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Journal articles on the topic 'Mouse model and breast cancer'

Author: Grafiati

Published: 10 December 2022

Last updated: 31 July 2025

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1

Wu, Min, and Murray O. Robinson. "Human-in-Mouse breast cancer model." Cell Cycle 8, no. 15 (2009): 2317–18. http://dx.doi.org/10.4161/cc.8.15.9206.

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Dabydeen, Sarah A., та Priscilla A. Furth. "Genetically engineered ERα-positive breast cancer mouse models". Endocrine-Related Cancer 21, № 3 (2014): R195—R208. http://dx.doi.org/10.1530/erc-13-0512.

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The majority of human breast cancers are estrogen receptor-positive (ER+), but this has proven challenging to model in genetically engineered mice. This review summarizes information on 21 mouse models that develop ER+ mammary cancer. Where available, information on cancer pathology and gene expression profiles is referenced to assist in understanding which histological subtype of ER+ human cancer each model might represent.ESR1,CCDN1, prolactin,TGFα,AIB1,ESPL1, andWNT1overexpression,PIK3CAgain of function, as well as loss ofP53(Trp53) orSTAT1are associated with ER+ mammary cancer. Treatment w

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3

Zhao, Minjun, Haizhi Qiao, and Jinku Zhang. "Research Progress on Mouse Models of Breast Cancer Metastasis." Proceedings of Anticancer Research 8, no. 6 (2024): 129–37. http://dx.doi.org/10.26689/par.v8i6.8882.

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Breast cancer metastasis is a major cause of treatment failure and patient mortality. Mouse tumor models largely replicate the pathophysiological processes of human tumors. Establishing mouse models of breast cancer metastasis helps to elucidate metastatic mechanisms, and in vivo imaging techniques enable dynamic monitoring of tumor cell metastasis in animals. This paper summarizes the mechanisms of breast cancer metastasis, the development, and application of various mouse breast cancer distant metastasis models over the past decade, and evaluates the characteristics and efficacy of each mode

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Hennighausen, Lothar. "Mouse models for breast cancer." Oncogene 19, no. 8 (2000): 966–67. http://dx.doi.org/10.1038/sj.onc.1203346.

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5

Alfred, Jane. "A new mouse model of BRCA1 breast cancer?" Molecular Medicine Today 5, no. 7 (1999): 284. http://dx.doi.org/10.1016/s1357-4310(99)01520-8.

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Burney, Maryam, Lata Mathew, Anjali Gaikwad, Elizabeth K. Nugent, Anneliese O. Gonzalez, and Judith A. Smith. "Evaluation Fucoidan Extracts From Undaria pinnatifida and Fucus vesiculosus in Combination With Anticancer Drugs in Human Cancer Orthotopic Mouse Models." Integrative Cancer Therapies 17, no. 3 (2017): 755–61. http://dx.doi.org/10.1177/1534735417740631.

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Objective: To determine the activity of fucoidan from Undaria pinnatifida (UPF) and Fucus vesiculosus (FVF) when given in combination of chemotherapy drugs using selected human breast or ovarian cancer orthotopic mouse models. Methods: Mice were inoculated with 1 × 106 cells of TOV-112d, MCF-7, or ZR-75 subcutaneously or SKOV3-GFP-Luc intraperitoneally on day 0. MCF-7 and ZR-75 mice were administered with estradiol valerate 2 mg/kg in 0.2 mL castor oil subcutaneously two days prior to cell inoculation. Mice were randomized to one of six arms (N = 10/arm) paclitaxel, UPF/paclitaxel, FVF/paclita

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Ye, Genlan, Chuangkun Li, Xiaoliang Zhao, Feng Wen, Leyu Wang, and Xiaozhong Qiu. "A Humanized Cancer-Bone Metastasis Mouse Model Based on Silica Nanoparticles-Incorporated Human Demineralized Bone Matrix." Journal of Biomedical Nanotechnology 15, no. 12 (2019): 2363–75. http://dx.doi.org/10.1166/jbn.2019.2860.

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Breast cancer tends to spread to other organs and bone metastasis has the highest frequency in breast cancer metastasis, while its mechanisms are not clear and the current treatments are not very effective. To better study the mechanisms and facilitate drug screening for breast cancer bone metastasis, an in vivo mouse model needs to be constructed. However, the construction of the humanized mouse model for cancer bone metastasis which will mimick real interactions between cancer tissue and bone tissue in the human microenvironment remains a challenge. In this study, we constructed a human engi

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Hámori, Lilla, Gyöngyi Kudlik, Kornélia Szebényi, et al. "Establishment and Characterization of a Brca1−/−, p53−/− Mouse Mammary Tumor Cell Line." International Journal of Molecular Sciences 21, no. 4 (2020): 1185. http://dx.doi.org/10.3390/ijms21041185.

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Breast cancer is the most commonly occurring cancer in women and the second most common cancer overall. By the age of 80, the estimated risk for breast cancer for women with germline BRCA1 or BRCA2 mutations is around 80%. Genetically engineered BRCA1-deficient mouse models offer a unique opportunity to study the pathogenesis and therapy of triple negative breast cancer. Here we present a newly established Brca1−/−, p53−/− mouse mammary tumor cell line, designated as CST. CST shows prominent features of BRCA1-mutated triple-negative breast cancers including increased motility, high proliferati

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Piazza, Gary A., Khalda Fadlalla, Adam B. Keeton та ін. "Abstract P1-02-27: A novel 1st-in-class RAS/β-catenin inhibitor concurrently targets cancer cells and MDSC to reverse the immunosuppressive tumor microenvironment: antitumor activity in mouse models of breast and other cancers". Clinical Cancer Research 31, № 12_Supplement (2025): P1–02–27—P1–02–27. https://doi.org/10.1158/1557-3265.sabcs24-p1-02-27.

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Abstract While RAS mutations rarely occur in breast cancers, RAS signaling is well-known to be involved in breast cancer development resulting from constitutive activation of receptor tyrosine kinases. The Wnt/β-catenin pathway is also activated and associated with more aggressive forms of breast cancer. We found that the cyclic nucleotide degrading enzyme, phosphodiesterase 10A (PDE10), is overexpressed in breast cancer cell lines and tumors compared with normal human mammary epithelial cells (HMEC) or tissues, respectively. PDE10 selective inhibitors and gene silencing inhibited the growth o

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Cuellar-Vite, Leslie, Kristen L. Weber-Bonk, Fadi W. Abdul-Karim, Christine N. Booth, and Ruth A. Keri. "Focal Adhesion Kinase Provides a Collateral Vulnerability That Can Be Leveraged to Improve mTORC1 Inhibitor Efficacy." Cancers 14, no. 14 (2022): 3374. http://dx.doi.org/10.3390/cancers14143374.

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The PI3K/AKT/mTORC1 pathway is a major therapeutic target for many cancers, particularly breast cancer. Everolimus is an mTORC1 inhibitor used in metastatic estrogen receptor-positive (ER+) and epidermal growth factor receptor 2-negative (HER2-) breast cancer. However, mTORC1 inhibitors have limited efficacy in other breast cancer subtypes. We sought to discover collateral sensitivities to mTORC1 inhibition that could be exploited to improve therapeutic response. Using a mouse model of breast cancer that is intrinsically resistant to mTORC1 inhibition, we found that rapamycin alters the expres

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Velazquez, Fabiola N., Leiqing Zhang, Valentina Viscardi, et al. "Loss of sphingosine kinase 1 increases lung metastases in the MMTV-PyMT mouse model of breast cancer." PLOS ONE 16, no. 5 (2021): e0252311. http://dx.doi.org/10.1371/journal.pone.0252311.

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Breast cancer is a very heterogeneous disease, and ~30% of breast cancer patients succumb to metastasis, highlighting the need to understand the mechanisms of breast cancer progression in order to identify new molecular targets for treatment. Sphingosine kinase 1 (SK1) has been shown to be upregulated in patients with breast cancer, and several studies have suggested its involvement in breast cancer progression and/or metastasis, mostly based on cell studies. In this work we evaluated the role of SK1 in breast cancer development and metastasis using a transgenic breast cancer model, mouse mamm

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Gkikopoulou, Evi, Anthi Kolokotroni, Vagelis Rinotas, Martina Rauner, and Eleni Douni. "Investigating breast cancer in an osteoporotic TgRANKL mouse model." Bone Reports 16 (May 2022): 101378. http://dx.doi.org/10.1016/j.bonr.2022.101378.

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Zou, Yiyu, Susan Fineberg, Alexander Pearlman, Richard D. Feinman, and Eugene J. Fine. "The effect of a ketogenic diet and synergy with rapamycin in a mouse model of breast cancer." PLOS ONE 15, no. 12 (2020): e0233662. http://dx.doi.org/10.1371/journal.pone.0233662.

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Background The effects of diet in cancer, in general, and breast cancer in particular, are not well understood. Insulin inhibition in ketogenic, high fat diets, modulate downstream signaling molecules and are postulated to have therapeutic benefits. Obesity and diabetes have been associated with higher incidence of breast cancer. Addition of anti-cancer drugs together with diet is also not well studied. Methods Two diets, one ketogenic, the other standard mouse chow, were tested in a spontaneous breast cancer model in 34 mice. Subgroups of 3–9 mice were assigned, in which the diet were impleme

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Regua, Angelina T., Austin Arrigo, Daniel Doheny, Grace L. Wong, and Hui-Wen Lo. "Transgenic mouse models of breast cancer." Cancer Letters 516 (September 2021): 73–83. http://dx.doi.org/10.1016/j.canlet.2021.05.027.

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Bennett, L. Michelle, and Roger W. Wiseman. "Mouse models for breast cancer susceptibility." Environmental Toxicology and Pharmacology 4, no. 3-4 (1997): 283–88. http://dx.doi.org/10.1016/s1382-6689(97)10024-2.

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Amundadottir, Laufey T., Glenn Merlino, and Robert B. Dickson. "Transgenic mouse models of breast cancer." Breast Cancer Research and Treatment 39, no. 1 (1996): 119–35. http://dx.doi.org/10.1007/bf01806083.

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Kim, Ik Soo, and Sung Hee Baek. "Mouse models for breast cancer metastasis." Biochemical and Biophysical Research Communications 394, no. 3 (2010): 443–47. http://dx.doi.org/10.1016/j.bbrc.2010.03.070.

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Son, Yeseon, Changwook Lee, In Tag Yu, Mijin Lee, and Hangun Kim. "Evaluation of Anti-cancer Efficacy of Potassium Usnate using NIR Imaging of Orthotopic Breast Cancer Mouse Model." Yakhak Hoeji 66, no. 5 (2022): 278–82. http://dx.doi.org/10.17480/psk.2022.66.5.278.

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Mouse cancer models are useful tools for evaluating in vivo tumor growth and metastasis, providing valuable information for preclinical testing. In this process, optical imaging enables the mouse models to easily identify the progress of disease in a non-invasive way. Here, we established an experimental bioimaging animal model of near-infrared (NIR) fluorescence by using a fluorescence-labeled organism bioimaging instrument (FOBI) and evaluated the anti-cancer effect of potassium usnate (KU) in an orthotopic breast cancer model. The cell viability assay revealed that KU had cytotoxicity with

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Chen, Hai, Jingmin Shu, Carlo C. Maley, and Li Liu. "A Mouse-Specific Model to Detect Genes under Selection in Tumors." Cancers 15, no. 21 (2023): 5156. http://dx.doi.org/10.3390/cancers15215156.

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The mouse is a widely used model organism in cancer research. However, no computational methods exist to identify cancer driver genes in mice due to a lack of labeled training data. To address this knowledge gap, we adapted the GUST (Genes Under Selection in Tumors) model, originally trained on human exomes, to mouse exomes via transfer learning. The resulting tool, called GUST-mouse, can estimate long-term and short-term evolutionary selection in mouse tumors, and distinguish between oncogenes, tumor suppressor genes, and passenger genes using high-throughput sequencing data. We applied GUST-

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Li, Juan, Dominique Davidson, Cleiton Martins Souza, et al. "Loss of PTPN12 Stimulates Progression of ErbB2-Dependent Breast Cancer by Enhancing Cell Survival, Migration, and Epithelial-to-Mesenchymal Transition." Molecular and Cellular Biology 35, no. 23 (2015): 4069–82. http://dx.doi.org/10.1128/mcb.00741-15.

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PTPN12 is a cytoplasmic protein tyrosine phosphatase (PTP) reported to be a tumor suppressor in breast cancer, through its capacity to dephosphorylate oncogenic receptor protein tyrosine kinases (PTKs), such as ErbB2. However, the precise molecular and cellular impact of PTPN12 deficiency in breast cancer progression remains to be fully clarified. Here, we addressed this issue by examining the effect of PTPN12 deficiency on breast cancer progressionin vivo, in a mouse model of ErbB2-dependent breast cancer using a conditional PTPN12-deficient mouse. Our studies showed that lack of PTPN12 in br

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Shigehiro, Tsukasa, Maho Ueno, Mayumi Kijihira, et al. "Immune State Conversion of the Mesenteric Lymph Node in a Mouse Breast Cancer Model." International Journal of Molecular Sciences 23, no. 19 (2022): 11035. http://dx.doi.org/10.3390/ijms231911035.

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Secondary lymphoid tissues, such as the spleen and lymph nodes (LNs), contribute to breast cancer development and metastasis in both anti- and pro-tumoral directions. Although secondary lymphoid tissues have been extensively studied, very little is known about the immune conversion in mesenteric LNs (mLNs) during breast cancer development. Here, we demonstrate inflammatory immune conversion of mLNs in a metastatic 4T1 breast cancer model. Splenic T cells were significantly decreased and continuously suppressed IFN-γ production during tumor development, while myeloid-derived suppressor cells (M

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Kwa, Mei Qi, Rafael Brandao, Trong H. Phung, Jianfeng Ge, Giuseppe Scieri та Cord Brakebusch. "MRCKα Is Dispensable for Breast Cancer Development in the MMTV-PyMT Model". Cells 10, № 4 (2021): 942. http://dx.doi.org/10.3390/cells10040942.

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MRCKα is a ubiquitously expressed serine/threonine kinase involved in cell contraction and F-actin turnover, which is highly amplified in human breast cancer and part of a gene expression signature for bad prognosis. Nothing is known about the in vivo function of MRCKα. To explore MRCKα function in development and in breast cancer, we generated mice lacking a functional MRCKα gene. Mice were born close to the Mendelian ratio and showed no obvious phenotype including a normal mammary gland formation. Assessing breast cancer development using the transgenic MMTV-PyMT mouse model, loss of MRCKα d

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Zhang, Yun, Jyotsna Godavarthi, Abie Williams-Villalobo, and Bin Liu. "Abstract P4-02-20: Investigating Age-Dependent Breast Cancer Dynamics in a Mouse Model." Clinical Cancer Research 31, no. 12_Supplement (2025): P4–02–20—P4–02–20. https://doi.org/10.1158/1557-3265.sabcs24-p4-02-20.

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Abstract Breast cancer incidence increases with age, but the relationship between age and breast cancer survival remains controversial. Additionally, while younger and older patients exhibit distinct molecular profiles, the intrinsic age-related molecular events in breast cancer are yet to be fully understood. To address this gap, we investigated the age-dependence of breast cancer in a controlled setting, aiming to uncover key signaling pathways. In this study, we utilized a breast cancer mouse model we previously published, which is highly relevant to human breast cancer. This model features

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Gwynne, William D., Mirza S. Shakeel, Adele Girgis-Gabardo, and John A. Hassell. "The Role of Serotonin in Breast Cancer Stem Cells." Molecules 26, no. 11 (2021): 3171. http://dx.doi.org/10.3390/molecules26113171.

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Breast tumors were the first tumors of epithelial origin shown to follow the cancer stem cell model. The model proposes that cancer stem cells are uniquely endowed with tumorigenic capacity and that their aberrant differentiation yields non-tumorigenic progeny, which constitute the bulk of the tumor cell population. Breast cancer stem cells resist therapies and seed metastases; thus, they account for breast cancer recurrence. Hence, targeting these cells is essential to achieve durable breast cancer remissions. We identified compounds including selective antagonists of multiple serotonergic sy

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Cheng, Xiaoqing (Cathy), Khooshbu Kantibhai Patel, Yiwei Fu, et al. "Abstract 2634: IL34-induced Arg1 positive macrophage cells at the edge of invasion in cerebellum metastasis model of HER2-positive breast cancer." Cancer Research 85, no. 8_Supplement_1 (2025): 2634. https://doi.org/10.1158/1538-7445.am2025-2634.

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Abstract Brain metastases occur in about 30% breast cancer patients. The cerebellum is a frequent location for metastases in HER2-positive breast cancer patients, but the mechanisms for this is unknown. We hypothesize that the cerebellar microenvironment plays a crucial role in promoting the growth of metastatic HER2+ breast cancer cells. To study the interaction between cerebellar cells and metastatic breast cancer, we developed a syngeneic, immunocompetent mouse model for breast cancer brain metastasis, by stereotactically injecting mouse breast cancer organoids with HER2V777L; PIK3CAH1047R

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Lanari, Claudia, Caroline A. Lamb, Victoria T. Fabris, et al. "The MPA mouse breast cancer model: evidence for a role of progesterone receptors in breast cancer." Endocrine-Related Cancer 16, no. 2 (2009): 333–50. http://dx.doi.org/10.1677/erc-08-0244.

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More than 60% of all breast neoplasias are ductal carcinomas expressing estrogen (ER) and progesterone receptors (PR). By contrast, most of the spontaneous, chemically or mouse mammary tumor virus induced tumors, as well as tumors arising in genetically modified mice do not express hormone receptors. We developed a model of breast cancer in which the administration of medroxyprogesterone acetate to BALB/c female mice induces mammary ductal carcinomas with a mean latency of 52 weeks and an incidence of about 80%. These tumors are hormone-dependent (HD), metastatic, express both ER and PR, and a

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Falconi, Sirin, Sabarish Ramachandran та Vadivel Ganapathy. "Abstract 2785: Carbidopa/α-methyltryptophan as an ideal combination therapy for breast cancer". Cancer Research 83, № 7_Supplement (2023): 2785. http://dx.doi.org/10.1158/1538-7445.am2023-2785.

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Abstract Background/Hypothesis: The amino acid transporter SLC6A14 is upregulated in estrogen receptor (ER)-positive breast cancer, a subtype that represents 75-80% of all breast cancers. Obesity/overweight increases the risk of breast cancer due to estrogen generated from fat cells that fuel the growth of the ER-positive breast cancer. Previous studies from our lab have demonstrated that blockade of the amino acid transporter SLC6A14 by the small molecule α-methyltryptophan reduces the growth of ER-positive breast cancer in mouse xenografts of human breast cancer cells and in a spontaneous mo

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Shi, Guilan, Xiufen Zhuang, Yanhong Wu та Richard Heller. "IFN-γ inhibit ALDHbr breast cancer cells in murine 4T1 tumor model". Journal of Immunology 202, № 1_Supplement (2019): 194.25. http://dx.doi.org/10.4049/jimmunol.202.supp.194.25.

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Abstract Background Due to the heterogeneity of breast cancer cells, cytotoxic treatments targeting proliferative cancer cells could not eradicate all cancer cells. Compelling evidence suggests that breast cancer stem cells (BCSCs) have a crucial impact in current shortcomings of cancer therapy because they are largely responsible for tumor initiation, relapse, metastasis, and chemo-resistance. Cytokines in the tumor microenvironment can regulate the self-renewal and survival of BCSCs in a variety of ways. Methods and Results We have utilized in vitro and mouse xenograft models (immunocompeten

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Fukui, Yukiko, Kosuke Kawaguchi, Ryuji Murakami, et al. "Abstract P3-08-07: Self-renewal signatures of peripheral blood T cells are associated with successful engraftment to establish a humanized mouse model of breast cancer." Cancer Research 83, no. 5_Supplement (2023): P3–08–07—P3–08–07. http://dx.doi.org/10.1158/1538-7445.sabcs22-p3-08-07.

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Abstract Background: Stable humanized immune mice transplanted with peripheral blood mononuclear cells (PBMCs) derived from breast cancer patients are important models for assessing the tumor immune responses and the tumor immune microenvironment in breast cancer, helping to advance both pre-clinical and clinical research. The PBMCs of breast cancer patients exhibit various differences from those of healthy individuals depending on the stage of cancer progression, subtype, and type of treatment. Recent studies indicate an association of the self-renewal signatures of T cells with successful ge

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Vila-Leahey, Ava, Sharon Oldford, Paola Marignani, and Jean Marshall. "Histamine receptor 2 blockade reduces breast tumor development and metastasis (TUM9P.1010)." Journal of Immunology 194, no. 1_Supplement (2015): 210.12. http://dx.doi.org/10.4049/jimmunol.194.supp.210.12.

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Abstract Histamine has multiple immunomodulatory roles that impact innate and acquired immunity. Histamine receptor antagonists are widely used clinically to treat allergic disease and gastrointestinal disorders, but their ability to alter effective immune function to breast tumors is unknown. We hypothesized that histamine receptor antagonist treatment could alter immune function in mouse models of breast cancer, therefore altering the growth and spread of breast cancer. Two injectable breast tumor models (the 4T1-BALB/c and E0771-C57BL/6 model) and a spontaneous breast cancer model (STK-/-/N

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Bimonte, Sabrina, Antonio Barbieri, Domenica Rea, et al. "Morphine Promotes Tumor Angiogenesis and Increases Breast Cancer Progression." BioMed Research International 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/161508.

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Morphine is considered a highly potent analgesic agent used to relieve suffering of patients with cancer. Severalin vitroandin vivostudies showed that morphine also modulates angiogenesis and regulates tumour cell growth. Unfortunately, the results obtained by these studies are still contradictory. In order to better dissect the role of morphine in cancer cell growth and angiogenesis we performedin vitrostudies on ER-negative human breast carcinoma cells, MDA.MB231 andin vivostudies on heterotopic mouse model of human triple negative breast cancer, TNBC. We demonstrated that morphinein vitroen

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Lujan, Daniel A., Joey L. Ochoa, Ellen J. Beswick, et al. "Cold-Inducible RNA Binding Protein Impedes Breast Tumor Growth in the PyMT Murine Model for Breast Cancer." Biomedicines 12, no. 2 (2024): 340. http://dx.doi.org/10.3390/biomedicines12020340.

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RNA binding proteins (RBPs) post-transcriptionally regulate gene expression by associating with regulatory sequences in the untranslated regions of mRNAs. Cold-inducible RBP (CIRP) is a stress-induced RBP that was recently shown to modulate inflammation in response to cellular stress, where it increases or decreases pro-tumorigenic (proinflammatory) cytokines in different contexts. CIRP expression is altered in several cancers, including breast cancer, but the effects of CIRP on inflammation in breast cancer is not known. Here, we investigate if CIRP alters growth and the inflammatory profile

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Doornebal, Chris W., Sjoerd Klarenbeek, Tanya M. Braumuller, et al. "A Preclinical Mouse Model of Invasive Lobular Breast Cancer Metastasis." Cancer Research 73, no. 1 (2012): 353–63. http://dx.doi.org/10.1158/0008-5472.can-11-4208.

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Su, Wenjie, Lianfu Zeng, and Weida Chen. "Moscatilin Suppresses the Breast Cancer Both In Vitro and In Vivo by Inhibiting HDAC3." Dose-Response 19, no. 1 (2021): 155932582110012. http://dx.doi.org/10.1177/15593258211001251.

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Moscatilin, a natural compound isolated from the orchid Dendrobium moscatum, has multiple pharmacological actions. The present study investigated the anti-tumor role of moscatilin in breast cancer and elucidated the underlying mechanisms. Cell proliferation, viability, and apoptosis of moscatilin treated MDA-MB-231 cells were determined by CCK-8 assay and flow cytometry. Histone deacetylases (HDACs) expression levels and global acetylated status of breast cancer cells were detected by Western blot and qPCR. Mouse xenograft model was established to evaluate the anti-cancer effects of moscatilin

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Bimonte, Sabrina, Antonio Barbieri, Giuseppe Palma, et al. "Dissecting the Role of Curcumin in Tumour Growth and Angiogenesis in Mouse Model of Human Breast Cancer." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/878134.

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Breast cancer is considered the most common cancer for women worldwide and it is now the second leading cause of cancer-related deaths among females in the world. Since breast cancer is highly resistant to chemotherapy, alternative anticancer strategies have been developed. In particular, many studies have demonstrated that curcumin, a derivative of turmeric, can be used as natural agent in treatment of some types of cancer by playing antiproliferative and antioxidant effects. In our study, we assessed the antitumor activities of curcumin in ER-negative human breast cancer cell line resistant

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Pathania, Shailja, Joshua Rivera, Stevension Tran, Carman Man Chung Li, Joan Brugge, and Kourosh Zarringhalam. "Abstract A065: Single cell transcriptomics reveals putative tumor promoting subpopulation in Brca1 mutant breast cancer mouse model." Cancer Research 84, no. 3_Supplement_1 (2024): A065. http://dx.doi.org/10.1158/1538-7445.advbc23-a065.

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Abstract Women with BRCA1 (B1) mutations have an exceptionally high risk of developing breast cancer. The only effective preventive strategy currently offered to these women is the life altering prophylactic mastectomy. Considering the limited treatment options available, it is critical that new preventive strategies be identified. Design of such strategies requires an understanding of early events in the breast cells that drive tumorigenesis. B1 heterozygous mouse models can help us identify these early changes however, despite the well-established association between B1 heterozygosity and ca

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Shrestha, Saroj Kumar, Kyung Hyun Min, Se Woong Kim, Hyoungsu Kim, William H. Gerwick, and Yunjo Soh. "Kalkitoxin: A Potent Suppressor of Distant Breast Cancer Metastasis." International Journal of Molecular Sciences 24, no. 2 (2023): 1207. http://dx.doi.org/10.3390/ijms24021207.

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Bone metastasis resulting from advanced breast cancer causes osteolysis and increases mortality in patients. Kalkitoxin (KT), a lipopeptide toxin derived from the marine cyanobacterium Moorena producens (previously Lyngbya majuscula), has an anti-metastatic effect on cancer cells. We verified that KT suppressed cancer cell migration and invasion in vitro and in animal models in the present study. We confirmed that KT suppressed osteoclast-soup-derived MDA-MB-231 cell invasion in vitro and induced osteolysis in a mouse model, possibly enhancing/inhibiting metastasis markers. Furthermore, KT inh

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Cao, Jingyan, Ran Wang, Ning Gao, et al. "A7RC peptide modified paclitaxel liposomes dually target breast cancer." Biomaterials Science 3, no. 12 (2015): 1545–54. http://dx.doi.org/10.1039/c5bm00161g.

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Karlsson, Jenny, Urs B. Hagemann, Véronique Cruciani, et al. "Efficacy of A HER2-Targeted Thorium-227 Conjugate in A HER2-Positive Breast Cancer Bone Metastasis Model." Cancers 15, no. 13 (2023): 3419. http://dx.doi.org/10.3390/cancers15133419.

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Human epidermal growth factor receptor 2 (HER2) is overexpressed in 15–30% of breast cancers but has low expression in normal tissue, making it attractive for targeted alpha therapy (TAT). HER2-positive breast cancer typically metastasizes to bone, resulting in incurable disease and significant morbidity and mortality. Therefore, new strategies for HER2-targeting therapy are needed. Here, we present the preclinical in vitro and in vivo characterization of the HER2-targeted thorium-227 conjugate (HER2-TTC) TAT in various HER2-positive cancer models. In vitro, HER2-TTC showed potent cytotoxicity

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Rivina, Leena, Michael Davoren, and Robert H. Schiestl. "Mouse Models for Radiation-Induced Breast Cancer." Cancer and Oncology Research 2, no. 6 (2014): 80–86. http://dx.doi.org/10.13189/cor.2014.020602.

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Hutchinson, John N., and William J. Muller. "Transgenic mouse models of human breast cancer." Oncogene 19, no. 53 (2000): 6130–37. http://dx.doi.org/10.1038/sj.onc.1203970.

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Jonkers, J. "201 Mouse Models of Metastatic Breast Cancer." European Journal of Cancer 48 (March 2012): S102. http://dx.doi.org/10.1016/s0959-8049(12)70269-1.

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Langsten, Kendall L., Lihong Shi, Adam S. Wilson, et al. "A Novel Metastatic Estrogen Receptor-Expressing Breast Cancer Model with Antiestrogen Responsiveness." Cancers 15, no. 24 (2023): 5773. http://dx.doi.org/10.3390/cancers15245773.

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Most women diagnosed with breast cancer (BC) have estrogen receptor alpha-positive (ER+) disease. The current mouse models of ER+ BC often rely on exogenous estrogen to encourage metastasis, which modifies the immune system and the function of some tissues like bone. Other studies use genetically modified or immunocompromised mouse strains, which do not accurately replicate the clinical disease. To create a model of antiestrogen responsive BC with spontaneous metastasis, we developed a mouse model of 4T1.2 triple-negative (TN) breast cancer with virally transduced ER expression that metastasiz

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Moela, Pontsho, Mayur Govender, and Melvin Ambele. "Abstract 2469: Investigating the effects of in vivo silencing of RBBP6 gene on tumor growth in the FVBN-Tg(MMTV PyVT)634MulJ breast cancer mouse model." Cancer Research 83, no. 7_Supplement (2023): 2469. http://dx.doi.org/10.1158/1538-7445.am2023-2469.

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Abstract Breast cancer is one of the most common causes of cancer mortality, with close to two million new cases and just over 600 000 cancer deaths projected in 2022 in the United States of America alone. Identifying prognostic markers for breast cancer is critical to reducing these numbers. Retinoblastoma binding protein 6 (RBBP6) is considered a potential cancer biomarker due to its association with cell proliferation and the fact that it is overexpressed at breast cancer sites where there is marked apoptosis and elevated p53. More information is emerging regarding the role of RBBP6 in canc

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Yang, N., F. E. Utama, A. F. Yanac, C. Liu, A. L. Rosenberg, and H. Rui. "Xenotransplantation of surgical specimens of human breast cancer directly into genetically engineered prolactin-humanized immunodeficient mice." Journal of Clinical Oncology 29, no. 27_suppl (2011): 76. http://dx.doi.org/10.1200/jco.2011.29.27_suppl.76.

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76 Background: Prolactin is an important hormone in mammary gland biology and is indispensible for lobulo-alveolar development during pregnancy and homeostasis during lactation. Prolactin has also been implicated in promoting proliferation, survival, and/ or differentiation of breast cancer. Importantly, murine and bovine prolactin, which are the major lactogens in current laboratory experimental conditions in vivo and in vitro, fail to effectively activate human prolactin receptors because of species incompatibility. Therefore, current established human breast cancer cell lines have been sele

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Ciccolini, Emma, Valérie Sabourin, David Patten та ін. "Abstract 1279: Investigating the impact of PGC-1α-coupled metabolic reprogramming on breast cancer metastasis". Cancer Research 83, № 7_Supplement (2023): 1279. http://dx.doi.org/10.1158/1538-7445.am2023-1279.

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Abstract Peroxisome proliferator-activated receptor γ coactivator 1 α (PGC-1α) is a transcriptional coactivator known to play a role in regulating cellular metabolism, contributing to pathways such as mitochondrial respiration, glutaminolysis, and lipogenesis. PGC-1α has been shown to promote cancer metastasis in mouse models of breast cancer while increasing both the global bioenergetic capacity and metabolic flexibility of breast cancer cells. However, the molecular mechanisms through which PGC-1α contributes to metabolic reprogramming to support breast cancer metastasis remain unknown. To a

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Henneman, Linda, Martine H. van Miltenburg, Ewa M. Michalak, et al. "Selective resistance to the PARP inhibitor olaparib in a mouse model for BRCA1-deficient metaplastic breast cancer." Proceedings of the National Academy of Sciences 112, no. 27 (2015): 8409–14. http://dx.doi.org/10.1073/pnas.1500223112.

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Metaplastic breast carcinoma (MBC) is a rare histological breast cancer subtype characterized by mesenchymal elements and poor clinical outcome. A large fraction of MBCs harbor defects in breast cancer 1 (BRCA1). As BRCA1 deficiency sensitizes tumors to DNA cross-linking agents and poly(ADP-ribose) polymerase (PARP) inhibitors, we sought to investigate the response of BRCA1-deficient MBCs to the PARP inhibitor olaparib. To this end, we established a genetically engineered mouse model (GEMM) for BRCA1-deficient MBC by introducing the MET proto-oncogene into a BRCA1-associated breast cancer mode

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Da Cruz, Raquel Santana, Odalys Dominguez, Apsra Nasir, et al. "Abstract 1429: DDT induces intergenerational epigenetic inheritance of cancer predisposition in a mouse model." Cancer Research 82, no. 12_Supplement (2022): 1429. http://dx.doi.org/10.1158/1538-7445.am2022-1429.

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Abstract DNA sequence accounts for the majority of disease heritability, including cancer. Yet, not all familial cancer cases can be explained by genetic factors. There is mounting evidence that environmentally-induced epigenetic inheritance occurs and that the progeny’s traits can be shaped by parental environmental experiences. In humans, epidemiologic studies have implicated endocrine disruptors and environmental toxicants such as the pesticide DDT in intergenerational cancer development, including breast and childhood tumors. Using a mouse model, we investigated whether paternal DDT exposu

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Singhal, Sharad S., Rachana Garg, Atish Mohanty, et al. "Recent Advancement in Breast Cancer Research: Insights from Model Organisms—Mouse Models to Zebrafish." Cancers 15, no. 11 (2023): 2961. http://dx.doi.org/10.3390/cancers15112961.

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Animal models have been utilized for decades to investigate the causes of human diseases and provide platforms for testing novel therapies. Indeed, breakthrough advances in genetically engineered mouse (GEM) models and xenograft transplantation technologies have dramatically benefited in elucidating the mechanisms underlying the pathogenesis of multiple diseases, including cancer. The currently available GEM models have been employed to assess specific genetic changes that underlay many features of carcinogenesis, including variations in tumor cell proliferation, apoptosis, invasion, metastasi

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Yan, Leqin, Sally Gaddis, Luis Della Coletta, et al. "ATF3-Induced Mammary Tumors Exhibit Molecular Features of Human Basal-Like Breast Cancer." International Journal of Molecular Sciences 22, no. 5 (2021): 2353. http://dx.doi.org/10.3390/ijms22052353.

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Basal-like breast cancer (BLBC) is an aggressive and deadly subtype of human breast cancer that is highly metastatic, displays stem-cell like features, and has limited treatment options. Therefore, developing and characterizing preclinical mouse models with tumors that resemble BLBC is important for human therapeutic development. ATF3 is a potent oncogene that is aberrantly expressed in most human breast cancers. In the BK5.ATF3 mouse model, overexpression of ATF3 in the basal epithelial cells of the mammary gland produces tumors that are characterized by activation of the Wnt/β-catenin signal

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