17β estradiol pellet

Manufactured by Innovative Research

Sourced in United States

17β-estradiol pellets are a type of laboratory equipment used for research purposes. They are formulated to release a controlled and consistent amount of the hormone 17β-estradiol over an extended period of time. The core function of these pellets is to provide a reliable source of this hormone for various experimental studies.

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Lab products found in correlation

Matrigel, by BD (17 mentions) Athymic nude mice, by Orient Bio (3 mentions) Female nu nu nude mice, by Charles River Laboratories (2 mentions) Matrigel, by Corning (2 mentions) Matrigel matrix, by Corning (2 mentions) Lsm 710, by Zeiss (2 mentions) Se 121, by Innovative Research (2 mentions) Placebo pellet, by Innovative Research (2 mentions) Rs 2000 x ray generator, by Rad Source (2 mentions) Nude foxn1nu, by Inotiv (1 mentions) Balb c athymic mice, by Charles River Laboratories (1 mentions) Ivis 200 imaging system, by PerkinElmer (1 mentions) Sucrose, by Merck Group (1 mentions) 17β estradiol, by Innovative Research (1 mentions) Isoflurane, by Performance Health (1 mentions) Mrl lpr mice, by Jackson ImmunoResearch (1 mentions) Female athymic nude mice, by Charles River Laboratories (1 mentions) Trametinib, by Santa Cruz Biotechnology (1 mentions) Rediject d luciferin, by PerkinElmer (1 mentions) Nod scid il2rγc nsg mice, by Jackson ImmunoResearch (1 mentions)

85 protocols using 17β estradiol pellet

Estrogen-induced Xenograft Tumor Models

Cited 1 time

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Experiments were performed under the regulations of the Animal Welfare Act and the Guide for the Care and Use of Laboratory Animals and approved by the Vanderbilt University Institutional Animal Care and Use Committee (IACUC). For the mammary fat pad study, 17β-estradiol pellets (0.36 mg/pellet; Innovative Research of America, Catalog No. SE-121) were subcutaneously implanted into female athymic nude mice 24 h prior to tumor inoculation [61 (link)]. The following day, 5 × 10⁵ tumor cells from each pooled cell line in 20 µl PBS + 50% matrigel (Fisher Scientific) were inoculated into the fourth mammary fat pad (n = 10 mice injected per group). Tumor volume was assessed by caliper measurement. Several mice had to be sacrificed early due to estrogen-induced toxicities resulting in MSCV = 8 mice, FLSEC = 7 mice, DNLS = 10 mice, DNLS + CTERM = 9 mice in the final analysis. For the intracardiac inoculation study, 6-week-old female athymic nude mice (Jackson, Catalog No. 7850) were injected with 1 × 10⁵ tumor cells from each pooled cell line as previously described [63 (link)] (n = 8–10 mice injected per group). The mice were subcutaneously implanted with a slow-release 17β-estradiol pellet (0.36 mg/pellet; Innovative Research of America, Catalog No. SE-121) 24 h prior to tumor cell injection [63 (link)].

Edwards C.M., Kane J.F., Smith J.A., Grant D.M., Johnson J.A., Diaz M.A., Vecchi LA I.I.I., Bracey K.M., Omokehinde T.N., Fontana J.R., Karno B.A., Scott H.T., Vogel C.J., Lowery J.W., Martin T.J, & Johnson R.W. (2024). PTHrP intracrine actions divergently influence breast cancer growth through p27 and LIFR. Breast Cancer Research : BCR, 26, 34.

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Establishment and Maintenance of Patient-Derived Xenograft Models

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The experimental protocol for this study was approved by the Institutional Animal Care and Use Committee (No. NCC-14-224, NCC-16-224, NCC-17-224). Surgically resected tumors or tumor biopsies were implanted into the mammary fat pad of 6-week-old female athymic Nude-Foxn1nu (Envigo, Tokyo, Japan), NOD/SCID/IL2Rγ-null, NSG or NOG mice (CIEA, Kawasaki, Japan) under isoflurane anesthesia (Hana Pharm Co. Ltd., Hwasung, Korea). Seven days before tumor inoculation, a 17β-estradiol pellet (Innovative Research of America, Sarasota, FL, USA) was subcutaneously implanted into the dorsal flank to support establishment of ER-positive tumors. These established PDX models were defined as passage 1 (F1). After inoculated tumors reached approximately 100–200 mm³ in size, they were collected, cut into ~20 mm³ fragments, and transferred to a sterile petri dish containing phosphate-buffered saline (PBS). Fragments of 40–60 mm³ were then transplanted into new recipient mice, a process that was serially repeated. The established PDX models were maintained at the National Cancer Center animal facility (Goyang, Korea).

Ryu J.S., Sim S.H., Park I.H., Lee E.G., Lee E.S., Kim Y.H., Kwon Y., Kong S.Y, & Lee K.S. (2019). Integrative In Vivo Drug Testing Using Gene Expression Signature and Patient-Derived Xenografts from Treatment-Refractory HER2 Positive and Triple-Negative Subtypes of Breast Cancer. Cancers, 11(4), 574.

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Estrogen-Driven Xenograft Tumor Model

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Animal experiments were approved by the Vanderbilt Institutional Animal Care and Use Committee. Female ovariectomized athymic mice (Harlan Sprague Dawley) were implanted s.c. with a 14-day-release, 0.17-mg, 17β-estradiol pellet (Innovative Research of America, Sarasota, FL). Twenty-four h later, 5×10⁶ MCF7 cells suspended in IMEM and matrigel (BD Biosciences, San Jose, California, USA) at 1:1 ratio were injected s.c. into the right flank of each mouse. Approximately 4 weeks later, mice bearing tumors measuring ≥150 mm³ were randomized to treatment with vehicle (control), volasertib (10 mg/kg/day via orogastric gavage), fulvestrant (5 mg/week s.c.), or both drugs. Animal weight and tumor diameters (with calipers) were measured twice weekly and tumor volume was calculated with the formula: volume = width² x length/2. After 6 weeks, tumors were harvested and snap-frozen in liquid nitrogen or fixed in 10% neutral buffered formalin followed by embedding in paraffin for immunohistochemical analysis.

Bhola N., Jansen V.M., Bafna S., Giltnane J.M., Balko J.M., Estrada M.V., Meszoely I., Mayer I., Abramson V., Ye F., Sanders M., Dugger T.C., Van Allen E, & Arteaga C.L. (2014). Kinome wide functional screen identifies role of Polo-like kinase 1 (PLK1) in hormone-independent, ER-positive breast cancer. Cancer research, 75(2), 405-414.

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Estrogen-Dependent Tumor Implantation Models

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Female nude mice (8 to 9 weeks of age) were implanted with a 0.36- or 0.72-mg 17β-estradiol pellet (Innovative Research of America) the day before implantation of tumor cells. Pellets were replaced at expiration date. MFP and brain implantations were performed as previously described (10 (link)). For liver tumors, 10⁶ BT474-Gluc cells were mixed with Matrigel (1:1 volume ratio) and injected in the subcapsular region of the liver parenchyma in the median lobe. For the intracarotid model, 100,000 BT474 cells were diluted in 50 to 100 μl of phosphate-buffered saline (PBS) and slowly injected into the right carotid artery of mice. All animal procedures were performed according to the guidelines of the Public Health Service Policy on Human Care of Laboratory Animals and in accordance with a protocol approved by the Institutional Animal Care and Use Committee of Massachusetts General Hospital (MGH).

Kodack D.P., Askoxylakis V., Ferraro G.B., Sheng Q., Badeaux M., Goel S., Qi X., Shankaraiah R., Cao Z.A., Ramjiawan R.R., Bezwada D., Patel B., Song Y., Costa C., Naxerova K., Wong C.S., Kloepper J., Das R., Tam A., Tanboon J., Duda D.G., Miller C.R., Siegel M.B., Anders C.K., Sanders M., Estrada M.V., Schlegel R., Arteaga C.L., Brachtel E., Huang A., Fukumura D., Engelman J.A, & Jain R.K. (2017). The brain microenvironment mediates resistance in luminal breast cancer to PI3K inhibition through HER3 activation. Science translational medicine, 9(391), eaal4682.

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Monitoring Breast Cancer Metastasis in Mice

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MCF7 Tet-Off p95HER2 cells expressing a short hairpin control or targeting ADAM17 were co-injected with MDA-MB-231 Luc cells into the right flanks of 6- to 8-week-old female BALB/c athymic mice (Charles River Laboratories, Paris, France) in addition to a 17β-estradiol pellet (Innovative Research of America, Sarasota, FL, USA). The expression of p95HER2 was repressed by adding doxycycline (50 mg/kg per day) to the drinking water until tumors were about 100 mm³. Tumor xenografts were measured with calipers every 3 days, and tumor volume was determined by using the formula: (length × width²) × (pi/6). Tumors were resected when they reached 300 mm³, and metastatic colonization was monitored by in vivo bioluminescence imaging with the IVIS-200 imaging system (PerkinElmer, Waltham, MA, USA). At the end of the experiment, animals were anesthetized with a 1.5 % isofluorane-air mixture and were sacrificed by cervical dislocation. Mice were maintained and treated in accordance with institutional guidelines of Vall d’Hebron University Hospital Care and Use Committee.

Morancho B., Martínez-Barriocanal Á., Villanueva J, & Arribas J. (2015). Role of ADAM17 in the non-cell autonomous effects of oncogene-induced senescence. Breast Cancer Research : BCR, 17(1), 106.

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Xenograft Models of Breast Cancer

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Animal studies were approved by the Dartmouth College IACUC. Female NOD-scid/IL2Rγ^−/− (NSG; NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ) mice (6–7 wks old; obtained from the Norris Cotton Cancer Center Transgenic & Genetic Construct Shared Resource) were subcutaneously injected with 5–10×10⁶ MCF-7 cells in matrigel (BD Biosciences), or orthotopically implanted with ~8-mm³ fragments of serially transplanted HCI-003 patient-derived xenograft tissue [a gift from Alana Welm, Univ. of Utah (27 (link))] in the inguinal #4 mammary fat pad; mice were subcutaneously implanted on the same day with a 17β-estradiol pellet (0.72 mg, 60-day-release; Innovative Research of America). In mice subcutaneously injected with T47D/FR cells, subcutaneous administration of 5 mg/wk fulv was initiated on the same day [clinical formulation; provides ER inhibition in MCF-7 tumors for ≥8 d (data not shown); kindly provided by AstraZeneca]. Mice bearing tumors 500–1,000 mm³ were randomized to treatment with vehicle, 5 mg/kg fulv QW, GDC-0941 (100 mg/kg QDx5d QW, 100 mg/kg BIDx3d QW, or 800 mg/kg QW, p.o. in 100 µL 0.5% methylcellulose/0.2%Tween-80), and combinations. Tumor volumes were measured twice weekly using calipers (volume = length²×width/2). Tumors were harvested and cut in pieces for snap-freezing or formalin fixation followed by paraffin embedding (FFPE).

Yang W., Hosford S.R., Dillon L.M., Shee K., Liu S.C., Bean J.R., Salphati L., Pang J., Zhang X., Nannini M.A., Demidenko E., Bates D., Lewis L.D., Marotti J.D., Eastman A.R, & Miller T.W. (2016). Strategically timing inhibition of phosphatidylinositol 3-kinase to maximize therapeutic index in estrogen receptor alpha-positive, PIK3CA-mutant breast cancer. Clinical cancer research : an official journal of the American Association for Cancer Research, 22(9), 2250-2260.

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Xenograft Breast Cancer Mouse Model

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Female nude (nu/nu) mice (Jackson Laboratories) were fed irradiated chow and water infused with trimethoprim/sulfamethoxazole (TMS) to minimize bacterial infection risk. At age 7 weeks, mice were implanted with a 17β-estradiol pellet (0.72 mg; Innovative Research of America), a dose generating systemic estrogen levels equivalent to that of human females mid-menstrual cycle [35 (link)], prior to inoculation with 1 × 10⁶ MCF-7 cells (stably overexpressing Cks2 or control) suspended in 30 μL of unsupplemented RPMI 1640 medium. The cells were injected into the fourth, right, inguinal mammary fat pad. Mice were randomly divided into four groups and biweekly intraperitoneal injection of 0.9% saline, methotrexate (50 mg/kg) [36 (link)], gemcitabine (80 mg/kg) [37 ], or the combination of methotrexate and gemcitabine began once tumor volume reached ∼50 mm³. Tumor volume was measured biweekly using digital calipers (Traceable) and calculated as (width² × length)/2 = mm³ [21 (link), 38 (link)]. Mice were weighed each time tumor volume was measured. Mice were euthanized 28 days after drug administration began, or if tumors size reached 1.5 cm in any direction, or if the tumor begins to ulcerate. Animal work complied with NIH and TSRI guidelines (TSRI is AAALAC accredited).

Tat J., Loriot C., Henze M., Spruck C., Felding B.H, & Reed S.I. (2017). CKS protein overexpression renders tumors susceptible to a chemotherapeutic strategy that protects normal tissues. Oncotarget, 8(70), 114911-114923.

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Xenograft Model of Breast Cancer in NOD/SCID Mice

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NOD/SCID mice were bred in-house and housed in pathogen-free rodent facilities at the University of Michigan. All supplies (cages, chow, and sterile water) were autoclaved, and all experiments were conducted according to standard protocol approved by the University Committee on the Use and Care of Animals. 5 × 10⁵ MCF7 or 5 × 10⁴ SUM159 cells were injected into the 4th mammary fat pads of 6-week-old female NOD/SCID mice. At the following day, mice were randomly selected to the Control or DOX cohort (n = 6). For mice transplanted with MCF7 cells, 17β-estradiol pellet (Cat# SE-121, 60-day release, 0.18 mg/pellet, Innovative Research of America) was implanted on the lateral side of neck between the ear and the shoulder of the mice on the day before tumor cell transplantation. Water containing DOX [2 mg/mL in 5% sucrose (w/v), Sigma-Aldrich] or Control (5% sucrose (w/v), Sigma-Aldrich) was administrated to each mouse cohort via bottled water supply at day 1 after tumor cell implantation. Tumor size was measured once a week with a caliper and calculated as tumor volume = Length × Width²/2.

Ma Y., Zhu Y., Shang L., Qiu Y., Shen N., Wang J., Adam T., Wei W., Song Q., Li J., Wicha M.S, & Luo M. (2023). LncRNA XIST regulates breast cancer stem cells by activating proinflammatory IL-6/STAT3 signaling. Oncogene, 42(18), 1419-1437.

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Orthotopic Xenograft Model for Breast Cancer

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Five week old ovariectomized athymic nude mice (Harlan Laboratories, Fredrick, MD) were injected orthotopically into the mammary fat pads with a suspension of 1 × 10⁶ LCC1 or LCC9 cells in Matrigel. Where appropriate, mice were supplemented with s.c. implantation of a 17β-estradiol pellet (0.72 mg, 60-day release; Innovative Research of America, Sarasota, FL). Mice were sacrificed after 9 weeks, and tumors removed at necropsy, fixed in neutral buffered formalin, and processed using routine histological methods.

Cook K.L, & Clarke R. (2014). Estrogen receptor-α signaling and localization regulates autophagy and unfolded protein response activation in ER+ breast cancer. Receptors & clinical investigation, 1(6), e316.

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Breast Cancer Cell Xenograft Model

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Female nude (nu/nu) mice (Charles River Laboratories) were implanted with an 17β-estradiol pellet (0.72 mg; Innovative Research of America) prior to inoculation with 3 × 10⁶ MCF-7 cells (stable Cks1 overexpressing or control) re-suspended in Matrigel (BD Biosciences) into the mammary fat pads. For drug treatments, mice were randomly divided into 2 groups and administered 5-FU (40mg/kg/week) or PBS (control) once tumor volume reached 100 mm³. Tumor volume was calculated as length (width²)/2=mm³. A portion of each tumor was frozen in liquid N₂ for Western blot analysis.

del Rincón S.V., Widschwendter M., Sun D., Ekholm-Reed S., Tat J., Teixeira L.K., Ellederova Z., Grolieres E., Reed S.I, & Spruck C. (2014). Cks Overexpression Enhances Chemotherapeutic Efficacy by Overriding DNA Damage Checkpoints. Oncogene, 34(15), 1961-1967.

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