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Academic literature on the topic 'Preclinical tumor models'

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Published: 8 June 2024

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Journal articles on the topic "Preclinical tumor models":

1

Varticovski, L., M. G. Hollingshead, M. R. Anver, A. I. Robles, J. E. Green, K. W. Hunter, G. Merlino, et al. "Preclinical testing using tumors from genetically engineered mouse mammary models." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 10067. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.10067.

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10067 Background: Mouse models have been used extensively in preclinical testing of anticancer drugs. However, few of these models reflect the progression of human disease, and even fewer predict the performance of these drugs in clinical trials. Testing anticancer therapies in genetically engineered mouse (GEM) holds the promise of improving preclinical models and guiding the design of clinical trials. Unfortunately, the use of tumor-bearing GEM is hampered by the difficulty in simultaneously obtaining sufficient numbers of animals with the same stage of tumor development. The additional complexity in testing breast cancer therapies in the mouse is that all 10 mammary glands can develop tumors, frequently at different times. Methods: To circumvent the variable tumor latency and lack of synchrony in GEM, we transplanted tumor fragments or cell suspensions from multiple mammary tumor-bearing GEM into the mammary fat pad or subcutaneously into naïve syngeneic, immunodeficient athymic nude, or scid mice. Results: Tumors transplanted as fragments or cell suspensions derived from anterior mammary gland grew faster than the posterior tumors for serial passages without any significant morphologic differences. Cell suspensions using fresh or frozen cells were equally effective in generating tumors, and increasing the numbers of transplanted cells resulted in faster tumor growth. The transplantation strategy was reproducible in multiple breast cancer mouse models, including MMTV-PyMT, -Her2/neu, -wnt1/p53, BRCA1/p53, and others. Metastatic disease in the lungs was evident after removing the primary tumors at different rates for each mouse model. The transplanted primary tumors and the tumors arising in the original GEM had similar morphologic appearance and sensitivity to several chemotherapeutic and novel molecular targeted agents. Conclusions: We have established transplantable synchronous mammary tumors from GEM which also develop metastatic disease. These valuable mouse models are suitable for studying tumor-host interactions, tumor progression, and preclinical testing in a well-characterized molecular and genetic background. Testing these GEM tumors for conventional and novel molecular targeted therapies will be discussed. No significant financial relationships to disclose.
2

Klenner, Marbod, Pia Freidel, Mariella G. Filbin, and Alexander Beck. "DIPG-39. New preclinical models for Diffuse Midline Glioma." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i27. http://dx.doi.org/10.1093/neuonc/noac079.096.

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Abstract Malignant brain tumors are the leading cause of childhood death in Germany, with Diffuse Midline Glioma (DMG) being the most lethal of all paediatric brain tumors. Current treatment strategies are limited to irradiation which prolongs survival only by a few months. Preclinical studies have identified effective drug candidates, but translation into the clinic remains a major obstacle. It is known that interactions between tumor cells and components of the TME (tumor microenvironment), such as cell to cell contacts between malignant and non-malignant cells or secreted factors, can increase therapy resistance and progression of brain tumors. However, these important factors are not present in most conventional cell culture models for drug testing. Consequently, there is a need for more realistic DMG models to improve the relevance and translational potential of current drug screening. Therefore, the goal of this study was to develop a new DMG model for drug testing, consisting of induced pluripotent stem cell (iPSC) derived human brain cells and patient derived DMG cells to better mimic the complex tumor microenvironment. We co-cultured three-dimensional cerebral organoids with DMG tumor spheres resulting in the formation of DMG-Brain-Organoids (DBO). Preliminary results show that co-culture induces distinct tumor cell subpopulations corresponding to those detected in DMG tumors by single cell RNA sequencing (Filbin et al., 2018). These subpopulations mainly differ in their proliferative capacity and their differential response to clinical interventions may be critical for therapeutic success. DBOs subjected to drug treatments (single or combination) were sectioned and individual therapy effects on tumor cell subpopulations and proliferative capacity were monitored using multiplexed immunofluorescence imaging. By observing drug effects in a realistic setup, we hope to improve the predictive power of our preclinical drug screens and to find new combination therapies for DMG.
3

Costa, Alice, Livia Gozzellino, Margherita Nannini, Annalisa Astolfi, Maria Abbondanza Pantaleo, and Gianandrea Pasquinelli. "Preclinical Models of Visceral Sarcomas." Biomolecules 13, no. 11 (November 6, 2023): 1624. http://dx.doi.org/10.3390/biom13111624.

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Visceral sarcomas are a rare malignant subgroup of soft tissue sarcomas (STSs). STSs, accounting for 1% of all adult tumors, are derived from mesenchymal tissues and exhibit a wide heterogeneity. Their rarity and the high number of histotypes hinder the understanding of tumor development mechanisms and negatively influence clinical outcomes and treatment approaches. Although some STSs (~20%) have identifiable genetic markers, as specific mutations or translocations, most are characterized by complex genomic profiles. Thus, identification of new therapeutic targets and development of personalized therapies are urgent clinical needs. Although cell lines are useful for preclinical investigations, more reliable preclinical models are required to develop and test new potential therapies. Here, we provide an overview of the available in vitro and in vivo models of visceral sarcomas, whose gene signatures are still not well characterized, to highlight current challenges and provide insights for future studies.
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Llaguno-Munive, Monserrat, Wilberto Villalba-Abascal, Alejandro Avilés-Salas, and Patricia Garcia-Lopez. "Near-Infrared Fluorescence Imaging in Preclinical Models of Glioblastoma." Journal of Imaging 9, no. 10 (October 6, 2023): 212. http://dx.doi.org/10.3390/jimaging9100212.

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Cancer is a public health problem requiring ongoing research to improve current treatments and discover novel therapies. More accurate imaging would facilitate such research. Near-infrared fluorescence has been developed as a non-invasive imaging technique capable of visualizing and measuring biological processes at the molecular level in living subjects. In this work, we evaluate the tumor activity in two preclinical glioblastoma models by using fluorochrome (IRDye 800CW) coupled to different molecules: tripeptide Arg-Gly-Asp (RGD), 2-amino-2-deoxy-D-glucose (2-DG), and polyethylene glycol (PEG). These molecules interact with pathological conditions of tumors, including their overexpression of αvβ3 integrins (RGD), elevated glucose uptake (2-DG), and enhanced permeability and retention effect (PEG). IRDye 800CW RGD gave the best in vivo fluorescence signal from the tumor area, which contrasted well with the low fluorescence intensity of healthy tissue. In the ex vivo imaging (dissected tumor), the accumulation of IRDye 800CW RGD could be appreciated at the tumor site. Glioblastoma tumors were presently detected with specificity and sensitivity by utilizing IRDye 800CW RGD, a near-infrared fluorophore combined with a marker of αvβ3 integrin expression. Further research is needed on its capacity to monitor tumor growth in glioblastoma after chemotherapy.
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Sewduth, Raj N., and Konstantina Georgelou. "Relevance of Carcinogen-Induced Preclinical Cancer Models." Journal of Xenobiotics 14, no. 1 (January 5, 2024): 96–109. http://dx.doi.org/10.3390/jox14010006.

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Chemical agents can cause cancer in animals by damaging their DNA, mutating their genes, and modifying their epigenetic signatures. Carcinogen-induced preclinical cancer models are useful for understanding carcinogen-induced human cancers, as they can reproduce the diversity and complexity of tumor types, as well as the interactions with the host environment. However, these models also have some drawbacks that limit their applicability and validity. For instance, some chemicals may be more effective or toxic in animals than in humans, and the tumors may differ in their genetics and phenotypes. Some chemicals may also affect normal cells and tissues, such as by causing oxidative stress, inflammation, and cell death, which may alter the tumor behavior and response to therapy. Furthermore, some chemicals may have variable effects depending on the exposure conditions, such as dose, route, and duration, as well as the animal characteristics, such as genetics and hormones. Therefore, these models should be carefully chosen, validated, and standardized, and the results should be cautiously interpreted and compared with other models. This review covers the main features of chemically induced cancer models, such as genetic and epigenetic changes, tumor environment, angiogenesis, invasion and metastasis, and immune response. We also address the pros and cons of these models and the current and future challenges for their improvement. This review offers a comprehensive overview of the state of the art of carcinogen-induced cancer models and provides new perspectives for cancer research.
6

Roosen, Mieke, Chris Meulenbroeks, Phylicia Stathi, Joris Maas, Julie Morscio, Jens Bunt, and Marcel Kool. "BIOL-11. PRECLINICAL MODELLING OF PEDIATRIC BRAIN TUMORS USING ORGANOID TECHNOLOGY." Neuro-Oncology 25, Supplement_1 (June 1, 2023): i8. http://dx.doi.org/10.1093/neuonc/noad073.030.

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Abstract Molecular characterization has resulted in improved classification of pediatric brain tumors, leading to many novel (sub)types with distinct oncodriving events. To study tumor biology and to perform translational research on each of these tumors, preclinical models are essential. However, we are currently lacking sufficient models, especially in vitro, to represent each (sub)type and their heterogeneity. To generate large series of preclinical in vitro models for pediatric brain tumors, we are using organoid technology. Cells from patient samples and patient-derived xenograft samples have been taken into culture to establish 3D organoids using tumor type specific culture conditions. These organoid lines retain the molecular characteristics of the original tumor tissue. They can be used to perform high-throughput drug screens, genetic manipulations, and co-cultures with, for instance, immune cells. Viable tissue is not always available for all tumor (sub)types and specific oncodrivers. To circumvent this lack of tissue, we can also induce tumors in vitro. Therefore, we generate cerebral and cerebellar brain organoids from human pluripotent stem cells. These organoids mimic human developing brain cells and can be genetically manipulated to model different brain tumor types. These genetically engineered brain tumor models allow us to study the cellular origins of pediatric brain tumors and the different tumor driving mechanisms. Tumors induced in the brain organoids histologically and molecularly resemble human patient samples based on (single cell) transcriptomic analyses. Moreover, the tumor cells are able to establish xenografts in mouse brains. In summary, organoid technology provides a novel avenue to establish in vitro models for pediatric brain tumors. At the meeting we will present data for various new ependymoma, medulloblastoma and embryonal brain tumor organoid models.
7

Stripay, Jennifer L., Thomas E. Merchant, Martine F. Roussel, and Christopher L. Tinkle. "Preclinical Models of Craniospinal Irradiation for Medulloblastoma." Cancers 12, no. 1 (January 5, 2020): 133. http://dx.doi.org/10.3390/cancers12010133.

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Medulloblastoma is an embryonal tumor that shows a predilection for distant metastatic spread and leptomeningeal seeding. For most patients, optimal management of medulloblastoma includes maximum safe resection followed by adjuvant craniospinal irradiation (CSI) and chemotherapy. Although CSI is crucial in treating medulloblastoma, the realization that medulloblastoma is a heterogeneous disease comprising four distinct molecular subgroups (wingless [WNT], sonic hedgehog [SHH], Group 3 [G3], and Group 4 [G4]) with distinct clinical characteristics and prognoses has refocused efforts to better define the optimal role of CSI within and across disease subgroups. The ability to deliver clinically relevant CSI to preclinical models of medulloblastoma offers the potential to study radiation dose and volume effects on tumor control and toxicity in these subgroups and to identify subgroup-specific combination adjuvant therapies. Recent efforts have employed commercial image-guided small animal irradiation systems as well as custom approaches to deliver accurate and reproducible fractionated CSI in various preclinical models of medulloblastoma. Here, we provide an overview of the current clinical indications for, and technical aspects of, irradiation of pediatric medulloblastoma. We then review the current literature on preclinical modeling of and treatment interventions for medulloblastoma and conclude with a summary of challenges in the field of preclinical modeling of CSI for the treatment of leptomeningeal seeding tumors.
8

Sitta, Juliana, Pier Paolo Claudio, and Candace M. Howard. "Virus-Based Immuno-Oncology Models." Biomedicines 10, no. 6 (June 18, 2022): 1441. http://dx.doi.org/10.3390/biomedicines10061441.

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Immunotherapy has been extensively explored in recent years with encouraging results in selected types of cancer. Such success aroused interest in the expansion of such indications, requiring a deep understanding of the complex role of the immune system in carcinogenesis. The definition of hot vs. cold tumors and the role of the tumor microenvironment enlightened the once obscure understanding of low response rates of solid tumors to immune check point inhibitors. Although the major scope found in the literature focuses on the T cell modulation, the innate immune system is also a promising oncolytic tool. The unveiling of the tumor immunosuppressive pathways, lead to the development of combined targeted therapies in an attempt to increase immune infiltration capability. Oncolytic viruses have been explored in different scenarios, in combination with various chemotherapeutic drugs and, more recently, with immune check point inhibitors. Moreover, oncolytic viruses may be engineered to express tumor specific pro-inflammatory cytokines, antibodies, and antigens to enhance immunologic response or block immunosuppressive mechanisms. Development of preclinical models capable to replicate the human immunologic response is one of the major challenges faced by these studies. A thorough understanding of immunotherapy and oncolytic viruses’ mechanics is paramount to develop reliable preclinical models with higher chances of successful clinical therapy application. Thus, in this article, we review current concepts in cancer immunotherapy including the inherent and synthetic mechanisms of immunologic enhancement utilizing oncolytic viruses, immune targeting, and available preclinical animal models, their advantages, and limitations.
9

Ortiz, Michael Vincent, Armaan Siddiquee, Daoqi You, Prabhjot Singh Mundi, Lianna Marks, Kristina Guillan, Daniel Diolaiti, et al. "Preclinical evaluation of XPO1 inhibition in Wilms tumors." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): 3580. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.3580.

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3580 Background: XPO1 is a nuclear export protein that selectively transports tumor and growth regulatory proteins out of the nucleus, thereby effectively inhibiting their function. We previously utilized the Virtual Inference of Protein-activity by Enriched Regulon analysis (VIPER) algorithm to discover that malignant rhabdoid tumors were dependent upon XPO1 inhibition and then evaluated a preclinical cohort using selinexor (KPT-330), the first-in-class selective inhibitor of nuclear export, to demonstrate that XPO1 inhibition was sufficient to cause cell cycle arrest, apoptosis, and disease control in multiple cell line and patient derived xenograft (PDXs) models. Our subsequent analysis revealed that the most common childhood kidney tumor, Wilms tumor, has even high higher inferred activity of XPO1 than rhabdoid tumors leading to our hypothesis that XPO1 inhibition is an effective therapeutic strategy to treat Wilms tumors. Methods: A panel of 9 Wilms tumor cell lines and 3 Wilms tumor PDXs were genomically characterized and tested to evaluate the pre-clinical efficacy of XPO1 inhibition in Wilms tumors. Results: Proliferation rate, increased XPO1 protein expression, and loss of function mutations in TP53 correlated with in vitro Wilms tumor cell line sensitivity to selinexor. Evaluation of co-segregation of all single nucleotide variant changes using with inferred activity of XPO1 on VIPER in all TGCA tumors demonstrates a strong association with TP53 alterations. XPO1 inhibition was effective in all Wilms tumor models tested, most significantly in MSKREN-57196, a favorable histology Wilms tumor PDX with somatic 1q gain as well as WTX and MYCN mutations, as well as in MSKREN-31827, a diffusely anaplastic TP53 mutant Wilms tumor PDX. Eltanexor (KPT-8602) is an XPO1 inhibitor with decreased CNS penetration and an improved toxicity profile; this drug was tested in these in vivo models and found to be at least as effective as selinexor. Conclusions: Somatic 1q gain in favorable histology Wilms tumors and TP53 mutations in diffusely anaplastic Wilms tumors have a particularly poor prognosis in the relapsed setting. Our study demonstrates that XPO1 inhibition may provide a rational therapeutic option to treat such high-risk Wilms tumors. Future clinical trials evaluating XPO1 inhibitors should evaluate its efficacy in children with relapsed Wilms tumors.
10

Bella, Ángela, Claudia Augusta Di Trani, Myriam Fernández-Sendin, Leire Arrizabalaga, Assunta Cirella, Álvaro Teijeira, José Medina-Echeverz, Ignacio Melero, Pedro Berraondo, and Fernando Aranda. "Mouse Models of Peritoneal Carcinomatosis to Develop Clinical Applications." Cancers 13, no. 5 (February 25, 2021): 963. http://dx.doi.org/10.3390/cancers13050963.

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Peritoneal carcinomatosis of primary tumors originating in gastrointestinal (e.g., colorectal cancer, gastric cancer) or gynecologic (e.g., ovarian cancer) malignancies is a widespread type of tumor dissemination in the peritoneal cavity for which few therapeutic options are available. Therefore, reliable preclinical models are crucial for research and development of efficacious treatments for this condition. To date, a number of animal models have attempted to reproduce as accurately as possible the complexity of the tumor microenvironment of human peritoneal carcinomatosis. These include: Syngeneic tumor cell lines, human xenografts, patient-derived xenografts, genetically induced tumors, and 3D scaffold biomimetics. Each experimental model has its own strengths and limitations, all of which can influence the subsequent translational results concerning anticancer and immunomodulatory drugs under exploration. This review highlights the current status of peritoneal carcinomatosis mouse models for preclinical development of anticancer drugs or immunotherapeutic agents.
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Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Preclinical tumor models":

1

MINOLI, LUCIA. "TUMOR MICROENVIRONMENT IN EXPERIMENTAL PRECLINICAL MOUSE MODELS OF HUMAN CANCER: MORPHOLOGICAL APPROACH." Doctoral thesis, Università degli Studi di Milano, 2020. http://hdl.handle.net/2434/704551.

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One of the recent advancements in oncological research has been the recognition of the tumor microenvironment (TME) as a relevant participant during all stages of the evolution of a neoplastic process. Indeed, over the past decades, tumors have been considered through a changing perspective: no longer as a growth of homogeneous neoplastic cells, but as an actual organ composed of different cell populations and structures: the parenchyma being the neoplastic population and the stroma, including the vascular network and infiltrating cells. The tumor microenvironment has a dual role in tumor biology, both promoting and antagonizing tumor development, growth, and local or distant invasiveness. According to its leading role in influencing tumor biology each component of the TME could be considered as a potential pharmacological target to be enhanced or antagonized, in order to influence tumor behavior. Accordingly, the study of the TME could provide new insights in the tumor biology and offers numerous potential targets for the development of novel therapeutic strategies. In this context, morphological techniques represent useful tools for the investigation of the TME, allowing the evaluation of the spatial distribution of the different elements, and provide useful complementary information to clinical and other data obtained in experimental in vivo studies. In this thesis, the three main classes of the TME components -tumor-associated vasculature, immune-inflammatory cells and tumor stroma- are illustrated in three different chapters and relevant experimental studies described. However, it should be considered that the various aspects of TME are not separate entities but are all involved in a dynamic system with complex structural and functional interactions. Chapter 1 – Tumor-associated vasculature Tumor angiogenesis has been identified as a hallmark of cancer, due to its central role in supporting tumoral growth, providing nutrient supply, removing catabolites and enabling tumoral metastatic dissemination. Most of the solid tumors are characterized by an “angiogenetic switch” in which an imbalance between pro- and anti-angiogenic factors sustains a dysregulated angiogenetic process, leading to the formation of an altered vascular network composed of structurally and functionally abnormal blood vessels. Drugs targeting tumor vasculature has been extensively studied as a mean to interfere with tumoral growth as well as to promote the delivery and/or effect of co-administered compounds to the tumor. In the first study of this chapter, we demonstrated the therapeutic efficacy and the antiangiogenic effect of a novel compound developed by binding sunitinib (a well-known antiangiogenic drug) to a selective binder of αVβ3 integrin thus promoting its delivery to the target site (tumors expressing αVβ3 integrin). The other studies of this chapter investigated the relation between tumor vasculature and tumor hypoxia. In particular, this relation was investigated to uncover the potential mechanism underlying the synergistic effect of the administration of an antiangiogenic compound (cediranib) with a poly-ADP ribose polymerase (PARP) inhibitor (olaparib) in a panel of patient-derived xenografts of ovarian carcinoma. Chapter 2 – Tumor immune microenvironment In most cancers, both innate and acquired immunity have a driving role during all stages of tumor development and progression. Depending on the cell population and/or molecular stimuli received, they can act in a dual way, antagonizing or promoting tumor growth. Three selected studies were described in chapter 2 and investigated: 1. The role of NK cells in hindering metastasis engraftment in a metastatic model of synovial sarcoma. After the combined administration of an heparanase-inhibitor with a tyrosine kinase inhibitor a significant reduction of lung metastases was observed and immunohistochemical analyses demonstrated the role of NK cells in this phenomenon. 2. The macrophage polarization status in a panel of xenotransplanted thyroid carcinoma tumors. The mononuclear-phagocyte populations infiltrating the tumors were evaluated by immunohistochemistry. 3. The role of inflammation in the development of colorectal cancer was evaluated in mice (wild type and EMILIN1-mutant), undergoing administration of AOM-SS (chemical carcinogenesis model). EMILIN1 mutant mice developed more numerous and more severe tumoral lesions compared to wild type, as well as increased inflammatory infiltrate was observed, unveiling a potential contribution of Emilin 1 in the pathogenesis of colorectal adenocarcinoma. Chapter 3 – Tumor stroma Tumor stroma represents not only the scaffold in which tumors growth, but also an intricate network of molecules and signals influencing tumor biology. The first study of this chapter investigated stroma-derived circulating molecules as a potential tool for the early diagnosis of pancreatic ductal adenocarcinoma (PDAC). Selected molecules (MMP-7, TIMP-1 and Throbospondin-2) were tested in KC genetically engineered mice (modeling the early stages of PDAC development) and patient-derived xenografts (modeling tumor progression), by serum ELISA and by immunohistochemistry. The second study evaluated the potential improvement in the biodistribution of chemotherapeutic drugs derived from the combined treatment with hyaluronidase. Tumor-bearing mice (ovarian carcinoma and pancreatic carcinoma models) were treated with chemotherapy alone (paclitaxel) or combined with hyaluronidase. Hyaluronidase treatment reduced the amount of stromal hyaluronic acid (as demonstrated by Alcian blue stain) and improved intratumor distribution of paclitaxel (as analyzed by mass spectrometry).
2

Chen, Liu Qi. "Development and Application of AcidoCEST MRI for Evaluating Tumor Acidosis in Pre-Clinical Cancer Models." Diss., The University of Arizona, 2014. http://hdl.handle.net/10150/323450.

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Tumor acidosis is an important biomarker in cancer. We have developed a noninvasive imaging method, termed acidosis Chemical Exchange Saturation Transfer (acidoCEST) MRI to measure extracellular pH (pHe) in the tumor microenvironment. Chapter 1 introduces the importance of measuring tumor acidosis and presents various imaging modalities and their shortcoming to measure pHe. Chapter 2 describes the optimization of acidoCEST MRI for in vivo pHe measurement. The acidoCEST MRI protocol consists of a CEST-FISP acquisition and Lorentzian line shape fittings. We determined the optimal saturation time, saturation power and bandwidth, 5 sec, 2.8 µT and 90 Hz respectively. We also tried various routes of administration to increase contrast agent uptake in the tumor. We decided upon 200 µL bolus followed by 150 µL/hr infusion. The optimized acidoCEST MRI protocol was tested on a mammary carcinoma mouse model of MDA- MB-231. Our method can detect an increase in pHe in the bladder and tumor of the mice treated with bicarbonate. We used this optimized acidoCEST MRI method to measure pHe in lymphoma tumor model of Raji, Ramos and Granta 519 as described in Chapter 3. Pixel-wise pHe maps showed tumor heterogeneity. The pHe of Raji, Ramos and Granta 519 were determined to be mildly acidic with no significant difference. Chapter 4 describes the evolution of pixel-wise analysis in more detail. Besides the pHe map and spatial heterogeneity, we were able to determine the % contrast agent uptake. We monitored these biomarkers in two different mammary carcinoma mouse models, MDA- MB-231 and MCF-7 longitudinally and made comparisons between the different tumor models: MCF-7 were more acidic, more heterogeneous and faster growing than MDA- MB-231.
3

Denton, Nicholas Lee Denton. "Modulation of tumor associated macrophages enhances oncolytic herpes virotherapy in preclinical models of Ewing sarcoma." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1523892800897524.

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4

TOSCA, ELENA MARIA. "Dynamic energy budget based models of tumor-in-host growth inhibition and cachexia onset in preclinical settings." Doctoral thesis, Università degli studi di Pavia, 2019. http://hdl.handle.net/11571/1242427.

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Il processo di sviluppo di un nuovo farmaco oncologico e' caratterizzato da un elevatissimo numero di fallimenti, principalmente dovuti alla scarsa efficacia o eccessiva tossicita' riscontrata durante le fasi di sperimentazione clinica. Tra le possibili cause di questo fenomeno vi sono l'utilizzo di modelli animali poco rappresentativi della condizione umana e la mancanza di un paradigma di traslazione dal contesto preclinico a quello clinico sufficientemente predittivo. L'utilizzo di modelli farmacometrici, capaci di estrapolare, sintetizzare e integrare le informazioni raccolte durante la sperimentazione preclinica, puo' essere un promettente tentativo di rispondere a queste problematiche. Inserendosi nell'ambito dell'uso della modellistica matematica a supporto del processo di sviluppo di nuovi farmaci antitumorali, questa tesi si concentra sulla costruzione, implementazione ed analisi di nuovi approcci matematici per l'analisi di dati sperimentali tradizionalmente ottenuti durante le fasi di sperimentazione preclinica. Focus specifico di questo lavoro e' la modellizzazione delle interazioni tra tumore e organismo ospitante durante la somministrazione di trattamenti antitumorali resa possibile dall'utilizzo di un set di leggi di bilancio energetico fornite dalla Dynamic Energy Budget theory. L'approccio proposto, opporunatamente declinato in diversi contesti sperimetali, e' capace di tenere simultaneamente in considerazione i differenti aspetti che caratterizzano gli studi di crescita tumorale in vivo: l'effetto citotossico o citostatico della terapia antitumorale sulle cellule tumorali, l'eventuale insorgere di fenomeni di cachexia come conseguenza del trattamento o del tumore stesso infine, l'influenza che la condizione dell'organismo ha sulla crescita tumorale. Piu' nel dettaglio, e' stato sviluppato ed analizzato dal punto di vista matematico un modello di interazione tumore-organismo capace di descrivere sia l'effetto inibitorio sulla crescita tumorale di un trattamento citotossico, sia il suo effetto tossico sull'organismo ospitante. Tale modello e' stato, in particolare, adottato per analizzare dati sperimentali circa l'effetto del farmaco etoposide su ratti Wistar. E' stato inoltre sviluppato un secondo modello, sempre basato sulle interazioni energetiche di tumore e organismo, per descrivere l'effetto citostatico di un trattamento anti-angiogenico. L'approccio meccanicistico alla base del modello proposto ha permesso di tenere in considerazioni l'insorgere di fenomeni di resistenza mediata dalla condizione di ipossia tumorale in seguito a trattamenti prolungati di bevacizumab. Infine, utilizzando i modelli di inibizione di crescita tumorale precedentemente sviluppati, e' stato proposto un nuovo approccio per analizzare esperimenti di combinazione e riconoscere eventuali interazioni tra farmaci anti-angiogenici e chemioterapici.
The anticancer drug development process is characterized by the highest attrition rates in the clinical setting, primarily due to adverse efficacy and safety results. Preclinical animal models slightly representative of the human condition and an inadequate predictive paradigm of preclinical to clinical translation may be likely causes of this. Pharmacometric models, able to extract, synthesize and integrate preclinical information, could support the transfer of the preclinical results to the clinical setting. Within the paradigm of the Model-Informed Drug Discovery and Development, my thesis deals with the development, implementation and analysis of new mathematical modeling approaches to exploit data routinely generated in the preclinical phases of anticancer drug development process. In all the described research activities it can be recognized the importance of PK/PD modeling in better characterizing, understanding and predicting PK/PD behaviour of oncology agents. The focus of this work is a mathematical modeling of interactions between tumor and host organism during anticancer drug treatments in preclinical experiments. To this aim, a tumor-in-host modeling approach is proposed on the basis of a set of tumor-host interaction rules taken from the Dynamic Energy Budget (DEB) theory. This framework, suitably adapted to several experimental contexts, is able to integrate the different aspects characterizing the in vivo tumor growth studies: the drug cytotoxic or cytostatic activity on the tumor, the eventually onset of cachexia due to the treatment, the effect of the tumor on the host and, viceversa, the influence of the host condition on tumor dynamics. In particular, a tumor-in-host DEB-based model describing the cachexia onset and tumor growth inhibition (TGI) after the administration of cell-killing agents has been developed, mathematically analysed and, subsequently, applied on a etoposide experiment in Wistar rats. The cytostatic anticancer effect of angiogenesis inhibitors in xenograft mice has been, also, modeled within the tumor-in-host DEB-based framework. This DEB-TGI anti-angiogenic model has proved to be extremely useful to describe and understand the complexities of an hypoxia-triggered resistance to bevacizumab. Finally, starting from the previous developed TGI models, a tumor-in-host approach to analyse combination experiments and assess possible drug-drug interaction between anti-angiogenic and chemotherapeutic agents is proposed.
5

Lahr, Christoph Alexander. "Tissue-engineering humanised bone sarcoma models in rodents-a preclinical study platform for orthopaedic research." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/207759/1/Christoph%20Alexander_Lahr_Thesis.pdf.

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This thesis is a step forward in preclinical in-vivo disease modelling, designed to find new diagnostic and therapeutic options, to ultimately improve the poor outcome of patients with primary bone cancer. Combining the principles of tissue-engineering, 3D-printing and advanced gene editing techniques the preclinical animal models developed in this thesis have important clinical implications that could shape future innovative treatment plans. Particularly the translation of a humanised osteosarcoma model from a mouse into a newly engineered severely immunocompromised rat will facilitate preclinical primary bone cancer research by opening up new experimental avenues for complex surgical resection and reconstruction models.
6

Laranga, Roberta <1985&gt. "Development of Preclinical Models of Mammary Carcinogenesis: Functional Role of Her2 and its Isoforms in Tumor Progression and in Drug Resistance." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2017. http://amsdottorato.unibo.it/7832/1/Laranga_Roberta_Tesi.pdf.

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Overexpression of huHER2 occurs in nearly 15–20% of breast cancers, and it is generally associated with poor patient survival. Existing therapies such as trastuzumab and lapatinib are currently used in the treatment of HER2-positive cancers, although issues with high recurrence and acquired resistance still remain. Elucidation of the molecular mechanisms underlying resistance is leading to the identification of therapies and strategies to manage resistance to HER2-targeted therapies. In addition to intrinsic and acquired resistance associated to HER2 oncogene, the induction of bypass pathways that reactivate growth factor-dependent signalling upon oncogene inhibition is likely pervasive across cancers and should be anticipated. Together, these findings underscore that many resistance mechanisms fall into predictable and therapeutically tractable themes, and can be effectively targeted with rationally designed combined therapies. It is, therefore, necessary to come back to dissect HER2 pathway and unravel key features contributing to its transforming capacity. The present thesis, is focused on the role played by HER2-loss variants and Delta16 isoform in mediating HER2 oncogenic activity and in conditioning the response to HER2 therapies in breast cancer. These HER2 phenotypes can drive differential drug responses of the tumor and of distant metastases. Thus, recent investigations on drug resistance and on tumor biology converged to the development of preclinical cancer models representative of cancer heterogeneity and able to mimic all possible scenarios observed in human tumors. In this project, thanks to the availability of several preclinical models representative of HER2 postive breast cancer, it was studied the contribute of HER2 and of its variants to cancer development and drug resistance. In addition, with the purpose of obtaining preclinical models that could best recapitulate human tumor heterogeneity a panel of breast cancer PDX was developed.
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Fuchs, Jeannette [Verfasser], and Thorsten [Akademischer Betreuer] Stiewe. "Establishment and characterization of preclinical mouse models for evaluation of oncogenic and tumor-suppressive properties of p53 family members / Jeannette Fuchs ; Betreuer: Thorsten Stiewe." Marburg : Philipps-Universität Marburg, 2017. http://d-nb.info/1131253272/34.

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Ferreira, Luís Pedro Correia Pinto. "Development of multicelular 3D cancer testing platforms for evaluation of new anti-cancer therapies." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/22713.

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Mestrado em Bioquímica Clínica
O cancro do pulmão (CP) é um dos cancros mais diagnosticados a nível mundial e também um dos mais mortíferos. Atualmente, as terapias administradas a nível clínico para o tratamento do CP são ainda extremamente ineficazes e limitadas no que diz respeito ao aumento da taxa de sobrevivência dos pacientes oncológicos. Esta realidade demonstra a necessidade de investigar ativamente novas terapias para o tratamento desta neoplasia. No entanto a validação pré-clínica de terapias inovadoras para o CP tem-se revelado extremamente difícil devido à inexistência de plataformas que sejam adequadas para testes a nível laboratorial, uma vez que as culturas celulares in vitro bidimensionais (2D), recomendadas pelas agências regulatórias são incapazes de mimetizar as caraterísticas principais dos tumores humanos. Estas limitações têm originado uma fraca correlação entre a performance das terapias nos estudos in vitro e a obtida em ensaios clínicos controlados. Neste contexto, os modelos de tumores tridimensionais (3D) in vitro têm vindo a ser reconhecidos como uma solução para este problema, pois podem recapitular várias componentes do microambiente tumoral. Das várias plataformas 3D in vitro de CP investigadas atualmente muito poucas avaliaram o papel da inclusão de células estaminais mesenquimais (MSCs). Para colmatar esta lacuna, o trabalho de investigação desenvolvido no âmbito desta dissertação descreve a produção e otimização de novos modelos hétero-celulares 3D in vitro. Estas plataformas são compostas por células tumorais do CP (A549) e do seu estroma, nomeadamente fibroblastos da pele e células estaminais mesenquimais derivadas da medula óssea (BM-MSCs). Estes três tipos de células foram co-cultivadas em micropartículas poliméricas de policaprolactona revestidas por ácido hialurónico, com o objetivo de incluir este componente da matriz extracelular que se encontra presente no microambiente do CP. Esta abordagem permitiu formar a nível laboratorial microtecidos multicelulares 3D híbridos que melhor mimetizam a heterogeneidade celular das neoplasias pulmonares. Os resultados obtidos demonstraram que os microtumores formados através da técnica de sobreposição-líquida são reprodutíveis em termos de morfologia e tamanho, apresentaram núcleos necróticos, organização celular 3D e produziram proteínas do microambiente tumoral. Além destas caraterísticas, os dados obtidos através de microscopia de fluorescência revelaram que as BM-MSCs migram para o interior dos microtumores ao longo do tempo. A avaliação da citotoxicidade da Doxorubicina, um fármaco anti-tumoral rotineiramente utilizado a nível clínico, demonstrou que a inclusão de micropartículas aumenta a resistência das células tumorais em modelos homotípicos. Nos modelos tri-cultura heterotípicos a citotoxicidade foi comparável à obtida em microtumores sem micropartículas. Estes resultados evidenciam assim o papel importante dos fibroblastos e das BM-MSCs na resposta dos microtumores. Numa visão global, os modelos 3D formados recapitulam com mais exatidão o microambiente do cancro do pulmão e poderão servir no futuro como plataformas de teste para descobrir ou aperfeiçoar novas terapias, ou combinações de terapêuticas, para este tipo de neoplasia.
Lung cancer (LC) is one the most commonly diagnosed cancers worldwide, being also one of the deadliest. Currently, clinically administered therapies for treatment of LC are still extremely ineffective and limited in increasing oncologic patients survival rates. This reality evidences the necessity of actively investigating novel therapies for the treatment of LC. However, preclinical validation of novel therapies as revealed itself as an extremely arduous process, due to the lack of suitable laboratory testing platforms since the recommend in vitro bi-dimensional (2D) cell cultures are unable to fully mimic the main hallmarks of human tumors. In this context, in vitro tridimensional (3D) tumor models are being increasingly recognized as a solution due to their ability to correctly recapitulate several characteristics of the tumor microenvironment (TME). Amongst currently developed 3D in vitro platforms for the study of LC, few have included or studied the role of mesenchymal stem cells (MSCs). To provide further insights into this hypothesis, the research work developed in this thesis describes the production and optimization of novel heterotypic in vitro 3D models, comprised by non-small-cell lung cancer cells (A549) and stromal cells, namely skin fibroblasts (HFs), and bone-marrow derived mesenchymal stem cells (BM-MSCs). These three diverse cell populations were co-cultured in hyaluronic acid coated polymeric polycaprolactone microparticles (LbL-MPs) as to include this key extracellular matrix component of LC TME. This approach allowed the formation of 3D multicellular heterotypic microtissues (3D-MCTS) that better recapitulate the cellular heterogeneity of LC TME in the laboratory. The obtained findings demonstrate that these models formed via the liquid-overlay technique were reproducible in terms of morphology and size, presented necrotic core formation, 3D cellular organization, and deposited matrix proteins in a similar manner as in the TME. Besides this, fluorescence microscopy data revealed that BM-MSCs migrated overtime into the microtumors core . Performed doxorubicin in vitro cytotoxicity assays revealed that the inclusion of LbL-MPs lead to an increased resistance of homotypic A549 monoculture models against this anti-cancer drug commonly used in clinical treatments. Alongside, the cytotoxicity obtained in triculture heterotypic models was comparable to that of microtumors without LbL-MPs inclusion, showcasing the role of HFs and BM-MSCs in microtumors response to therapy. Globally, the herein bioengineered 3D models were able to recapitulate with an increased precision the TME of LC, making them suitable test platforms for development or improvement of standalone or combinatorial therapies for this type of neoplasia.
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Wolska-Krawczyk, Malgorzata [Verfasser], and Arno [Akademischer Betreuer] Bücker. "Evaluation of liver tumor perfusion by intraarterial transcatheder magnetic resonance angiography during transarterial chemoembolization in patients with hepatocellular carcinoma : Preclinical instrument validation in vascular models and clinical study / Malgorzata Wolska-Krawczyk. Betreuer: Arno Bücker." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2014. http://d-nb.info/1056906979/34.

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Dobosz, Michael [Verfasser], Vasilis [Akademischer Betreuer] Ntziachristos, and Hans-Jürgen [Akademischer Betreuer] Wester. "The application of in vivo and ex vivo multispectral epi-fluorescence imaging for the preclinical discovery and development of monoclonal antibodies in tumor xenograft models / Michael Dobosz. Betreuer: Vasilis Ntziachristos. Gutachter: Hans-Jürgen Wester ; Vasilis Ntziachristos." München : Universitätsbibliothek der TU München, 2014. http://d-nb.info/1080903682/34.

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Books on the topic "Preclinical tumor models":

1

Fiebig, H. H. Revelance Of Tumor Models For Anticancer Drug Development (CONTRIBUTIONS TO ONCOLOGY). Edited by H. H. Fiebig. Karger, 1999.

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Holland, Eric C. Mouse Models of Human Cancer. Wiley-Liss, 2004.

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Powell, Craig M. PTEN and Autism With Macrocepaly. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0010.

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Phosphatase and Tensin homolog deleted on chromosome 10 (PTEN) is a gene encoding an intracellular signaling molecule. PTEN was originally discovered as the gene responsible for a subset of familial hamartoma (tumor) syndromes associated with increased risk for certain cancers (Nelen et al., 1997) and as a gene often mutated in human cancers and tumor cell lines (Li et al., 1997; Steck et al., 1997). More recently, mutations in PTEN have been linked genetically to the clinical phenotype of autism or developmental delay with macrocephaly (Boccone et al., 2006; Butler et al., 2005; Buxbaum et al., 2007; Goffin, Hoefsloot, Bosgoed, Swillen, & Fryns, 2001; Herman, Butter, et al., 2007; McBride et al., 2010; Orrico et al., 2009; Stein, Elias, Saenz, Pickler, & Reynolds, 2010; Varga, Pastore, Prior, Herman, & McBride, 2009; Zori, Marsh, Graham, Marliss, & Eng, 1998). This chapter examines the role of PTEN in intracellular signaling, the link between PTEN signaling pathways and other autism-related genes and signaling pathways, the genetic relationship between PTEN and autism, model systems in which effects of Pten deletion on the brain have been studied, and promising preclinical data identifying therapeutic targets for patients with autism/macrocephaly associated with PTEN mutations.

Book chapters on the topic "Preclinical tumor models":

1

Teicher, Beverly A. "Preclinical Tumor Response End Points." In Tumor Models in Cancer Research, 571–605. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_23.

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Morton, Christopher L., and Peter J. Houghton. "The Pediatric Preclinical Testing Program." In Tumor Models in Cancer Research, 195–213. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_8.

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Gerner, Eugene W., Natalia A. Ignatenko, and David G. Besselsen. "Preclinical Models for Chemoprevention of Colon Cancer." In Tumor Prevention and Genetics, 58–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55647-0_6.

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Boss, Mary-Keara, Gregory M. Palmer, and Mark W. Dewhirst. "Imaging the Hypoxic Tumor Microenvironment in Preclinical Models." In Hypoxia and Cancer, 157–78. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-9167-5_7.

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Nathanson, S. David. "Preclinical Models of Regional Lymph Node Tumor Metastasis." In Cancer Metastasis And The Lymphovascular System: Basis For Rational Therapy, 129–56. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-69219-7_10.

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Hillman, Gilda G. "Experimental Animal Models for Investigating Renal Cell Carcinoma Pathogenesis and Preclinical Therapeutic Approaches." In Tumor Models in Cancer Research, 287–305. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_12.

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Sadekar, Shraddha, Isabel Figueroa, and Harish Shankaran. "Evaluation of Tumor Growth Inhibition in Preclinical Tumor Models: A Quantitative Approach." In Development of Antibody-Based Therapeutics, 171–86. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-0496-5_8.

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Parchment, Ralph E. "Bone Marrow as a Critical Normal Tissue that Limits Drug Dose/Exposure in Preclinical Models and the Clinic." In Tumor Models in Cancer Research, 521–52. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-968-0_21.

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Chambers, Ann F., Eva A. Turley, John Lewis, and Leonard G. Luyt. "Preclinical Cell and Tumor Models for Evaluating Radiopharmaceuticals in Oncology." In Monoclonal Antibody and Peptide-Targeted Radiotherapy of Cancer, 397–417. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470613214.ch11.

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Jacoberger-Foissac, Celia, Bertrand Allard, David Allard, and John Stagg. "Assessing the Efficacy of Immune Checkpoint Inhibitors in Preclinical Tumor Models." In Methods in Molecular Biology, 151–69. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2914-7_11.

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Conference papers on the topic "Preclinical tumor models":

1

Bagley, Rebecca G., Yi Ren, Leslie Kurtzberg, William Weber, Dinesh Bangari, and Beverly A. Teicher. "Abstract 1596: Human choriocarcinomas: Placental growth factor-dependent preclinical tumor models." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1596.

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Faia, Kerrie, Alberto Toso, Kristina Fetalvero, Marly Roche, Steven Bench, Erin O'Hearn, Qiongfang Cao, et al. "Abstract 1717: MAP4K1 inhibition enhances immune cell activation and anti-tumor immunity in preclinical tumor models." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1717.

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Welm, Alana L. "Abstract IA07: Breast tumor grafts as preclinical models for anti-metastasis therapy." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-ia07.

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Doody, Jacqueline, Sneha Mathew, Lan Wu, Yanxia Li, Ying Wang, Kris Persaud, Douglas Burtrum, et al. "Abstract 3539: Anti-CSF-1R antibodies reduce tumor-associated macrophages and inhibit tumor growth in preclinical models." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3539.

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Li, Yanxia, Sneha Mathew, Lan Wu, Ying Wang, Jessica Kearney, Kris Persaud, Douglas Burtrum, et al. "Abstract C224: Anti-CSF-1R antibodies reduce tumor-associated macrophages and inhibit tumor growth in preclinical models." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-c224.

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Li, Yanxia, Sneha Mathew, Lan Wu, Ying Wang, Kris Persaud, Douglas Burtrum, Paul Balderes, et al. "Abstract A235: Anti-CSF-1R antibodies reduce tumor-associated macrophages and inhibit tumor growth in preclinical models." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-a235.

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Staniszewska, Anna, Joshua Armenia, Matthew King, Chrysiis Michaloglou, Maneesh Singh, Maryann San Martin, Zena Wilson, et al. "Abstract 967: Anti-tumor and immune effects of olaparib +/- anti-PD-L1 in preclinical BRCA1mut tumor models." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-967.

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Heuer, Timothy S., Richard Ventura, Joanna Waszczuk, Kasia Mordec, Julie Lai, Russell Johnson, Lilly Hu, et al. "Abstract 1815: Efficacy of FASN-selective small molecule inhibitors in preclinical tumor models." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1815.

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Sriram, Venkataraman, Michael E. Bigler, Holly Cherwinski, Erin Murphy, Terrill K. McClanahan, and Joseph H. Phillips. "Abstract 5025: Dissecting the dynamics of anti-PD1 immunotherapy in preclinical tumor models." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5025.

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Heuer, Timothy S., Minchao Chen, Richard Ventura, Joanna Waszczuk, Satya Yendluri, Julie Lai, Samnang Tep, et al. "Abstract B261: Characterization of FASN-selective small-molecule inhibitors in preclinical tumor models." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b261.

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