Relevant bibliographies by topics / Preclinical cancer models

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Academic literature on the topic 'Preclinical cancer models'

Author: Grafiati
Published: 1 March 2025

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Journal articles on the topic "Preclinical cancer models"

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KARNEZIS, ANTHONY N., and KATHLEEN R. CHO. "Preclinical Models of Ovarian Cancer." Clinical Obstetrics and Gynecology 60, no. 4 (December 2017): 789–800. http://dx.doi.org/10.1097/grf.0000000000000312.

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Sedlack, Andrew J. H., Samual J. Hatfield, Suresh Kumar, Yasuhiro Arakawa, Nitin Roper, Nai-Yun Sun, Naris Nilubol, et al. "Preclinical Models of Adrenocortical Cancer." Cancers 15, no. 11 (May 23, 2023): 2873. http://dx.doi.org/10.3390/cancers15112873.

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Adrenocortical cancer is an aggressive endocrine malignancy with an incidence of 0.72 to 1.02 per million people/year, and a very poor prognosis with a five-year survival rate of 22%. As an orphan disease, clinical data are scarce, meaning that drug development and mechanistic research depend especially on preclinical models. While a single human ACC cell line was available for the last three decades, over the last five years, many new in vitro and in vivo preclinical models have been generated. Herein, we review both in vitro (cell lines, spheroids, and organoids) and in vivo (xenograft and genetically engineered mouse) models. Striking leaps have been made in terms of the preclinical models of ACC, and there are now several modern models available publicly and in repositories for research in this area.
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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.
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Jeon, Min Ji, and Bryan R. Haugen. "Preclinical Models of Follicular Cell-Derived Thyroid Cancer: An Overview from Cancer Cell Lines to Mouse Models." Endocrinology and Metabolism 37, no. 6 (December 31, 2022): 830–38. http://dx.doi.org/10.3803/enm.2022.1636.

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The overall prognosis of thyroid cancer is excellent, but some patients have grossly invasive disease and distant metastases with limited responses to systemic therapies. Thus, relevant preclinical models are needed to investigate thyroid cancer biology and novel treatments. Different preclinical models have recently emerged with advances in thyroid cancer genetics, mouse modeling and new cell lines. Choosing the appropriate model according to the research question is crucial to studying thyroid cancer. This review will discuss the current preclinical models frequently used in thyroid cancer research, from cell lines to mouse models, and future perspectives on patient-derived and humanized preclinical models in this field.
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McIntyre, Rebecca E., Simon J. A. Buczacki, Mark J. Arends, and David J. Adams. "Mouse models of colorectal cancer as preclinical models." BioEssays 37, no. 8 (June 26, 2015): 909–20. http://dx.doi.org/10.1002/bies.201500032.

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Zhu, Shaoming, Zheng Zhu, Ai-Hong Ma, Guru P. Sonpavde, Fan Cheng, and Chong-xian Pan. "Preclinical Models for Bladder Cancer Research." Hematology/Oncology Clinics of North America 35, no. 3 (June 2021): 613–32. http://dx.doi.org/10.1016/j.hoc.2021.02.007.

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Rodriguez, Cynthia, Paloma Valenzuela, Natzidielly Lerma, and Giulio Francia. "Preclinical Models to Study Breast Cancer." Clinical Cancer Drugs 1, no. 2 (May 31, 2014): 90–99. http://dx.doi.org/10.2174/2212697x113026660005.

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Kim, Minlee, Andrea L. Kasinski, and Frank J. Slack. "MicroRNA therapeutics in preclinical cancer models." Lancet Oncology 12, no. 4 (April 2011): 319–21. http://dx.doi.org/10.1016/s1470-2045(11)70067-5.

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Joshi, Kirtan, Tejas Katam, Akshata Hegde, Jianlin Cheng, Randall S. Prather, Kristin Whitworth, Kevin Wells, et al. "Pigs: Large Animal Preclinical Cancer Models." World Journal of Oncology 15, no. 2 (April 2024): 149–68. http://dx.doi.org/10.14740/wjon1763.

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Sedlack, Andrew J. H., Kimia Saleh-Anaraki, Suresh Kumar, Po Hien Ear, Kate E. Lines, Nitin Roper, Karel Pacak, et al. "Preclinical Models of Neuroendocrine Neoplasia." Cancers 14, no. 22 (November 17, 2022): 5646. http://dx.doi.org/10.3390/cancers14225646.

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Neuroendocrine neoplasia (NENs) are a complex and heterogeneous group of cancers that can arise from neuroendocrine tissues throughout the body and differentiate them from other tumors. Their low incidence and high diversity make many of them orphan conditions characterized by a low incidence and few dedicated clinical trials. Study of the molecular and genetic nature of these diseases is limited in comparison to more common cancers and more dependent on preclinical models, including both in vitro models (such as cell lines and 3D models) and in vivo models (such as patient derived xenografts (PDXs) and genetically-engineered mouse models (GEMMs)). While preclinical models do not fully recapitulate the nature of these cancers in patients, they are useful tools in investigation of the basic biology and early-stage investigation for evaluation of treatments for these cancers. We review available preclinical models for each type of NEN and discuss their history as well as their current use and translation.
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Dissertations / Theses on the topic "Preclinical cancer models"

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Chaffee, Beth K. "Preclinical Modeling of Musculoskeletal Cancer." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376844544.

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Delgado, San Martin Juan A. "Mathematical models for preclinical heterogeneous cancers." Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=230139.

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Cancer is a deadly, complex disease with 14 million new cases diagnosed every year and the endeavour to develop a cure is a global multidisciplinary effort. The complexity of cancer and the resulting vast volume of data derived from its research necessitates a robust and cutting-edge system of mathematical and statistical modelling. This thesis proposes novel mathematical models of quantification and modelling applied to heterogeneous preclinical cancers, focusing on the translation of animal studies into patients with particular emphasis on tumour stroma. The first section of this thesis (quantification) will present different techniques of extracting and quantifying data from bioanalytical assays. The overall aim will be to present and discuss potential methods of obtaining data regarding tumour volume, stromal morphology, stromal heterogeneity, and oxygen distribution. Firstly, a 3D scanning technique will be discusses. This technique aims to assess tumour volume in mice more precisely than the current favoured method (callipers) and record any cutaneous symptoms as well, with the potential to revolutionise tumour growth analysis. Secondly, a series of image processing methods will be presented which, when applied to tumour histopathology, demonstrate that tumour stromal morphology and its microenvironment play a key role in tumour physiology. Lastly, it will be demonstrated through the integration of in-vitro data from various sources that oxygen and nutrient distribution in tumours is very irregular, creating metabolic niches with distinct physiologies within a single tumour. Tumour volume, oxygen, and stroma are the three aspects central to the successful modelling of tumour drug responses over time. The second section of this thesis (modelling) will feature a mathematical oxygen-driven model - utilising 38 cell lines and 5 patient-derived animal models - that aims to demonstrate the relationship between homogeneous oxygen distribution and preclinical tumour growth. Finally, all concepts discussed will be merged into a computational tumour-stroma model. This cellular automaton (stochastic) model will demonstrate that tumour stroma plays a key role in tumour growth and has both positive (at a molecular level) and negative (at both a molecular and tissue level) effects on cancers. This thesis contains a useful set of algorithms to help visualise, quantify, and understand tissue phenomena in cancer physiology, as well as providing a series of platforms to predict tumour outcome in the preclinical setting with clinical relevance.
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PEDERZOLI, FILIPPO. "Microbiome and bladder cancer." Doctoral thesis, Università Vita-Salute San Raffaele, 2021. http://hdl.handle.net/20.500.11768/121778.

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The microbiome has gained increasing momentum in cancer research, as it has become clear that microorganisms residing within our body are involved in mediating the cellular and tissue metabolism in health and disease. In bladder cancer research, there are different microbial communities that may mediate cancer pathobiology and response to therapy: the gut microbiome, the urinary microbiome, the urothelium-bound microbiome. These bacterial communities may mediate the processes of carcinogenesis or recurrence, modify the response to local intravesical therapies or influence the activity of systemic anticancer protocols. Based on these premises, my research project aimed to unveil the urinary and urothelium-bound microbiome in therapy-naïve bladder cancer patients, describing the differently enriched bacterial communities using a sex-based stratification. Compared to healthy controls, I found that the urine of men affected by bladder cancer were enriched in the order Opitutales and subordinate family Opitutaceae, together with the isolated class Acidobacteria-6, while in female patients I found enriched the genus Klebsiella. Notably, the bladder cancer tissue was enriched in the genus Burkholderia in both men and women, when compared to non-neoplastic, paired urothelium biopsies. Then, I also characterized the gut microbiome of bladder cancer patients undergoing neoadjuvant pembrolizumab to understand if the intestinal bacteria may influence the immune-mediated anticancer activity. In this set, I have reported that antibiotic therapy has a negative effect on immunotherapy efficacy. Second, the gut microbiome of patients not responding to neoadjuvant pembrolizumab was characterized by a higher abundance of Ruminococcus bromii, while patients who showed a response were enriched in the genus Sutterella. Lastly, I started the implementation of in vivo and in vitro systems to test the mechanistic role of the bacteria identified in human samples. This thesis work reported innovative data on the role of different microbial communities (urinary/urothelium-bound/fecal) in bladder cancer and bladder cancer therapy, and provided novel in vivo and in vitro models to validate those finding and uncover the complex microbiome-host cells crosstalk in bladder cancer patients.
The microbiome has gained increasing momentum in cancer research, as it has become clear that microorganisms residing within our body are involved in mediating the cellular and tissue metabolism in health and disease. In bladder cancer research, there are different microbial communities that may mediate cancer pathobiology and response to therapy: the gut microbiome, the urinary microbiome, the urothelium-bound microbiome. These bacterial communities may mediate the processes of carcinogenesis or recurrence, modify the response to local intravesical therapies or influence the activity of systemic anticancer protocols. Based on these premises, my research project aimed to unveil the urinary and urothelium-bound microbiome in therapy-naïve bladder cancer patients, describing the differently enriched bacterial communities using a sex-based stratification. Compared to healthy controls, I found that the urine of men affected by bladder cancer were enriched in the order Opitutales and subordinate family Opitutaceae, together with the isolated class Acidobacteria-6, while in female patients I found enriched the genus Klebsiella. Notably, the bladder cancer tissue was enriched in the genus Burkholderia in both men and women, when compared to non-neoplastic, paired urothelium biopsies. Then, I also characterized the gut microbiome of bladder cancer patients undergoing neoadjuvant pembrolizumab to understand if the intestinal bacteria may influence the immune-mediated anticancer activity. In this set, I have reported that antibiotic therapy has a negative effect on immunotherapy efficacy. Second, the gut microbiome of patients not responding to neoadjuvant pembrolizumab was characterized by a higher abundance of Ruminococcus bromii, while patients who showed a response were enriched in the genus Sutterella. Lastly, I started the implementation of in vivo and in vitro systems to test the mechanistic role of the bacteria identified in human samples. This thesis work reported innovative data on the role of different microbial communities (urinary/urothelium-bound/fecal) in bladder cancer and bladder cancer therapy, and provided novel in vivo and in vitro models to validate those finding and uncover the complex microbiome-host cells crosstalk in bladder cancer patients.
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Benoni, Alexandra. "Oxytocin, as a hormonal treatment for cachexia in preclinical models." Electronic Thesis or Diss., Sorbonne université, 2022. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2022SORUS290.pdf.

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L'ocytocine (OT), une hormone neurohypophysaire, affecte le système nerveux central (SNC), l'utérus et les glandes mammaires. Il a été récemment démontré que l'OT favorise la différenciation myogénique et la régénération musculaire. En effet, les niveaux d'OT diminuent avec l'âge et son administration exogène contrecarre la sarcopénie chez les souris âgées. La cachexie est un syndrome caractérisé par une sévère fonte musculaire. Nous avons remarqué des niveaux inférieurs d'OT circulant chez les patients cachectiques atteints de cancer. Pour prouver que l'OT inhibe les facteurs dérivés de la tumeur, nous avons d'abord effectué des expériences in vitro montrant que l'inhibition de la différenciation myogénique exercée par le milieu conditionné par la tumeur C26 (CM) est inversée par le cotraitement avec l'OT. Ceci a été confirmée in vivo, car l'OT accélérait la régénération musculaire suite à une lésion focale, inhibé par le TNF. Dans un modèle préclinique, OT a restauré la masse musculaire squelettique, la taille des fibres et inhibé le catabolisme protéique. Nous nous sommes concentrés sur les effets de la tumeur et d’OT sur le métabolisme des protéines, en marquant spécifiquement les protéines nouvellement synthétisées. Dans les myoblastes co-cultivés avec des cellules tumorales, nous avons observé une diminution des protéines nouvellement synthétisées, contrecarré par le traitement OT. Nous montrons pour la première fois que l'OT est efficace pour contrecarrer les effets des facteurs dérivés de la tumeur
Oxytocin (OT), a neurohypophyseal hormone, affects the central nervous system (CNS), uterus, and mammary glands. OT has recently been shown to promote myogenic differentiation and muscle regeneration. Indeed, OT levels decrease with age and its exogenous administration counteracts sarcopenia in aged mice. Cachexia is a syndrome characterized by severe muscle wasting. We noticed lower levels of circulating OT in cachectic cancer patients. To prove that OT inhibits tumor-derived factors, we first performed in vitro experiments showing that the inhibition of myogenic differentiation exerted by C26 tumor-conditioned medium (CM) is reversed by co-treatment with OT. We confirmed in vivo that OT accelerated muscle regeneration following focal injury, inhibited by TNF. In a preclinical model, OT restored skeletal muscle mass, fiber size, and inhibited protein catabolism. We focused on the effects of tumor and OT on protein metabolism, specifically labeling newly synthesized proteins. In myoblasts co-cultured with tumor cells, we observed a decrease in newly synthesized proteins, counteracted by OT treatment. We show for the first time that OT is effective in counteracting the effects of tumor-derived factors
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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).
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Casagrande, Naike. "Anticancer activity of liposomal cisplatin in preclinical models of cervical and ovarian cancer." Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423785.

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Cisplatin-based chemotherapy improves survival in cervical and ovarian cancer; however, treatment is associated with tumor resistance and significant toxicity. Lipoplatin (Regulon Inc., Mountain View, California) is a liposomal encapsulated form of cisplatin, developed in an effort to reduce cisplatin‟s systemic toxicity, while simultaneously improving the targeting of drugs to primary tumor and metastasis. Lipoplatin has been successfully administered in several randomized Phase II and III clinical trials, but not in cervical and ovarian cancer. The aim of this project was to analyze the antitumoral activity of lipoplatin in cisplatin-sensitive and cisplatin-resistant cervical and ovarian cancer cells. I evaluated the antiproliferative activity of lipoplatin, with cisplatin as reference drug, in the ME-180 cervical cancer cell line and its cisplatin-resistant clone R-ME-180, and in a panel of ovarian cancer cell lines: A2780, its cisplatin-resistant clone A2780cis, MDAH, OVACR3, OVCAR5, SKOV3, and TOV21G. Results demonstrated that lipoplatin exhibited a potent antitumoral activity in all the tested cell lines, including cisplatin-resistant cells, indicating that there is no cross-resistance between the two drugs. Lipoplatin induced apoptosis, as evaluated by Annexin-V staining and DNA fragmentation. In particular, it induced the mitochondrial apoptotic pathway causing mitochondrial membrane permeabilization, cytochrome-c release, Bcl-2 down-regulation, but Bax up-regulation, and caspases 9 and 3 activation. At the same experimental conditions cisplatin induced apoptosis only in cisplatin-sensitive cells. Moreover, lipoplatin, but not cisplatin, increased reactive oxygen species (ROS) accumulation and inhibited the enzymatic activity of thioredoxin reductase (TrxR), an enzyme involved in ROS detoxification and over-expressed in many tumor cells contributing to drug resistance. Furthermore, lipoplatin reduced EGFR expression and inhibited both migration and invasion. Multiple drug treatment is widely used in chemotherapy to obtain an additive or a synergistic effect (more than additive). I combined lipoplatin with the chemotherapeutic agents mostly used in ovarian cancer treatment. The results showed that the combination of lipoplatin with doxorubicin or abraxane demonstrated a synergistic effect, whereas the combination of lipoplatin with docetaxel or paclitaxel was less effective or at best additive. In the ascites of ovarian cancer patients there are multicellular aggregates or spheroids that are involved in tumor progression. Thus, spheroid-based assays are more predictive of in vivo therapeutic efficacy because they more closely resemble tumor microenvironment. Furthermore, cancer stem cells (CSC), rare tumor cells involved in initiating cancer growth, drug resistance, and disease recurrence, are also present in spheroids. The treatment with lipoplatin reduced stem cell markers in a dose-dependent manner and inhibited spheroid formation in both cervical and ovarian cancer models. Furthermore, it decreased ovarian cancer spheroid growth, vitality, and migration. Finally, lipoplatin treatment of nude mice with cervical and ovarian tumors significantly inhibited tumor growth in vivo, with low toxicities. Moreover, even after treatment interruption the tumors did not show any regrowth. In conclusion, in this project lipoplatin demonstrated an antitumoral activity in monolayer cultures, three-dimensional spheroids, and in vivo studies using cisplatin-resistant cervical and ovarian cancer cells. These promising results suggest lipoplatin as a novel chemotherapeutic agent for the treatment of cervical and ovarian cancer.
Il cisplatino è uno dei farmaci più utilizzati per il trattamento del carcinoma della cervice e dell‟ovaio. Purtroppo il suo utilizzo in chemioterapia presenta importanti limitazioni, quali l‟elevata tossicità e l‟insorgenza di resistenza intrinseca o acquisita. Il lipoplatino è una formulazione liposomiale del cisplatino (Regulon, Inc., Mt. View, U.S.A), sintetizzata allo scopo di ridurre la tossicità sistemica del cisplatino e contemporaneamente di incrementarne l‟accumulo nel tumore primario e nelle metastasi. Studi clinici di Fase II e III sono stati effettuati in diversi tumori ma non nel carcinoma della cervice uterina e dell‟ovaio. In questo lavoro è stata analizzata l‟attività antitumorale del lipoplatino in modelli preclinici di carcinoma della cervice uterina e carcinoma ovarico sensibili e resistenti al cisplatino. L‟attività antiproliferativa del lipoplatino è stata studiata nella linea cellulare derivata da carcinoma della cervice uterina ME-180 e nel suo clone resistente al cisplatino R-ME-180, come pure in un pannello di linee cellulari derivanti da carcinoma ovarico: A2780, il suo clone cisplatino-resistente A2780cis, MDAH, OVACR3, OVCAR5, SKOV3, e TOV21G. Il cisplatino è stato introdotto nello studio come farmaco di riferimento. I risultati hanno dimostrato che il lipoplatino esibisce una potente attività antitumorale in tutte le linee cellulari analizzate, incluse le cisplatino-resistenti, dimostrando assenza di cross-resistenza con il farmaco cisplatino. Il lipoplatino induce apoptosi, valutata tramite l‟esternalizzazione della fosfatidilserina (marcatore precoce di apoptosi) e la frammentazione del DNA. In particolare, il lipoplatino attiva la via mitocondriale dell'apoptosi, come dimostrato dalla depolarizzazione della membrana mitocondriale, il rilascio del citocromo-c , la diminuzione dell‟espressione della proteina anti-apoptotica Bcl-2, l‟incremento dell‟espressione della molecola pro-apoptotica Bax e l‟attivazione delle caspasi 9 e 3. Nelle stesse condizioni sperimentali il cisplatino attiva l‟apoptosi soltanto in cellule sensibili al cisplatino. L‟enzima tioredoxina reduttasi (TrxR) svolge una funzione ossidoriduttiva proteggendo la cellula da stress ossidativo. Un elevato livello dell‟enzima si osserva in diversi tipi di tumore e sembra essere associato alla resistenza al cisplatino. I miei studi hanno dimostrato che il lipoplatino, ma non il cisplatino, inibisce l‟attività enzimatica della TrxR incrementando la produzione di radicali liberi dell‟ossigeno (ROS). Inoltre il lipoplatino riduce l‟espressione del recettore del fattore di crescita dell‟epidermide (EGFR), un recettore di membrana over-espresso nei tumori, coinvolto nella proliferazione e nella migrazione delle cellule tumorali. Anche la migrazione e l‟invasione cellulare vengono ridotte dal trattamento con lipoplatino. Molto spesso in chemioterapia si somministra una combinazione di più farmaci (polichemioterapia) per ottenere un effetto additivo e/o sinergico. Si è quindi combinato il lipoplatino con i chemioterapici più utilizzati nel trattamento del carcinoma ovarico. La combinazione del lipoplatino con i farmaci doxorubicina e abraxane dimostra effetti sinergici, mentre la combinazione con docetaxel e paclitaxel è meno efficace con effetti quasi additivi. Nell‟ascite di pazienti affette da carcinoma ovarico si possono ritrovare aggregati multicellulari, o sferoidi, che sembrano essere coinvolti nella progressione tumorale. Gli sferoidi rappresentano un valido modello sperimentale con caratteristiche biologiche e molecolari simili ai tumori solidi, tra queste la presenza di cellule staminali cancerose, ossia cellule con grandi capacità rigenerative e di resistenza alle terapie in grado di alimentare la crescita del tumore. Il trattamento con lipoplatino diminuisce in maniera dose-dipendente i marcatori di staminalità e inibisce la formazione di sferoidi in entrambi i modelli sperimentali. Inoltre riduce la dimensione, la vitalità e la disseminazione di sferoidi di carcinoma ovarico. Infine il lipoplatino diminuisce la crescita di tumori xenografi derivanti da cellule di carcinoma della cervice uterina e dell‟ovaio con ridotta tossicità. Anche in seguito all‟interruzione del trattamento i tumori non riprendono la crescita. Concludendo il lipoplatino dimostra un‟attività antitumorale in colture cellulari tradizionali, in colture tridimensionali o sferoidi ed in vivo, sia di cellule derivanti da carcinoma della cervice uterina cisplatino-resistenti che da carcinoma ovarico. Questi risultati molto promettenti suggeriscono un potenziale utilizzo di questa formulazione liposomiale di cisplatino per il trattamento di pazienti affette dalle suddette patologie.
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García, Parra Jetzabel 1983. "PARP1 expression in breast cancer and effects of its inhibition in preclinical models." Doctoral thesis, Universitat Pompeu Fabra, 2012. http://hdl.handle.net/10803/84173.

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Breast cancer is the main cause of cancer death in women. Improved treatments, prevention programs and earlier detection are reducing the rate of death; however, there is still a high percentage of mortality by this cancer. Identification of novel targets to predict response to specific treatments is a key goal for personalizing breast cancer therapy and to improve survival. Few years ago, PARP inhibitors appeared as a promising therapy, particularly in BRCA-mutated cancers. However, there was a clear need to conduct further preclinical and translational work to improve the rational development of PARP inhibition in breast cancer. In this work we described PARP1 expression in breast tumour samples and characterized the effects of its inhibition in preclinical models. We found that nuclear PARP1 protein overexpression was associated with malignant transformation and poor prognosis in breast cancer. PARP1 overexpression was more common in triple negative subtype, but was also detectable in small subsets of estrogen receptor positive and HER2 positive breast cancers. In preclinical models, PARP1 played distinct roles in different molecular subtypes of breast cancer. Moreover, we described that olaparib (novel PARP inhibitor) had antitumour effects in different breast cancer subtypes, and its combination with trastuzumab (anti-HER2 antibody) enhanced the antitumour effects of this therapy.
El càncer de mama és la principal causa de mort per càncer en dones. La millora dels tractaments i la detecció precoç estan reduint la taxa de mort, però segueix sent elevada. Identificar noves dianes per predir la resposta a tractaments és clau per millorar les teràpies contra aquest càncer i la supervivència. Els inhibidors de PARP van aparèixer com una teràpia prometedora, particularment en càncers BRCA-mutants, però, cal dur a terme més estudis preclínics i translacionals per fomentar un desenvolupament racional d’aquesta teràpia en càncer de mama. Aquest treball descriu l’expressió de PARP1 en mostres de tumors mamaris i caracteritza els efectes de la seva inhibició a models preclínics. Vam observar que la sobreexpressió nuclear de la proteïna PARP1 fou associada amb: la transformació maligna; mal pronòstic en càncer de mama; i fou més freqüent al subtipus triple-negatiu, però també es va detectar en un subgrup de càncers de mama receptors d’estrogen positius i HER2 positius. En models preclínics, PARP1 va exercir rols diferents als diferents subtipus de càncer de mama. Per altra banda, vam descriure que olaparib (inhibidor de PARP) té efectes antitumorals en els diversos subtipus, i combinat amb trastuzumab (anticòs anti-HER2) potencia els efectes antitumorals d’aquesta teràpia.
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Jawad, Dhafer Sahib. "Chemopreventive effect of resveratrol in preclinical colorectal cancer models with different genetic drivers." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/40308.

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Previous reports indicate resveratrol can modulate many processes and targets in colorectal cancer (CRC) cells and rodent models but it is uncertain whether these effects translate to humans in vivo. The lack of relevant experimental models, particularly premalignant colorectal cells, the major targets for prevention, is a significant obstacle to translation of effective preventive agents to the clinic. Development of improved 3-dimensional organoid models with discrete mutational drivers (Apc, Apc+Kras and Braf) representing different subtypes of early CRC is an aim of this thesis. A further aim is to evaluate resveratrol across these models and examine in greater detail the ability of resveratrol to interfere with the development of cancers driven by mutant BrafV600E. Organoid cultures using intestinal cells isolated from genetically engineered mice and human cancer/adenoma tissue were successfully established and conditions optimised to allow long-term maintenance. Notably, the organoids derived from adenomas arising in Villin-Cre/BrafV600E mice constitute a novel preclinical model of CRC. After first demonstrating that resveratrol had anti-proliferative activity across a panel of human CRC cell lines with different mutation profiles it was tested in the organoids at clinically-achievable concentrations for effects on autophagy, senescence, apoptosis and stem cells. Administration of a high-fat diet to Villin-Cre/BrafV600E mice enhanced Braf-induced cryptal hyperplasia in a short-term study and this was significantly reduced by resveratrol. In a follow-up survival study, high dose resveratrol greatly prolonged the lifespan of Villin-Cre/BrafV600E mice on high-fat diet. However, resveratrol had no effect on the survival of mice given standard diet. Overall, these findings suggest a specific interaction between mutant Braf expressed in mouse intestine and high-fat, and that the effects are blocked by high dose resveratrol. Future studies are needed to investigate underlying mechanisms. Results suggest resveratrol may have value in the prevention of colorectal adenomas/cancers with different genetic alterations, including mutant BrafV600E.
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Gronbach, Leonie [Verfasser]. "Organotypic head and neck cancer models for advanced preclinical drug testing / Leonie Gronbach." Berlin : Freie Universität Berlin, 2021. http://d-nb.info/1230407316/34.

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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.
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Books on the topic "Preclinical cancer models"

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Tuli, Hardeep Singh, ed. Drug Targets in Cellular Processes of Cancer: From Nonclinical to Preclinical Models. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7586-0.

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A, Jones Peter, and Michael Lübbert. Epigenetic Therapy of Cancer: Preclinical Models and Treatment Approaches. Springer London, Limited, 2013.

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A, Jones Peter, and Michael Lübbert. Epigenetic Therapy of Cancer: Preclinical Models and Treatment Approaches. Springer, 2016.

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A, Jones Peter, and Michael Lübbert. Epigenetic Therapy of Cancer: Preclinical Models and Treatment Approaches. Springer, 2014.

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Tuli, Hardeep Singh. Drug Targets in Cellular Processes of Cancer: From Nonclinical to Preclinical Models. Springer Singapore Pte. Limited, 2020.

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Tuli, Hardeep Singh. Drug Targets in Cellular Processes of Cancer: From Nonclinical to Preclinical Models. Springer Singapore Pte. Limited, 2021.

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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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Lee, Gregory. Epitope/Peptide-Based Monoclonal Antibodies for Immunotherapy of Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0007.

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Two monoclonal antibodies, RP215 and GHR106, were selected, respectively, for the research and development of anti-cancer drugs targeting ovarian cancer and other types of human cancer. RP215 was shown to react with a carbohydrate-associated epitope located mainly in the variable regions of immunoglobulin heavy chains expressed on the surface of almost all cancer cells in humans. GHR106 was generated against a synthetic peptide corresponding to N1-29 amino acid residues in the extracellular domains of human GnRH receptor, which is surface-expressed by most cancer cells as well as the anterior pituitary. This monoclonal antibody was shown to serve as a bioequivalent analog to GnRH-derived decapeptides currently used clinically. The molecular mechanisms of action of these two antibody-based anti-cancer drug candidates were well elucidated following numerous biochemical, immunological, and molecular biological studies, mainly by using ovarian cancer as the model. Further preclinical studies with humanized forms of these two antibodies are essential.
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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.
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Book chapters on the topic "Preclinical cancer models"

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Mika, Joanna, Wioletta Makuch, and Barbara Przewlocka. "Preclinical Cancer Pain Models." In Cancer Pain, 71–93. London: Springer London, 2013. http://dx.doi.org/10.1007/978-0-85729-230-8_6.

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Cheng, Menglin, and Kristine Glunde. "Magnetic Resonance Spectroscopy Studies of Mouse Models of Cancer." In Preclinical MRI, 331–45. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7531-0_20.

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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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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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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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Yang, Ying, Wen-Jian Meng, and Zi-Qiang Wang. "Preclinical Models in Colorectal Cancer Drug Discovery." In Handbook of Animal Models and its Uses in Cancer Research, 1097–106. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-3824-5_56.

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Yang, Ying, Wen-Jian Meng, and Zi-Qiang Wang. "Preclinical Models in Colorectal Cancer Drug Discovery." In Handbook of Animal Models and its Uses in Cancer Research, 1–10. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-1282-5_56-1.

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Juvekar, Aarti S., Joyce Thompson, Clinton F. Stewart, and Peter J. Houghton. "Preclinical Models for Evaluating Topoisomerase I-Targeted Drugs." In Camptothecins in Cancer Therapy, 127–51. Totowa, NJ: Humana Press, 2005. http://dx.doi.org/10.1385/1-59259-866-8:127.

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Carbajal, Eletha, and Eric C. Holland. "Mouse Models in Preclinical Drug Development: Applications to CNS Models." In Genetically Engineered Mice for Cancer Research, 549–67. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-69805-2_26.

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Conference papers on the topic "Preclinical cancer models"

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Bouvet, Michael, and Robert M. Hoffman. "Preclinical fluorescent mouse models of pancreatic cancer." In Biomedical Optics (BiOS) 2007, edited by Samuel Achilefu, Darryl J. Bornhop, Ramesh Raghavachari, Alexander P. Savitsky, and Rebekka M. Wachter. SPIE, 2007. http://dx.doi.org/10.1117/12.708060.

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Duchamp, Olivier, Gael Krysa, Robin Artus, Hugo Quillery, Maxime Ramelet, Valerie Boullay, Laure Levenez, et al. "Abstract 5638: Liver preclinical models - acute, chronic and cancer 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.am2020-5638.

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Rosen, JM. "Abstract DL-1: Leveraging Preclinical Models of Breast Cancer." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-dl-1.

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Bamberg, C., I. Witzel, A. Wöckel, S. Seiler, S. Loibl, K. Thiele, A. Diemert, and PC Arck. "Breast cancer during pregnancy: from preclinical models to clinical studies." In 64. Kongress der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe e. V. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1756750.

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Nguyen, Holly M., Colm Morrissey, Peter S. Nelson, Xiaotun Zhang, Paul H. Lange, Robert L. Vessella, and Eva Corey. "Abstract 1214: Preclinical models of prostate cancer: New patient-derived xenografts for preclinical studies and evaluation of prostate cancer biology." 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.am2014-1214.

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KHOO, Bee Luan, and Jing Zhang. "Anti-inflammatory combinatorial therapy to enhance killing efficacy with patient-derived preclinical models." In The 1st International Electronic Conference on Cancers: Exploiting Cancer Vulnerability by Targeting the DNA Damage Response. Basel, Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/iecc2021-09204.

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Trachet, Erin E., Sumithra Urs, Alden Wong, Scott Wise, and Maryland Rosenfeld Franklin. "Abstract 1928: Radiation response in preclinical orthotopic models of brain cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1928.

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Trachet, Erin E., Sumithra Urs, Alden Wong, Scott Wise, and Maryland Rosenfeld Franklin. "Abstract 1928: Radiation response in preclinical orthotopic models of brain cancer." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1928.

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Shannon, Kevin. "Abstract IA14: Preclinical models for targeting oncogenic Ras signaling in cancer." In Abstracts: AACR Special Conference on Hematologic Malignancies: Translating Discoveries to Novel Therapies; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.hemmal14-ia14.

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Freed-Pastor, William A., Laurens Lambert, Ana P. Garcia, George Eng, Omer Yilmaz, and Tyler Jacks. "Abstract PR14: Preclinical models to dissect immune escape in pancreatic cancer." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-pr14.

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Reports on the topic "Preclinical cancer models"

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Gregerson, Karen A. Human-Compatible Animal Models for Preclinical Research on Hormones in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada574629.

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Jiang, Weiqin, and Zongjian Zhu. Exploitation of Nontraditional Crop, Yacon, in Breast Cancer Prevention Using Preclinical Rat Model. Fort Belvoir, VA: Defense Technical Information Center, July 2010. http://dx.doi.org/10.21236/ada541863.

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Abate-Shen, Corry. Preclinical Studies of Signaling Pathways in a Mutant Mouse Model of Hormone-Refractory Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2011. http://dx.doi.org/10.21236/ada549157.

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Kumar, Aishani, Thendral Yalini, and Sunil Kumar C. Unlocking Cellular Control: The Promise of PROTACs in Disease Intervention. Science Reviews - Biology, May 2024. http://dx.doi.org/10.57098/scirevs.biology.3.2.1.

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The discovery of proteolysis-targeting chimeras (PROTACs) is among the most exciting and promising avenues in cancer therapy. These fascinating compounds signify a paradigm shift from traditional approaches to medication development, offering a new idea that leverages the complexities of biological mechanisms to accomplish highly focused degradation of particular proteins implicated in pathological processes. This novel strategy has the potential to address a number of drawbacks with conventional therapy techniques, such as the development of drug resistance and unexpected adverse effects resulting from interactions that are not intended. The fundamental attraction of PROTACs is their distinct mode of action, which is based on controlling the cell's own machinery for protein degradation. This orchestrated degradation translates to a substantial reduction in the levels of disease-driving proteins, often leading to the disruption of critical pathways involved in cancer growth and progression. The in-depth principles underlying PROTAC technology are thoroughly explored in this review study, which also provides insight into the complex chemical mechanisms that enable these chimeric molecules to specifically degrade certain proteins while leaving others intact. Showcasing the potential of PROTACs as a revolutionary force in targeted cancer therapy, and focusing on its application in prostate and breast cancer especially, the article draws from a comprehensive compilation of preclinical and clinical studies, advancements, and breakthroughs in the field. The methods used to create and refine PROTACs for various cancer types will be examined throughout the review, along with the subtleties of the ligand and linker choices that are crucial to their effectiveness and selectivity. The difficulties and possibilities of transferring this ground-breaking technology from the lab to clinical practice will also be thoroughly examined, with an emphasis on issues like bioavailability, administration strategies, and potential resistance mechanisms. Through the integration of perspectives from various studies, the objective is to present a thorough but succinct review of the state of ongoing PROTAC research, emphasizing both, noteworthy advancements and the important issues that still need to be resolved. In the end, our investigation into PROTACs aims to shed light on how they can change the face of cancer therapy by providing a preview of a day when targeted protein degradation of disease-causing proteins would lead the way in novel therapeutic approaches.
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