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Female nod scid mice

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Female NOD/SCID mice are a strain of immunodeficient laboratory mice. They lack functional T and B cells, which makes them useful for research involving the transplantation of human cells or tissue samples.

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Lab products found in correlation

Matrigel, by BD (4 mentions) Ivis instrument, by PerkinElmer (1 mentions) D3100 camera, by Nikon (1 mentions) Matrigel matrix, by Corning (1 mentions) Positively charged slides, by Thermo Fisher Scientific (1 mentions) Axio observer z1 fluorescence microscope, by Zeiss (1 mentions) Cm1510s cryostat, by Leica (1 mentions) 4 6 diamidino 2 phenylindole (dapi), by Merck Group (1 mentions) Tissue tek oct, by Sakura Finetek (1 mentions) H 2kd, by BD (1 mentions) Doxycycline diet, by Inotiv (1 mentions) Matrigel, by Corning (1 mentions)

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Female BLT-NOD-scid IL2Rg−/− (NSG) mice NOD/SCID/γ−/− (NSG) male and female mice NOD.Cg-Prkdc scid Il2rg tm1Wjl/SzJ (NSG) female mice NOD/SCID/IL2yR−/− female mice NOD-SCID-IL2Rg-/- (NSG) female mice Female NOD-SCID-γc−/− (NSG) mice NOD/SCID/IL2γR−/− female mice NOD-scid IL2Rgammanull (NSG) female mice Female NOD/SCID/IL-2Rγ−/− (NSG) mice Female NOD/scid immunodeficient mice

17 protocols using female nod scid mice

1

Combination therapy for breast cancer

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Female NOD/SCID mice (Jackson Labs) were given orthotopic mammary fat pad injections of 2×106 SUM-159PT cells suspended in 50% matrigel. Mice were housed and treated in accordance with protocols approved by the Institutional Care and Use Committee for animal research at the University of North Carolina. Once tumor volume reached approximately 100 mm3 mice were treated daily with 2.0 mg/kg trametinib by oral gavage (vehicle: 0.5% hydroxypropylmethylcellulose, 0.2% tween 80 in diH2O) or 30mg/kg I-BET151 by IP injection (vehicle: 5% tween 80, 5% DMSO in saline) as single agents or in combination. Tumor volume was calculated daily by caliper measurements ((width)2 × length))/2 until tumors reached maximum size of 2,000 mm3 or at the end of treatment. Tumors used for long-term growth study were snap-frozen in liquid nitrogen and stored at −80°C. Tumors used for riboTRAP and RNA sequencing were treated 48 hours and fresh tissue was harvested for downstream analysis. Tumor number for Fig. 6A: vehicle: n=5, trametinib: n=6, I-BET151: n=4, trametinib+I-BET151 combination: n=3.
Zawistowski J.S., Bevill S.M., Goulet D.R., Stuhlmiller T.J., Beltran A.S., Olivares-Quintero J.F., Singh D., Sciaky N., Parker J.S., Rashid N.U., Chen X., Duncan J.S., Whittle M.C., Angus S.P., Velarde S.H., Golitz B.T., He X., Santos C., Darr D.B., Gallagher K., Graves L.M., Perou C.M., Carey L.A., Earp H.S, & Johnson G.L. (2017). Enhancer Remodeling During Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacological Targeting of the P-TEFb Complex. Cancer discovery, 7(3), 302-321.
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2

Modeling BCR-ABL1 Leukemia in Mice

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Female Nod-SCID mice were purchased from Jackson Labs at 9 weeks of age. At 12 weeks of age, mice were injected by tail vein with 1×106 Ba/F3 cells transduced with pMIG-BCR-ABL1T315I/H396R and pMMP-luciferase-hygromycin (Ridges et al., 2012 (link)) (kindly provided by Dr. Michael Engel, The University of Utah). Oral drug delivery was initiated 72 hr later. Mice received 50 μL of drug in solvent SCIE (66.25 mM sucrose, 13.25 mM citric acid, 40% isopropanol, and 6.7% ethanol; see below). Animals were dosed with asciminib (30 mg/kg), ponatinib (25 mg/kg), or the combination once daily. Luciferase was imaged on days 14 and 21 post-injection on a PerkinElmer (Waltham, MA) IVIS instrument. Dosing was held if mice lost >10% of body weight and maintained this loss on two consecutive days or if a mouse lost 4 grams in 24 hours. Mice were re-enrolled if they gained two grams or more. Mice were euthanized upon exhibiting signs of suffering, generally including lack of response to stimuli and/or lethargy.
Eide C.A., Zabriskie M.S., Savage Stevens S.L., Antelope O., Vellore N.A., Than H., Schultz A.R., Clair P., Bowler A.D., Pomicter A.D., Yan D., Senina A.V., Qiang W., Kelley T.W., Szankasi P., Heinrich M.C., Tyner J.W., Rea D., Cayuela J.M., Kim D.W., Tognon C.E., O’Hare T., Druker B.J, & Deininger M.W. (2019). Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy Against Highly Resistant BCR-ABL1 Mutants. Cancer cell, 36(4), 431-443.e5.
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3

Intramammary Xenograft Studies in NOD/SCID Mice

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The intramammary xenograft studies were conducted as per the approved institutional Animal Care and Use Committee protocol (WVU #1603001644) and using the procedure described by us recently (20 (link)). Female NOD/SCID mice were purchased from the Jackson laboratories and approximately 106 cells mixed in a 1:1 ratio with matrigel (BD Biosciences) were injected into the mammary fat pad of each mouse using a hypodermic needle. After transplantation, tumor growth monitoring was conducted as described above.
Zhao H., Martin E., Matalkah F., Shah N., Ivanov A., Ruppert J.M., Lockman P.R, & Agazie Y.M. (2018). Conditional knockout of SHP2 in ErbB2 transgenic mice or inhibition in HER2-amplified breast cancer cell lines blocks oncogene expression and tumorigenesis. Oncogene, 38(13), 2275-2290.
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4

Tumor Regression in NOD/SCID Mice

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Female NOD/SCID mice were purchased from Jackson Labs. The Animal Care and Use Committee of the Massachusetts Institute of Technology approved all animal procedures. For tumor regression studies, 1×106 cells were injected bilaterally into the mammary fat pad of 6–8-wk-old Female NOD/SCID mice. After reaching 60–80 mm3, tumors were treated with PERKi (7.5 mg/kg/tumor) or DMSO by intratumoral injection on days 1, 2, 4, 5, 8, 9, 11, and 12, and Dox (2.5 mg/kg) or PBS by intraperitoneal (IP) injection on days 2, 5, 9, and 12 unless otherwise specified. Tumor volume over time and average tumor weight at sacrifice were measured and presented as the average ± standard error of mean for 10 tumors per treatment group.
Del Vecchio C.A., Feng Y., Sokol E.S., Tillman E.J., Sanduja S., Reinhardt F, & Gupta P.B. (2014). De-Differentiation Confers Multidrug Resistance Via Noncanonical PERK-Nrf2 Signaling. PLoS Biology, 12(9), e1001945.
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5

Xenograft Model of Tumor Formation

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Female NOD/SCID mice (Jackson Laboratory, Bar Harbor, ME, USA; body weight, 125–150 g; age, 7–8 weeks) were maintained in pathogen-free vinyl isolators under a 12/12-h day/night cycle at 22±1°C, and had access to sterilized laboratory chow and water ad libitum. Eight mice from each group were used for the present study. The FACS-purified SP and MP CD133+ cells were mixed with Matrigel Matrix (Corning Life Sciences, Tewksbury MA, USA) and administered into these mice by subcutaneous injection (15 (link)). Mice were injected once with 5×103 SP cells or 5×104 MP cells in a 500 µl volume, using a 25–26-gauge needle. The density of cells injected and mouse growth were monitored, according to a previously described protocol (15 (link)). The tumor volumes were measured according to the following formula: V = 1/2 ab2, in which a represents the long diameter of the tumor and b represents the short diameter of the tumor. After 2 weeks, the mice were sacrificed by carbon dioxide asphyxiation, tumors were harvested and measured, and images were captured with a Nikon D3100 camera (Nikon Corporation, Tokyo, Japan).
LIU C.T., XIN Y., TONG C.Y., LI B., BAO H.L., ZHANG C.Y, & WANG X.H. (2016). Production of interleukin-4 in CD133+ cervical cancer stem cells promotes resistance to apoptosis and initiates tumor growth. Molecular Medicine Reports, 13(6), 5068-5076.
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6

Tumor Growth in NOD/SCID Mice

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Female NOD/SCID mice (Jackson Laboratory, USA), age 7–10 weeks, weighing 20–25 g were used. The mice were kept in individually ventilated, pathogen-free cages where they had free access to food and water ad libitum. All the experiments were approved by the Norwegian Committee for Animal Research (FOTS project number: 23135440). Bodyweight, activity, tumor size and skin changes were monitored carfully throughout the experiments. No animals showed any signs of illness following tumor formation and metastasis and none died due to the experimental procedure.
Yttersian Sletta K., Tveitarås M.K., Lu N., Engelsen A.S., Reed R.K., Garmann-Johnsen A, & Stuhr L. (2017). Oxygen-dependent regulation of tumor growth and metastasis in human breast cancer xenografts. PLoS ONE, 12(8), e0183254.
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7

Detecting NSC and Viral Presence in Tumor Xenografts

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Female NOD-SCID mice (Jackson Labs) that were 6–8 weeks old were inoculated with 2 million OVCAR8.EGFP.ffluc cells via i.p. injection. Alternatively, female B6 mice (National Cancer Institute [NCI]) that were 7–8 weeks old were inoculated with 5 million ID8.EGFP.ffluc cells via i.p. injection. After 3 weeks, mice (n = 3) were administered i.p. 2e6 DiI-labeled NSC.CRAd-S-pk7. Two days after NSC injection, tumors were harvested. Three tumors per mouse were digested using proteinase K, DNA was extracted (DNA Extraction from fixed tissues kit; Puragene), quantified using a NanoDrop, and then amplified by PCR using primers for v-myc and hexon to test for the presence of NSCs and viral particles, respectively. GAPDH was used as a loading control (351 bp). Primer sequences are listed. An additional three tumors per mouse were frozen in Tissue Tek OCT (Sakura Finetek USA) and sectioned on a Leica CM1510 S cryostat (Leica Biosystems). Sections (10 μm thick) were collected on positively charged slides (Thermo Fisher Scientific), immunostained for hexon (Goat Anti-Adenovirus FITC Conjugated Polyclonal Antibody, AB1056F; Millipore), counterstained with DAPI (1 μg/mL; Sigma), and then imaged using the Zeiss Axio Observer Z1fluorescence microscope (ZEISS Microscopy).
Mooney R., Majid A.A., Batalla-Covello J., Machado D., Liu X., Gonzaga J., Tirughana R., Hammad M., Lesniak M.S., Curiel D.T, & Aboody K.S. (2018). Enhanced Delivery of Oncolytic Adenovirus by Neural Stem Cells for Treatment of Metastatic Ovarian Cancer. Molecular Therapy Oncolytics, 12, 79-92.
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8

Xenograft Mouse Model for Cancer

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Female NOD SCID mice (Jackson) of 20 ± 2 g were used. Animals were housed in individual HEPA ventilated cages (Innocage® IVC, Innovive USA). Fluorescent lighting was provided on a 12-h cycle. Temperature and humidity were monitored and recorded daily and maintained to the maximum extent possible between 20 and 23°C and 30–70% humidity, respectively. 2920X.10 18% soy irradiated rodent feed (Harlan) and autoclaved acidified water (pH 2.5–3.0) were provided ad libitum. Cells from PA5363 and PA5366 (77,000 and 56,000 cells/mouse, respectively, in 200 μL) from the bank cryovals of Crown Bioscence were washed in PBS and counted in cold PBS. Cell suspensions were mixed with an equal volume of Cultrex ECM and kept on ice to avoid the solidification of ECM. Vehicle and ST8176AA1 or trastuzumab (15 mg/kg) were intraperitoneally injected every 4 days for 5 times, starting 28 or 35 days after tumor transplantation for PA5363 and PA5366, respectively.
Milazzo F.M., Vesci L., Anastasi A.M., Chiapparino C., Rosi A., Giannini G., Taddei M., Cini E., Faltoni V., Petricci E., Battistuzzi G., Salvini L., Carollo V, & De Santis R. (2020). ErbB2 Targeted Epigenetic Modulation: Anti-tumor Efficacy of the ADC Trastuzumab-HDACi ST8176AA1. Frontiers in Oncology, 9, 1534.
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9

Oncolytic Virus Therapy in Xenograft Mice

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Female NOD-SCID mice (Jackson Laboratory, Bar Harbor, ME, USA) were subcutaneously inoculated with A673 cells into right flank. When average tumor volume reached >150 mm3, one dose of VMG was administered IT at 2e5 or 2e6 TCID50 in 50 μL PBS or PBS only in the control group (day 0). Tumor dimensions were measured by digital caliper three times per week and tumor volume calculated. Mouse body weight and clinical observations were also recorded three times per week. Study was concluded at day 15.
Watters C.R., Barro O., Elliott N.M., Zhou Y., Gabere M., Raupach E., Baker A.T., Barrett M.T., Buetow K.H., Jacobs B., Seetharam M., Borad M.J, & Nagalo B.M. (2023). Multi-modal efficacy of a chimeric vesiculovirus expressing the Morreton glycoprotein in sarcoma. Molecular Therapy Oncolytics, 29, 4-14.
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10

Evaluating LRP8 Knockdown Effects on Tumor Growth

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The animal studies were conducted following the protocols approved by the University Committee on the Use and Care of Animals at the University of Michigan. Female NOD/SCID mice (Jackson Laboratory, Bar Harbor, ME, USA) were used to evaluate the effects of LRP8 knockdown on tumor growth and tumorigenicity. Briefly, 5000 SUM149 cells carrying doxycycline-inducible control or LRP8 shRNA were injected into the inguinal mammary fat pad of 6–8-week-old mice. Doxycycline diet (625 mg/kg) (Envigo, Haslett, MI, USA) was given to mice starting from 5 weeks after implantation when palpable tumors were observed. At the end of tumor growth monitoring, tumors were harvested and dissociated by using Tumor Dissociation Kit, human (Miltenyi Biotec, Auburn, CA, USA), and then DAPI and H-2Kd (BD Biosciences) double-negative live human cancer cells were sorted by flow cytometry. Limiting dilution assay was conducted by inoculating the sorted and serially diluted cancer cells (2,500, 500 and 100 cells/inoculation) into the inguinal mammary fat pad of tumor-free mice. Tumor formation was monitored for 3 months. The frequency of tumor-initiating cells was calculated by using Extreme Limiting Dilution Analysis (ELDA) [25 ].
Lin C.C., Lo M.C., Moody R., Jiang H., Harouaka R., Stevers N., Tinsley S., Gasparyan M., Wicha M, & Sun D. (2018). Targeting LRP8 inhibits breast cancer stem cells in triple-negative breast cancer. Cancer letters, 438, 165-173.
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