Cb17 scid mice

Manufactured by Taconic Biosciences

Sourced in United States, Denmark

CB17 SCID mice are a strain of immunodeficient mice developed by Taconic Biosciences. They lack functional T and B cells, making them useful for a variety of research applications that require a severely compromised immune system.

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Lab products found in correlation

Matrigel, by BD (5 mentions) D luciferin, by PerkinElmer (3 mentions) Prism 8, by GraphPad (3 mentions) Nod scid gamma mice, by Jackson ImmunoResearch (2 mentions) Rpmi 1640 medium, by BD (2 mentions) Matrigel suspension, by Corning (2 mentions) Wild type balb c, by Jackson ImmunoResearch (1 mentions) Nod ltj mice, by Jackson ImmunoResearch (1 mentions) Cb17 scid mice, by Jackson ImmunoResearch (1 mentions) Lg1049, by Jackson ImmunoResearch (1 mentions) Benchmark ultra, by Roche (1 mentions) Balb cbyj, by Jackson ImmunoResearch (1 mentions) C57bl 6 mice, by Jackson ImmunoResearch (1 mentions) Celecoxib, by Novartis (1 mentions) C57bl 6 mice, by Inotiv (1 mentions) Balb c mice, by Inotiv (1 mentions) Erlotinib, by Selleck Chemicals (1 mentions) Wild type c57bl 6j, by Jackson ImmunoResearch (1 mentions) C 129s6 b6 rag2tm1fwa n12, by Taconic Biosciences (1 mentions) Ivis spectrum, by PerkinElmer (1 mentions)

Spelling variants of this product

SCID mice (30 citations) CB17-SCID male mice (4 citations) CB17 mice (2 citations) Female CB17 SCID mice (2 citations) CB17-Prkdc < scid > mice (2 citations)

61 protocols using cb17 scid mice

Lung Colonization Kinetics Modulated by ERRα Knockdown

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All animal work was performed in accordance with protocols approved by the Institutional Animal Care and Use Committee-Children’s Hospital Boston. Female CB17 SCID mice were purchased from Taconic. MDA-MB-231 cells-LUC control cells or MDA-MB-231 cells-LUC cells with stable ERRα knockdown were collected, suspended in 100 μl PBS (5×10⁶ ml⁻¹), and injected intravenously into mice (n=5 per group). Lung colonization was monitored using bioluminescent live imaging at 1, 6 and 24 h post-cell injection. Ten minutes prior to imaging, animals were injected with D-luciferin (Perkin Elmer, 120 mg kg⁻¹, i.p.). Bioluminescent signals were recorded using the Xenogen IVIS 200 System. Total photon flux of chest area was analyzed. Mice were administrated with vehicle or rapamycin (6 mg kg⁻¹, i.p.) after imaging at 1-h post-cell inoculation. The photon flux at the chest regions was evaluated.

Berman A.Y., Manna S., Schwartz N.S., Katz Y.E., Sun Y., Behrmann C.A., Yu J.J., Plas D.R., Alayev A, & Holz M.K. (2017). ERRα regulates the growth of triple-negative breast cancer cells via S6K1-dependent mechanism. Signal Transduction and Targeted Therapy, 2, 17035-.

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Glucose Monitoring in Mouse Models

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Wild-type Balb/c and NOD/LtJ mice were purchased from The Jackson Laboratory (Bar Harbor, ME). Breeding colonies of these mice were also established and maintained in a pathogen-free facility of the biological resources laboratory (BRL) of the University of Illinois at Chicago (Chicago, IL). CB-17 SCID mice were purchased from Taconic (Hudson, NY). Glucose levels in the tail vein blood samples of mice were monitored with the ACCU-CHEK blood glucose test strips with a blood glucose meter. The animal studies were approved by the animal care and use committee of the University of Illinois at Chicago.

Bhattacharya P., Fan J., Haddad C., Essani A., Gopisetty A., Elshabrawy H.A., Vasu C, & Prabhakar B.S. (2014). A novel pancreatic β-cell targeting bispecific-antibody (BsAb) can prevent the development of Type 1 diabetes in NOD mice. Clinical immunology (Orlando, Fla.), 153(1), 187-198.

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Xenograft Tumor Growth Assay

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We resuspended stably-transduced Melan-a/MEL270/MEL202 cells (1M cells) with doxycycline-inducible shRNAs, cDNAs, or sgRNAs in 100 μl of a 1:1 mix of medium and Matrigel (BD Biosciences) and subcutaneously and bilaterally injected the mix into the flanks of 7-week-old female CB17-SCID mice (Taconic). For doxycycline-regulated shRNA induction, we used doxycycline-containing diets (625mg/kg diet, Envigo). To assess tumor growth, at least five mice per group were injected for a total of ten tumors per group. No randomization or blinding was used in the analysis of tumor growth. Tumors were measured with calipers every 7 days. Growth curves were visualized with Prism GraphPad 8.0. Tumor volume was calculated using the formula; Volume = π(length)(width)(height)/6.

Inoue D., Chew G.L., Liu B., Michel B.C., Pangallo J., D’Avino A.R., Hitchman T., North K., Lee S.C., Bitner L., Block A., Moore A.R., Yoshimi A., Escobar-Hoyos L., Cho H., Penson A., Lu S.X., Taylor J., Chen Y., Kadoch C., Abdel-Wahab O, & Bradley R.K. (2019). Spliceosomal disruption of the non-canonical BAF complex in cancer. Nature, 574(7778), 432-436.

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Xenograft Tumor Establishment in SCID Mice

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Human tumor xenografts were established by transplanting cancer cells ectopically into the flank of C.B17 SCID mice (Taconic Farms) as described previously (Nomura et al., 2010b (link)). Briefly, cells were washed two times with PBS, trypsinized, and harvested in serum-containing medium. Next, the harvested cells were washed two times with serum-free medium and resuspended at a concentration of 2.0 × 10⁴ cells/μl and 100 μl was injected. Growth of the tumors was measured every 3–6 days with calipers.

Mulvihill M.M., Benjamin D.I., Ji X., Le Scolan E., Louie S.M., Shieh A., Green M., Narasimhalu T., Morris P.J., Luo K, & Nomura D.K. (2014). Metabolic Profiling Reveals PAFAH1B3 as a Critical Driver of Breast Cancer Pathogenicity. Chemistry & biology, 21(7), 831-840.

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Xenograft Mouse Model for Tumor Growth

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All animal work was performed in accordance with protocols approved by the University of Cincinnati Standing Committees on Animals. Female nude CD-1 mice (Charles River) (A549 cell line), NOD/SCID-gamma mice (Jackson Lab) (LAM 621-101 cell line), and CB17-scid mice (Taconic) (RT4 and ELT3-luciferase cell lines), 6 to 8 weeks of age, were used. 2×10⁶ cells were subcutaneously inoculated into the posterior back regions of each mouse. Once the tumor is formed three to five weeks post inoculation, tumor length and width were measured using a digital caliper. Tumor volume was calculated using the formula: volume = (length × (width)²/2). For the drug treatment experiment, mice were randomized into two groups after tumor formation and treated with either vehicle control (100 µl of 1% DMSO in PBS) or SRPIN340 (100 µl of 20 µg/ml; 1% DMSO in PBS) by daily peritumoral injection as previously described (Gammons et al., 2014 (link)). SRPIN340 was dissolved as 2 mg/ml in DMSO, and this stock solution was diluted 1:1,000 using PBS prior to inject. For the bioluminescent imaging of ELT3-luciferase tumors, luciferin (120 mg/kg, Xenogen) was intraperitoneally injected into the mouse 10 min prior to imaging. Bioluminescent signals were recorded using the Xenogen IVIS System and the total photon flux of tumors was analyzed as previously described (Yu et al., 2009 (link)).

Lee G., Zheng Y., Cho S., Jang C., England C., Dempsey J.M., Yu Y., Liu X., He L., Cavaliere P.M., Chavez A., Zhang E., Isik M., Couvillon A., Dephoure N.E., Blackwell T.K., Yu J.J., Rabinowitz J.D., Cantley L.C, & Blenis J. (2017). Post-transcriptional regulation of de novo lipogenesis by mTORC1-S6K1-SRPK2 signaling. Cell, 171(7), 1545-1558.e18.

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Evaluating Novel Cancer Therapeutics in PDX Models

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All animal studies were conducted in an AAALAC accredited facility. All procedures performed on these animals were in accordance with regulations and established guidelines and were reviewed and approved by Pfizer Institutional Animal Care and Use Committee. Four or five animals per cohort were used in all the efficacy studies. For BxPC3 xenograft model, 2 million cells were implanted subcutaneously into 5-6 weeks old female CB17/SCID mice (The Jackson Laboratory) until the tumor sizes reached 250-300 mm3 before treatment started. Non-small cell lung carcinoma PDX models LG1049 (which harbors the EGFR Exon19del/T790M mutations), LG1179 (Kras G13R mutation, paclitaxel resistant) and LG0551 (squamous carcinoma) were acquired from The Jackson Laboratory. The NSCLC PDX model CTG1014 (EGFR L858R/T790M mutations) and colorectal cancer PDX model CTG0334 (Kras wild-type) were acquired from Champion Oncology. For PDX models, 1-2 mm3 of tumor fragments were implanted subcutaneously into the lateral flanks of female CB17/SCID mice from Taconic. Animals were randomized by tumor sizes once they reached ∼300 mm3 or otherwise indicated, and RN765C and other agents were administered through bolus tail vein injection. Tumor volume was calculated with the following formula: Tumor volume = (length x width ²) / 2. Animals were humanely euthanized before their tumor volumes reached 2000 mm³.

Wong O.K., Tran T.T., Ho W.H., Casas M.G., Au M., Bateman M., Lindquist K.C., Rajpal A., Shelton D.L., Strop P, & Liu S.H. (2018). RN765C, a low affinity EGFR antibody drug conjugate with potent anti-tumor activity in preclinical solid tumor models. Oncotarget, 9(71), 33446-33458.

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Prostate Cancer Tumor Progression Assay

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PCa cells (1 × 10⁶), including PC3-vector, PC3-shTNC clones, C4-2b-vector or C4-2b-TNC cells, were injected into the prostate of 6- to 7-week-old male CB.17 scid mice (Taconic Biosciences) [55 (link)]. A total of 10 mice in each group was used, in which 5 mice per cage were randomly allocated as control or experimental group. Control and experimental groups were not blinded to the investigators. Animals were excluded from the analysis when there was no tumor take. Tumor growth was monitored by bioluminescence imaging. DNA was isolated from individual femurs using DNeasy kit. Human-specific Alu qPCR was performed to determine the number of tumor cells in each femur as previously described [11 (link)]. Animal studies were performed in compliance with protocols approved by the Institutional Animal Care and Use Committee at M.D. Anderson Cancer Center.

Lee Y.C., Lin S.C., Yu G., Zhu M., Song J.H., Rivera K., Pappin D.J., Logothetis C.J., Panaretakis T., Wang G., Yu-Lee L.Y, & Lin S.H. (2021). Prostate tumor-induced stromal reprogramming generates Tenascin C that promotes prostate cancer metastasis through YAP/TAZ inhibition. Oncogene, 41(6), 757-769.

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Lentiviral Infection and Xenograft Assay for Organoid Research

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Organoids were infected with the indicated lentivirus, selected with puromycin and further selected with FACS. For histology and immunohistochemistry, organoids were processed as described previously^{5 (link),16 (link)}. Immunohistochemistry was performed using a Ventana BenchMark ULTRA. The anti-CK8/18 antibody was purchased from Abcam (ab53280). In vivo xenograft experiments were performed as described previously^{23 (link)}, using 7-week-old male C.B17 SCID mice (Taconic): one million cells were injected into the flank for a total of ten tumours per shRNA and cell type. Once tumours were palpable, tumour volume was measured weekly using a Peira TM900 system (Peira, Belgium). The maximal tumour volume permitted by our Institutional Animal Care and Use Committee under protocol 06-07-012 was 2 cm³, beyond which mice were euthanized. All animal experiments were performed in compliance with the guidelines of the Research Animal Resource Center of Memorial Sloan Kettering Cancer Center.

Bose R., Karthaus W.R., Armenia J., Abida W., Iaquinta P.J., Zhang Z., Wongvipat J., Wasmuth E.V., Shah N., Sullivan P.S., Doran M.G., Wang P., Patruno A., Zhao Y., Zheng D., Schultz N, & Sawyers C.L. (2017). ERF mutations reveal a balance of ETS factors controlling prostate oncogenesis. Nature, 546(7660), 671-675.

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Xenograft Model of Castrated SCID Mice

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L(−)ID4 cells (2 × 10⁶) suspended in 100 μL of serum‐free RPMI 1640 medium containing matrigel (1 : 1 v/v; BD Biosciences, San Jose, CA, USA) were injected subcutaneously into the lower flanks of 4‐week‐old castrated (C) male C.B‐17 SCID mice (Taconic Biosciences, Rensselaer, NY, USA) using a 27‐gauge syringe. The C.B‐17 SCID mice were maintained at the Mercer University Vivarium. All studies were approved by the Clark Atlanta and Mercer University Committee for the use and care of animals.

Joshi J.B., Patel D., Morton D.J., Sharma P., Zou J., Hewa Bostanthirige D., Gorantla Y., Nagappan P., Komaragiri S.K., Sivils J.C., Xie H., Palaniappan R., Wang G., Cox M.B, & Chaudhary J. (2017). Inactivation of ID4 promotes a CRPC phenotype with constitutive AR activation through FKBP52. Molecular Oncology, 11(4), 337-357.

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Breast Cancer Xenograft Model in SCID Mice

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Experiments were performed on 6-week-old female CB17 SCID mice (Taconic Biosciences, Lille Skensved, Denmark). Mice were maintained at a constant temperature (22°C±1°C), relative humidity 55%±10%, and a photoperiod (12 h light/dark cycle). Animals were acclimatized for 7 days before each experiment. The animals were provided with auto-claved rodent chow (Diet 4RF25; Mucedola, Milan, Italy) and purified water ad libitum. Animal experiments were approved by the Animal Care and Use Committee of the State Food and Veterinary Service (approval No G2-29), and all procedures were in accordance with the guidelines for animal research set out in the European Union Directive 2010/63/EU and national regulations. Mice were inoculated with 2×10⁶ MDA-MB-231 cells in a volume of 200 µL growth medium into adipose tissue around the nipple using 23G needles. The tumor volume was estimated by measuring three orthogonal diameters (L [length], W [width], H [height]) with calipers; the volume (V) was calculated as follows: V = (L × W × H) ×0.523. The migration studies were performed when the tumor size reached 300 mm³, generally 50–60 days after inoculation. At least five mice were used in the experimental groups.

Dapkute D., Steponkiene S., Bulotiene D., Saulite L., Riekstina U, & Rotomskis R. (2017). Skin-derived mesenchymal stem cells as quantum dot vehicles to tumors. International Journal of Nanomedicine, 12, 8129-8142.

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