibitor BAY was prepared in a 6:1:3 (v/v/v) mixture of PEG400, Ethanol and ultrapure water at a concentration of 3.75 mg/ml. When tumors grew to 300 mm3, BAY (30 mg/kg) was administrated (p.o.) for 3 days. Control animals received equal volumes of vehicle. Tumors were collected to perform immunoblotting.
Li L., Hu X., Nkwocha J., Sharma K., Kmieciak M., Mann H., Zhou L, & Grant S. (2023). Non-canonical role for the ataxia-telangiectasia-Rad3 pathway in STAT3 activation in human multiple myeloma cells. Cellular Oncology (Dordrecht), 46(5), 1369-1380.
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