Relevant bibliographies by topics / Tumor chemoresistance

Academic literature on the topic 'Tumor chemoresistance'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "Tumor chemoresistance"

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Yeldag, Gulcen, Alistair Rice, and Armando Del Río Hernández. "Chemoresistance and the Self-Maintaining Tumor Microenvironment." Cancers 10, no. 12 (November 28, 2018): 471. http://dx.doi.org/10.3390/cancers10120471.

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The progression of cancer is associated with alterations in the tumor microenvironment, including changes in extracellular matrix (ECM) composition, matrix rigidity, hypervascularization, hypoxia, and paracrine factors. One key malignant phenotype of cancer cells is their ability to resist chemotherapeutics, and elements of the ECM can promote chemoresistance in cancer cells through a variety of signaling pathways, inducing changes in gene expression and protein activity that allow resistance. Furthermore, the ECM is maintained as an environment that facilitates chemoresistance, since its constitution modulates the phenotype of cancer-associated cells, which themselves affect the microenvironment. In this review, we discuss how the properties of the tumor microenvironment promote chemoresistance in cancer cells, and the interplay between these external stimuli. We focus on both the response of cancer cells to the external environment, as well as the maintenance of the external environment, and how a chemoresistant phenotype emerges from the complex signaling network present.
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Oplt, Alyssa, Elizabeth Stock, Hollie Noia, Patrick Cannon, Gregory Longmore, and Katherine C. Fuh. "Abstract 3235: The role of DDR2 in chemoresistant ovarian cancer." Cancer Research 82, no. 12_Supplement (June 15, 2022): 3235. http://dx.doi.org/10.1158/1538-7445.am2022-3235.

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Abstract Ovarian cancer is the fifth leading cause of cancer death for women in the United States. As many as 80% of ovarian cancer patients experience recurrent disease and the majority of recurrences become resistant to treatment. Once patients no longer respond to chemotherapy, there are minimal treatment options and they succumb to their disease. Therefore, there is a need to create new targeted therapies to overcome chemoresistance in ovarian cancer and improve patient survival. We have assembled a tumor microarray from 164 patient tumors to characterize the changes in protein expression that lead to resistance in clinical samples. We have found using IHC staining, that patients with high tyrosine kinase receptor discoidin domain receptor 2 (DDR2) protein expression (>70%) have significantly shorter overall survival times regardless of stage at diagnosis (HR= 2.108, p=0.002) as well as reduced platinum free interval (p=0.046). Additionally, platinum refractory tumors have higher DDR2 protein expression than platinum sensitive tumors (p=0.036). To further understand the mechanisms of chemoresistance, we created a novel, chemoresistant, syngeneic, mouse ovarian cancer cell line derived from ID8 trp53-/-BRCA2-/- GFP LUC cells from Walton et. al 2016, and have designated them CHRP5. DDR2 expression assessed via western blot increased significantly in the chemoresistance cells, suggesting that DDR2 is associated with chemoresistance. We knocked down DDR2 using a stable shRNA transfection in CHRP5 and used MTS survival assays to determine if decreased DDR2 expression increases sensitivity to chemotherapy. CHRP5 shDDR2 cells were significantly more sensitive to carboplatin than CHRP5 shControl cells (CHRP5 shControl IC50=213.6uM, CHRP5 shDDR2 IC50=128.5uM, p<0.000001), suggesting that DDR2 is involved in regulating chemoresistance in these cells. Additionally, we have submitted matched chemoresistant and chemosensitive mouse tumor samples for RNA-sequencing. We will use this data to determine which chemoresistant mechanisms are utilized, and if DDR2 is involved in regulating those mechanisms. In the future, we plan to rescue DDR2 in the knockdown cells to confirm that off target effects are not influencing the change in sensitivity. We also have access to a specific, allosteric inhibitor of DDR2 and plan to use this drug to determine if inhibiting DDR2 pharmacologically can overcome chemoresistance and reduce tumor burden in vivo and in vitro. In conclusion, DDR2 is more highly expressed in chemoresistant patients, and higher DDR2 expression correlates with reduced survival and platinum free interval. Additionally, knocking down DDR2 in chemoresistant cells increases sensitivity to chemotherapy. Therefore, DDR2 is a potential new target for ovarian cancer therapy and may be targeted to overcome chemoresistant disease and extend patient survival. Citation Format: Alyssa Oplt, Elizabeth Stock, Hollie Noia, Patrick Cannon, Gregory Longmore, Katherine C. Fuh. The role of DDR2 in chemoresistant ovarian cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 3235.
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Gronlund, B., E. V. S. Høgdall, I. J. Christensen, J. S. Johansen, B. Nørgaard-Pedersen, S. A. Engelholm, and C. Høgdall. "Pre-Treatment Prediction of Chemoresistance in Second-Line Chemotherapy of Ovarian Carcinoma: Value of Serological Tumor Marker Determination (Tetranectin, YKL-40, CASA, CA 125)." International Journal of Biological Markers 21, no. 3 (July 2006): 141–48. http://dx.doi.org/10.1177/172460080602100302.

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Objective To examine if the determination of the levels of serological tumor markers at time of relapse had any predictive value for chemoresistance in the second-line treatment of ovarian cancer patients. Methods From a registry of consecutive single-institution patients with epithelial ovarian carcinoma pretreated with paclitaxel plus platinum, we selected 82 patients with (a) solid tumor recurrence, and (b) second-line chemotherapy consisting of topotecan (platinum-resistant disease) or paclitaxel plus carboplatin (platinum-sensitive disease). Stored serum samples were analyzed for the biochemical tumor markers tetranectin, YKL-40, CASA (cancer-associated serum antigen), and CA 125. The serum tumor marker levels at time of relapse were correlated with response status at landmark time after 4 cycles of second-line chemotherapy. Univariate and multivariate logistic regression analyses (chemoresistant vs non-chemoresistant disease) were performed. Results At landmark time, 26% of patients had progression according to the GCIG (Gynecologic Cancer Intergroup) progression criteria. In univariate logistic regression analysis, the tumor markers tetranectin (OR 0.4; 95% CI: 0.2–0.8; p=0.008), YKL-40 (OR 1.8; 95% CI: 1.0–3.3; p=0.045), and CASA (OR 1.8; 95% CI: 1.2–2.7; p=0.007) had predictive value for second-line chemoresistance, whereas serum CA 125 had no predictive value. In a multivariate logistic regression analysis, serum tetranectin and CASA both had independent predictive value for chemoresistance. The combined determination of tetranectin and CASA had a specificity of 90% with 33% sensitivity for the prediction of chemoresistance (area under the receiver operating characteristic curve = 0.78; 95% CI: 0.66–0.91; p=0.001). Conclusion Low serum levels of tetranectin, or high serum levels of CASA or YKL-40, are associated with increased risk of second-line chemoresistance in patients with ovarian cancer.
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Wu, Qitong, Sumit Siddharth, and Dipali Sharma. "Triple Negative Breast Cancer: A Mountain Yet to Be Scaled Despite the Triumphs." Cancers 13, no. 15 (July 23, 2021): 3697. http://dx.doi.org/10.3390/cancers13153697.

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Metastatic progression and tumor recurrence pertaining to TNBC are certainly the leading cause of breast cancer-related mortality; however, the mechanisms underlying TNBC chemoresistance, metastasis, and tumor relapse remain somewhat ambiguous. TNBCs show 77% of the overall 4-year survival rate compared to other breast cancer subtypes (82.7 to 92.5%). TNBC is the most aggressive subtype of breast cancer, with chemotherapy being the major approved treatment strategy. Activation of ABC transporters and DNA damage response genes alongside an enrichment of cancer stem cells and metabolic reprogramming upon chemotherapy contribute to the selection of chemoresistant cells, majorly responsible for the failure of anti-chemotherapeutic regime. These selected chemoresistant cells further lead to distant metastasis and tumor relapse. The present review discusses the approved standard of care and targetable molecular mechanisms in chemoresistance and provides a comprehensive update regarding the recent advances in TNBC management.
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Belisario, Dimas Carolina, Joanna Kopecka, Martina Pasino, Muhlis Akman, Enrico De Smaele, Massimo Donadelli, and Chiara Riganti. "Hypoxia Dictates Metabolic Rewiring of Tumors: Implications for Chemoresistance." Cells 9, no. 12 (December 4, 2020): 2598. http://dx.doi.org/10.3390/cells9122598.

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Hypoxia is a condition commonly observed in the core of solid tumors. The hypoxia-inducible factors (HIF) act as hypoxia sensors that orchestrate a coordinated response increasing the pro-survival and pro-invasive phenotype of cancer cells, and determine a broad metabolic rewiring. These events favor tumor progression and chemoresistance. The increase in glucose and amino acid uptake, glycolytic flux, and lactate production; the alterations in glutamine metabolism, tricarboxylic acid cycle, and oxidative phosphorylation; the high levels of mitochondrial reactive oxygen species; the modulation of both fatty acid synthesis and oxidation are hallmarks of the metabolic rewiring induced by hypoxia. This review discusses how metabolic-dependent factors (e.g., increased acidification of tumor microenvironment coupled with intracellular alkalinization, and reduced mitochondrial metabolism), and metabolic-independent factors (e.g., increased expression of drug efflux transporters, stemness maintenance, and epithelial-mesenchymal transition) cooperate in determining chemoresistance in hypoxia. Specific metabolic modifiers, however, can reverse the metabolic phenotype of hypoxic tumor areas that are more chemoresistant into the phenotype typical of chemosensitive cells. We propose these metabolic modifiers, able to reverse the hypoxia-induced metabolic rewiring, as potential chemosensitizer agents against hypoxic and refractory tumor cells.
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Trevino, J. G., S. R. Pillai, and S. P. Chellappan. "Effect of nicotine on chemoresistant phenotype as mediated through Src-dependent Id1 expression in pancreatic adenocarcinoma cells." Journal of Clinical Oncology 29, no. 4_suppl (February 1, 2011): 216. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.216.

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216 Background: The signaling pathways contributing to DNA-binding protein inhibitor Id1 expression and chemoresistance in pancreatic cancer remain unknown. Id1 plays a role in pancreatic tumor progression with tumor-promoting effects of nicotine regulating protein tyrosine kinase Src activation and Id1 expression, both associated with chemoresistance in other systems. We hypothesize Id1 expression regulates chemoresistance in pancreatic cancer through a nicotine-promoting Src-dependent pathway. Methods: We probed pancreatic cancer cell lines (L3.6pl, PANC-1, Mia-PaCa-2) for innate gemcitabine chemoresistance with cell viability MTT assay and western blot analysis of PARP cleavage programmed cell death. Gemcitabine-sensitive cells were exposed to rising gemcitabine concentrations to establish a resistant subtype, L3.6plGemRes. Protein analysis and mRNA expression were determined by western blot analysis and RT-PCR respectively. Induction of Src phosphorylation or Id1 expression was performed with nicotine (1 μM). Results: Inhibition of c-Src expression was performed with short-interfering RNA (siRNA). Nicotine-induced Src phosphorylation and Id1 expression. Inhibition of Src by siRNA resulted in decreased nicotine-induced Id1 expression. Inhibition of Src and Id1 expression by siRNA in innate or established gemcitabine resistant pancreatic cancer cells resulted in gemcitabine sensitization. To determine if nicotine contributes to gemcitabine chemoresistance, we exposed gemcitabine-sensitive cells to nicotine with subsequent exposure to gemcitabine IC50, 250 ng/ml, and cell viability assays confirmed a 2-fold increase in cell prolilferation and a 4.5-fold reduction in apoptosis. Further, nicotine induced phosphorylation of key signaling enzymes involved in proliferation and apoptosis, Erk1/2 and Akt respectively. Conclusions: In summary, we demonstrate that Id1, through a nicotine-promoting Src-dependent pathway, is necessary for establishment of a chemoresistant phenotype in pancreatic cancer cells. Understanding the signaling pathways involved in pancreatic tumor chemoresistance will lead to therapies resulting in improved tumor responses. No significant financial relationships to disclose.
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Ji, Ping, Kristen M. Turner, and Wei Zhang. "OverAKT3: tumor progression and chemoresistance." Cell Cycle 14, no. 13 (June 4, 2015): 1993–94. http://dx.doi.org/10.1080/15384101.2015.1046787.

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Brown, Elizabeth, and Maurie Markman. "Tumor chemosensitivity and chemoresistance assays." Cancer 77, no. 6 (March 15, 1996): 1020–25. http://dx.doi.org/10.1002/(sici)1097-0142(19960315)77:6<1020::aid-cncr3>3.0.co;2-l.

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Cree, Ian A., Russell D. Petty, Christian M. Kurbacher, and Michael Untch. "Tumor chemosensitivity and chemoresistance assays." Cancer 78, no. 9 (November 1, 1996): 2031–32. http://dx.doi.org/10.1002/(sici)1097-0142(19961101)78:9<2031::aid-cncr27>3.0.co;2-x.

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Kern, David H. "Tumor chemosensitivity and chemoresistance assays." Cancer 79, no. 7 (April 1, 1997): 1447–49. http://dx.doi.org/10.1002/(sici)1097-0142(19970401)79:7<1447::aid-cncr23>3.0.co;2-z.

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Dissertations / Theses on the topic "Tumor chemoresistance"

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Chau, Wing-ka, and 周穎嘉. "Characterization of ovarian tumor-initiating cells and mechanisms of chemoresistance." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/197834.

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Chemoresistance remains a major clinical obstacle to effective management of ovarian cancer. Cancer stem cells (or tumor-initiating cells, TICs) have been discovered recently, and have played a pivotal role in changing the view of cancer development; however, the molecular mechanisms by which these cells escape conventional therapies remain elusive. In this study, TICs were isolated from ovarian cancer cells as tumor spheres with specific stem properties under TIC-selective conditions. Unlike non-TICs, TICs strongly express stem cell factor (SCF) and c-Kit. Blocking SCF-c-Kit by SCF neutralizing antibodies, c-Kit small interfering RNA (siRNA) or imatinib (Gleevec), a clinical drug that inhibits c-Kit signaling, significantly inhibited TIC proliferation. Although cisplatin and paclitaxel killed the non-TICs, they did not eliminate TICs. Importantly, the combination of cisplatin/paclitaxel with c-Kit siRNA or imatinib inhibited the growth of both non-TICs and TICs. Similar results were obtained when patient-derived TICs were used. The findings also indicate that tumor-predisposing microenvironment, such as hypoxia, may promote ovarian TICs through upregulating c-Kit expression. Furthermore, I have showed that c-Kit expression induced activation of Phosphatidylinositol 3-kinases (PI3K)/Akt, -catenin, and ATP-binding cassette G2, which could be reversed by treatment with the PI3K/Akt inhibitor or -catenin siRNA. I further studied potential gene expression in TICs using cDNA and microRNA (miRNA) microarrays. The result from these microarrays provided a general profile in gene expression of TICs compared with the bulk tumor cells. In particular, let-7a, b, and c were shown to be downregulated in TICs compared to bulk tumor cells, suggesting that their loss may contribute to ovarian cancer development. Together, this study reveals a previously undescribed therapeutic effect of SCF-c-Kit signaling blockade to prevent ovarian cancer progression by eliminating TICs and the altered genes or miRNAs may represent possible molecular targets.
published_or_final_version
Biological Sciences
Master
Master of Philosophy
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Cox, Megan Christine. "Modeling the Heterogeneous Brain Tumor Microenvironment to Analyze Mechanisms of Vascular Development and Chemoresistance." Diss., Virginia Tech, 2018. http://hdl.handle.net/10919/95947.

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Regulation of cancer cell phenotype by the tumor microenvironment has motivated further investigation into how microenvironmental factors could contribute to tumor initiation, development, and therapeutic resistance. Analyzing how the microenvironment drives tumor development and cancer cell heterogeneity is particularly important in cancers such as glioblastoma multiforme (GBM) that have no known risk factors and are characterized by a high degree of heterogeneity. GBM patients have a median survival of 15 months and therefore are in great need of more effective therapeutic options. The goal of this research is to generate in vitro models of the heterogeneous brain tumor microenvironment, with a focus on vascular dynamics, to probe the impact of microenvironmental cues on tumor progression and to integrate the tumor models with highly sensitive analytical tools to characterize the epigenome of discrete phenotypic subpopulations that contribute to intratumoral cellular heterogeneity. As GBM tumors are characterized by a dense vasculature, we delved into microenvironmental factors that may be promoting angiogenesis. The correlations emerging between inflammation and cancer led to analysis of the inflammatory molecule lipopolysaccharide (LPS). We utilized 3D micro-tissue models to simulate vascular exposure to ultra-low chronic inflammatory levels of LPS and observed an increase in vascular formation when brain endothelial cells were exposed to ultra-low doses of LPS. We also utilized our micro-tissue models to analyze histone methylation changes across the epigenome in response to microenvironmental cues, namely culture dimensionality and oxygen status. The H3K4me3 modification we analyzed is associated with increased gene transcription, therefore the alterations we observed in H3K4me3 binding across the genome could be a mechanism by which the tumor microenvironment is regulating cancer cell phenotype. Lastly, we developed a microfluidic platform in which vascular dynamics along with microenvironmental heterogeneities can be modeled in a more physiologically relevant context. We believe the studies presented in this dissertation provide insight into how vasculature primed by chronic inflammation and epigenetic alterations in tumor cells could both contribute to enhanced tumor development. Modeling these biological processes in our advanced microfluidic platform further enables us to better understand microenvironmental regulation of tumor progression, uncovering new potential therapeutic targets.
PHD
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BRIVIO, SIMONE. "Molecular mechanisms of cholangiocarcinoma progression: emphasizing the role of tumor-stroma interactions." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/199031.

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Il colangiocarcinoma (CCA) è una neoplasia epiteliale che origina dai dotti biliari, ed è caratterizzata da una prognosi infausta, imputabile alla spiccata invasività e alla resistenza alla chemioterapia. L’aggressività delle cellule di CCA è esacerbata dallo stroma desmoplastico che si sviluppa contestualmente alla crescita tumorale, contenente fibroblasti cancro-associati (CAF), macrofagi tumore-associati e cellule endoteliali linfatiche (LEC). Durante il mio dottorato, ho analizzato la natura e la rilevanza biologica dei segnali paracrini intercorrenti tra cellule stromali e tumorali nel CCA, nel tentativo di chiarire i meccanismi molecolari che guidano la progressione tumorale. In un primo studio, abbiamo esaminato la citochina pleiotropica Leukemia Inhibitory Factor (LIF), che abbiamo scoperto essere secreta non solo dalle cellule di CCA, ma anche dalle cellule infiammatorie e dai CAF all’interno del microambiente tumorale. Abbiamo dimostrato che il LIF ostacolava l’induzione di apoptosi in cellule di CCA trattate con gemcitabina e cisplatino, tramite attivazione del pathway PI3K/Akt, e conseguente up-regolazione della proteina anti-apoptotica Myeloid Cell Leukemia (Mcl)-1. In un secondo studio, abbiamo considerato un tipico readout delle interazioni stroma-tumore, ovvero la transizione epitelio-mesenchimale (EMT) delle cellule carcinomatose, un fenomeno alla base dell’invasione tumorale. In precedenza, avevamo dimostrato che S100A4, un biomarcatore della EMT, promuove attivamente l’invasività del CCA quando espresso nel nucleo delle cellule tumorali. Abbiamo quindi osservato che la nuclearizzazione di S100A4 era dipendente dalla sua SUMOilazione, che poteva essere inibita trattando le cellule di CCA con dosi nanomolari di paclitaxel. La riduzione dei livelli nucleari di S100A4 si associava ad una diminuzione dell’attività di RhoA e Cdc42, della secrezione della metalloproteinasi della matrice (MMP)-9, e dell’espressione della MMP di membrana di tipo 1. Inoltre, il paclitaxel a basse dosi attenuava l’invasività delle cellule di CCA, sia in vitro sia in un modello xenograft. In un terzo studio, abbiamo ipotizzato che la comunicazione tra cellule di CCA e CAF potesse promuovere la linfoangiogenesi tumorale, un processo di fondamentale importanza per la metastatizzazione del CCA. Abbiamo dimostrato che, dopo stimolazione con il Platelet-Derived Growth Factor (PDGF)-D, un mediatore cruciale del reclutamento dei CAF da parte delle cellule di CCA, i fibroblasti incrementavano la secrezione del Vascular Endothelial Growth Factor (VEGF)-A e del VEGF-C, in virtù dell’attivazione delle chinasi ERK1/2 e JNK. Coerentemente, il medium condizionato derivato da fibroblasti trattati con il PDGF-D promuoveva la migrazione delle LEC e il loro assemblaggio in strutture vascolari 3D, ed entrambi gli effetti erano prevenuti bloccando il recettore β del PDGF a livello dei fibroblasti, o i recettori 2 e 3 dei VEGF a livello delle LEC. Anche la permeabilità di LEC in monostrato era aumentata dai fibroblasti stimolati con il PDGF-D, così da favorire la migrazione trans-endoteliale delle cellule di CCA. In conclusione, i nostri risultati confermano che lo stroma tumorale è in grado di alimentare la progressione del CCA, sia modulando direttamente il comportamento delle cellule tumorali, sia allestendo un microambiente favorevole alla diffusione metastatica. Una piena comprensione delle interazioni tra cellule neoplastiche e stromali nel CCA potrebbe portare in futuro allo sviluppo di terapie innovative e “multi-target” in grado di eradicare più efficacemente il tumore.
Cholangiocarcinoma (CCA) is an epithelial cancer arising from the biliary tree. CCA carries a poor prognosis, owing to early and pronounced invasiveness, and resistance to chemotherapy. The aggressiveness of CCA cells is exacerbated by the desmoplastic stroma developing in conjunction with tumor outgrowth, which mainly consists of cancer-associated fibroblasts (CAFs), tumor-associated macrophages, and lymphatic endothelial cells (LECs). During my PhD studies, I sought to dissect the nature and the biological relevance of the dense paracrine communications between stromal and cancer cells in CCA, in an effort to unveil the molecular mechanisms driving tumor progression. In a first study, we focused on a pleiotropic cytokine named leukemia inhibitory factor (LIF), which we found to be released not only by CCA cells, but also by inflammatory cells and CAFs within the tumor microenvironment. We showed that LIF hindered the induction of apoptosis in CCA cells treated with gemcitabine plus cisplatin, an effect dependent on the up-regulation of the anti-apoptotic protein myeloid cell leukemia (Mcl)-1, occurring downstream of PI3K activation. Therefore, targeting the LIF/PI3K/Mcl-1 axis may represent a feasible strategy to increase CCA responsiveness to chemotherapy. In a second study, we considered a classic readout of tumor-stroma interactions, i.e., the epithelial-to-mesenchymal transition (EMT) of cancer cells, a process underlying carcinoma invasion and metastasis. Previously, we had shown that S100A4, an EMT biomarker, acts as a mechanistic determinant of CCA invasiveness when expressed in the nucleus of cancer cells. We then demonstrated that the nuclearization of S100A4 was dependent on its SUMOylation, which could be inhibited by treating CCA cells with paclitaxel at nanomolar doses. Down-modulation of nuclear S100A4 hampered the activity of RhoA and Cdc42, the secretion of matrix metalloproteinase (MMP)-9, and the expression of membrane-type (MT)1-MMP. Moreover, low-dose paclitaxel significantly impaired CCA cell invasiveness, both in vitro and in a SCID mouse xenograft model, implying that a selective reduction in S100A4 nuclear expression may prevent tumor dissemination in CCA patients. In a third study, we aimed at clarifying whether the interplay between CCA cells and CAFs could drive tumor lymphangiogenesis, a process of utmost importance for CCA metastatization. We showed that, upon stimulation with platelet-derived growth factor (PDGF)-D, a major mediator of CAF recruitment by CCA cells, fibroblasts increased the secretion of vascular endothelial growth factor (VEGF)-A and VEGF-C, due to the activation of ERK1/2 and JNK. Consistently, conditioned medium from PDGF-D-treated fibroblasts promoted the recruitment of LECs, along with their assembly in 3-D vascular structures, and both effects could be prevented by antagonizing either PDGF receptor β on fibroblasts, or VEGF receptors 2 and 3 on LECs. The permeability of LEC monolayers was also increased by PDGF-D-treated fibroblasts, supporting the trans-endothelial migration of CCA cells. Overall, we unveiled the presence of a sequential cross-talk among CCA cells, CAFs and LECs, whose disruption may interfere with CCA metastatic spread. In conclusion, our results validate the notion that the tumor stroma strongly promotes the progression of CCA, both by directly shaping the behavior of cancer cells, and by setting up a microenvironment conducive to metastasis. Hopefully, a comprehensive understanding of the mutual interactions between cancer and stromal cells will lead to the development of innovative, multitargeted therapies that may more effectively eradicate the tumor.
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Chauhan, Vikash Pal Singh. "Re-Engineering the Tumor Microenvironment to Enhance Drug Delivery." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10405.

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Tumors are similar to organs, with unique physiology giving rise to an unusual set of transport barriers to drug delivery. Cancer therapy is limited by non-uniform drug delivery via blood vessels, inhomogeneous drug transport into tumor interstitium from the vascular compartment, and hindered transport through tumor interstitium to the target cells. Four major abnormal physical and physiological properties contribute to these transport barriers. Accumulated solid stress compresses blood vessels to diminish the drug supply to many tumor regions. Immature vasculature with high viscous and geometric resistances and reduced pressure gradients leads to sluggish and heterogeneous blood flow in tumors to further limit drug supply. Nonfunctional lymphatics coupled with highly permeable blood vessels result in elevated hydrostatic pressure in tumors to abrogate convective drug transport from blood vessels into and throughout most of the tumor tissue. Finally, a dense structure of interstitial matrix and cells serves as a tortuous, viscous, and steric barrier to diffusion of therapeutic agents. In this dissertation, I discuss the origins and implications of these barriers. I then highlight strategies I have developed for overcoming these barriers by modulating either drug properties or the tumor microenvironment itself to enhance the delivery and effectiveness of drugs in tumors.
Engineering and Applied Sciences
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Kopp, Florian. "Novel insights into the role of microRNAs in chemoresistance, tumor progression and cancer therapy." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-163243.

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Han, Chae Young. "The Role of Hexokinase II in the Regulation of Glycolysis and Cisplatin Sensitivity in Ovarian Cancer." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38574.

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OVCA is the most lethal gynecological cancer, due primarily to late diagnosis and chemoresistance (Canada, 2014; Society, 2014b). CDDP resistance is a major hurdle to successful therapy (MayoClinic, 2014). The mechanism of chemoresistance is multi-factorial including defects in apoptotic pathway and key tumor suppressor as well as dysregulation of metabolism (Borst et al., 2000; Galluzzi et al., 2012a; Siddik, 2003). Elevated aerobic glycolysis is a major source for fulfilling high energy demand of cancer, but the role of metabolic reprogramming and its regulatory mechanism in OVCA cells remain unknown. p53 is a key tumor suppressor involved in apoptosis and frequent defect of p53 (> 80%) exist in epithelial OVCA. HKII is a key metabolic enzyme involved in the first step of glycolysis and its frequent presence in the mitochondria (80% >) has been reported in multiple cancers. We demonstrate here that CDDP-induced, p53-mediated HKII down-regulation and mitochondrial p53-HKII interaction are determinants of chemosensitivity in OVCA. CDDP decreased HKII (mRNA abundance, protein level), altered its cellular localization and glycolysis in p53-wt chemosensitive OVCA cells, a response loss or attenuated in p53 deficient cells. HKII depletion sensitized chemoresistant cells to CDDP -induced apoptosis in a p53- dependent manner. In addition, p53 binds to HKII and facilitates its nuclear localization. Mechanistically, our data suggest that CDDP-activated p53 (phosphorylated p53; P-p53 Ser15) interacts with HKII in the nucleus for its regulation. Upon entry to the nucleus, P-p53(Ser15) transcriptionally regulates HKII by promoter binding, contributing to the regulation of HKII and aerobic glycolysis, eliciting apoptosis in chemosensitive OVCA cells. Conversely, this response is compromised in p53 defect chemoresistant cells. Using proximity ligation assay (PLA) in human OVCA cell lines and primary tumor cells and tumor sections from OVCA patients, we have demonstrated that nuclear HKII-P-p53(Ser15) intracellular trafficking is associated with chemosensitivity in vitro and in vivo. Furthermore, the nuclear HKII-P-p53(Ser15) interaction may be useful as a biomarker for chemosensitivity in multiple epithelial subtypes of OVCA.
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Li, Xia. "Role of tumor-surrounding adipocytes in breast cancer chemoresistance : molecular mechanisms and regulation by obesity." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30136.

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Le cancer du sein est le cancer le plus fréquemment observé chez les femmes en France et dans le monde. Bien que le nombre de cas observés chaque année a tendance à diminuer depuis 2005, notamment grâce au dépistage organisé, cette maladie reste la première cause de décès par cancer chez les femmes. De nombreux travaux ont montré que la progression tumorale est dépendante des cellules tumorales mais également des cellules " saines " du microenvironnement (ou stroma) qui entourent la tumeur. Dans le cas du cancer du sein, les adipocytes, type cellulaire majeur du stroma mammaire, représentent des acteurs émergents dans la progression tumorale. Mon équipe est l'une des premières à avoir montré que les adipocytes péritumoraux étaient impliqués dans l'agressivité des cancers du sein. Du dialogue bidirectionnel qui s'instaure entre les adipocytes et les cellules cancéreuses mammaires résulte des modifications des deux types cellulaires : (i) les cellules tumorales " éduquées " par les adipocytes présentent des capacités invasives augmentées et une plus grande résistance aux traitements et (ii) les adipocytes co-cultivés avec les cellules tumorales acquièrent un phénotype activé avec des modifications spécifiques telles que délipidation, perte de marqueurs adipocytaires, surexpression de cytokines pro-inflammatoires et sécrétion de protéines de la matrice extracellulaire, qui nous ont amené à les nommer CAA pour " Cancer-Associated Adipocytes ". De façon intéressante, le dialogue paracrine entre les tumeurs et les adipocytes pourrait être amplifié dans l'obésité, où l'équilibre normal des protéines sécrétées par le tissu adipeux est perturbé. Dans le cancer du sein, l'obésité est associée à une augmentation des risques de survenue après la ménopause et une aggravation du pronostic indépendamment du statut ménopausique s'expliquant par une augmentation de la dissémination locale et à distance et par une réponse diminuée aux traitements, notamment par une résistance plus importante. L'objectif de ma thèse a été d'évaluer le rôle des adipocytes dans la chimiorésistance des cellules tumorales mammaires. En effet, la résistance est une limite majeure à l'efficacité des traitements et contribue à l'apparition de rechutes, lesquelles sont augmentée chez les patientes obèses. Au moyen d'un modèle de co-culture en 2D, nous avons montré que les adipocytes sont capables de promouvoir une résistance pléïotropique (doxorubicine, paclitaxel, 5-fluorouracile et cyclophosphamide) dans diverses lignées tumorales mammaires, indépendamment du type de tumeur. Grâce aux propriétés de fluorescence des anthracyclines, nous avons montré que cette résistance implique une augmentation de l'efflux de doxorubicine, l'empêchant d'agir au niveau de son site d'action nucléaire. Ce mécanisme d'efflux implique un processus original, qui fait intervenir la protéine de voûte majeure MVP / LRP (Major vault protein / Lung resistance protein), un transporteur nucléocytoplasmique dont la fonction reste à ce jour mal comprise. Suite à l'efflux nucléaire de drogue, celle-ci s'accumule dans des vésicules cytoplasmiques avant d'être effluée hors de la cellule via des vésicules extra cellulaires. Nous avons également pu montrer que cette résistance médiée par MVP s'explique par la sécrétion de facteurs solubles adipocytaires et est amplifiée en conditions d'obésité. En conclusion, nos résultats montrent que les adipocytes péritumoraux sont capables d'influencer la progression tumorale en favorisant la chimiorésistance via un mécanisme original impliquant la protéine MVP, qui pourrait potentiellement devenir un marqueur de résistance aux traitements. Ces travaux pourraient expliquer, au moins en partie, le mauvais pronostic des cancers du sein chez les patientes obèses et ouvrent donc, à plus long terme, des perspectives thérapeutiques intéressantes, destinées à interrompre le dialogue délétère entre adipocytes et cellules tumorales, en particulier chez les patients obèses
Breast cancer is the most common cancer among women in France, as well as in the European Union and the United States. Although the number of cases observed each year has tended to decrease since 2005, notably due to organized screening, this disease remains the leading cause of cancer death in women. Many studies have shown that tumor progression is dependent on tumor cells but also on the "healthy" cells of the microenvironment (or stroma) that surround the tumor. In the case of breast cancer, adipocytes, the major cell type of the mammary stroma, represent emerging actors in tumor progression. My team is one of the first to have shown that peritumoral adipocytes were involved in the aggressiveness of breast cancers. From the bi-directional dialogue that takes place between adipocytes and mammary cancer cells results some changes in both cell types : (i) the tumor cells "educated" by the adipocytes have increased invasive capacities and greater resistance to treatments and (ii) the adipocytes co-cultured with the tumor cells acquire an activated phenotype with specific modifications such as delipidation, loss of adipocyte markers, overexpression of pro-inflammatory cytokines and secretion of proteins of the extracellular matrix, which led us to name them CAA for "Cancer-Associated Adipocytes". Interestingly, the paracrine dialogue between tumors and adipocytes could be amplified in obesity, where the normal balance of proteins secreted by adipose tissue is disrupted. In breast cancer, obesity is associated with an increased risk of occurrence after menopause and a worsening prognosis independent of menopausal status due to increased dissemination (local and remote) and decreased response to treatments, in particular by a greater resistance. The objective of my thesis was to evaluate the role of adipocytes in the chemoresistance of mammary tumor cells. Indeed, resistance is a major limit to the effectiveness of treatments and contributes to the onset of relapses, which are increased in obese patients. Using a 2D co-culture model, we have shown that adipocytes are able to promote pleiotropic resistance (doxorubicin, paclitaxel, 5-fluorouracil and cyclophosphamide) in various mammary tumor lines, irrespective of tumor type. By taking advantage of the fluorescence properties of anthracyclines, we have shown that this resistance implies an increase in the doxorubicin efflux, preventing it from acting at its site of nuclear action. This efflux mechanism implies an original process involving the major vault protein MVP / LRP (Major Vault Protein / Lung Resistance Protein), a nucleocytoplasmic transporter whose function remains poorly understood to date. Following nuclear drug efflux, it accumulates in cytoplasmic vesicles before before being expelled from the cell via extracellular vesicles. We also showed that this resistance mediated by MVP could be explained by the soluble factors secreted from adipocytes and is amplified in obesity conditions. In conclusion, our findings highlight that peritumoral adipocytes are able to influence tumor progression by promoting chemoresistance via an original mechanism involving the MVP protein, which could potentially become a marker of resistance to treatments. This work may explain, at least in part, the poor prognosis of breast cancers in obese patients and thus could provide interesting therapeutic perspectives, in order to interrupt the deleterious dialogue between adipocytes and tumor cells, particularly in obese patients
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PAZIENZA, VALERIO. "Impact of engineered food on tumor growth and chemoresistance in the frame of pancreatic cancer." Doctoral thesis, Università di Foggia, 2017. http://hdl.handle.net/11369/361941.

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L’impatto della dieta (in particolare quella associate a cicli di restrizione calorica) sui benefici della salute sono stati già dimostrati. Questi includono il miglioramento delle malattie cardiovascolari, insulino resistenza, diabete, disordini immuni, rallentamento dei processi di invecchiamento ed in particolare il ridotto rischio per il cancro. Recenti studi in modelli animali ed in modelli in vitro hanno scoperto un nesso tra i cicli di restrizione calorica ed il ridotto rischio di cancro ed un migliorata efficacia della chemioterapia che è stata già descritta per alcuni tipi di cancro. L’obiettivo di questo progetto di ricerca è stato quello di elucidare il ruolo dei cicli di restrizione calorica nelle vie di segnale intracellulari coinvolti nei meccanismi di chemioresistenza del cancro del pancreas che è tra i cancri più aggressivi ed è classificato come la quarta causa di morte cancro-correlata al fine di implementare una formulazione nutrizionale che mimasse la restrizione calorica in grado di reversare la chemioresistenza o di inibire la crescita tumorale. Avvantaggiandoci di modelli animali xenograft e di linee cellulari del cancro del pancreas, mediante l’utilizzo di approcci biochimici e biomolecolari abbiamo inizialmente cercato di comprendere a fondo il ruolo dei cicli di restrizione calorica nella progressione del cancro del pancreas in un modello murino predisposto e poi elucidato i meccanismi molecolari coinvolti nella chemioresistenza. A doggi è di fondamentale importanza identificare i targets potenziali che posso essere utilizzati come predittori di malattia utili per la prevenzione, la prognosi ed il trattamento. I risultati di questo progetto saranno di aiuto per gli scienziati impegnati nell’identificazione di nuovi target terapeutici.
The impact of nutrition (particularly associated with short term starvation (STS)) on major health benefits have been already demonstrated. These include amelioration of cardiovascular diseases, diabetes, insulin resistance, immune disorders, slowing of the aging process and in particular reduced risks of cancer. Recent studies in rodent and in in vitro models uncovered a potential link between STS and improved efficacy of chemotherapy which has already been demonstrated for some types of cancer. The broader objective of the research project developed during the PhD program was to elucidate the role of fasting (or short term starvation, STS) on the intracellular signaling events involved in the chemo-resistance of pancreatic cancer (PC) amidst the most aggressive types of cancer ranked as the fourth leading cause of cancer-related deaths worldwide, in order to implement a new diet formulation, mimicking calories restriction, in order to reverse chemoresistance or inhibit tumor growth. Taking advantage of in vivo xenograft mouse model for pancreatic cancer and in vitro PC cell lines, using biochemical and biomolecular approaches we first aimed to understand in depth the role of STS during the onset of pancreatic cancer in an ad hoc murine model and we then elucidate the molecular mechanisms involved in PC chemoresistance. It is important to systematically identify potential targets, which could serve as biomarkers for cancer prevention, prognosis and treatment. By elucidating the mechanisms involved in PC chemoresistance the results of this study will help scientists to identify new therapeutic targets.
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Veaco, Jennifer Mitchell. "Prospective Detection of Chemoradiation Resistance in Patients with Locally Advanced Esophageal Adenocarcinoma." Thesis, The University of Arizona, 2017. http://hdl.handle.net/10150/623577.

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A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
Approximately 25% of patients with locoregional esophageal adenocarcinoma (EC) are resistant (marked by minimal tumor regression; TRG 3) to preoperative chemoradiation, including 5FU‐based and CROSS regimens. Previously, an immunohistochemistry (IHC) test that accurately identifies patients as responders (TRG 0‐2) or non‐responders (TRG 3) to neoadjuvant CTRT was developed and validated. The current study was designed to identify gene expression profile (GEP) signatures able to predict response to preoperative treatment. Methods: Formalin‐fixed, paraffin‐embedded (FFPE) tumor tissue from 24 diagnostic biopsies (14 responders, 10 non‐responders) was collected. RNA was isolated, and RT‐PCR performed to assess the expression of 96 candidate genes chosen from in silicoanalysis. Genetic signatures incorporating genes with significant expression differences in pathologically determined responders versus non‐responders were identified, and linear and non‐linear predictive modeling methods were used to assess the accuracy of the signatures for predicting treatment response. Cross validation was performed to attain corrected accuracy values. Ten‐, 18‐, and 24‐gene signatures were identified with significantly different gene expression levels in responders compared to non‐responders (p < 0.05). Functional groups represented by the signatures included DNA damage repair, extracellular matrix remodeling, and 5FU metabolism. Partial Least Squares (PLS) prediction of treatment response was compared to pathologic TRG determined by blinded pathologic reading, and resulted in an area under the curve (AUC) of 0.99 and overall accuracy of 100% for the 24‐gene signature. Corrected AUC of 0.99 and accuracy of 95% resulted from five‐fold cross validation with 20 iterations. Heatmap analysis of the 24‐gene signature separated the EC cases into two distinct clusters, the first with 93% responders and the second with 90% non‐responders. The current study identifies novel gene signatures able to accurately predict EC patient response to preoperative treatment. The GEP may allow non‐responders to avoid unnecessary toxicities associated with chemoradiation therapy.
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Kopp, Florian [Verfasser], and Ernst [Akademischer Betreuer] Wagner. "Novel insights into the role of microRNAs in chemoresistance, tumor progression and cancer therapy / Florian Kopp. Betreuer: Ernst Wagner." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2013. http://d-nb.info/1045153052/34.

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Books on the topic "Tumor chemoresistance"

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Reader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny, and Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.

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Ovarian adenocarcinoma is typified by detection at late stages with dissemination of cancer cells into the peritoneal cavity and frequent acquisition of chemoresistance. A number of studies show the importance of the tumor microenvironment and innate immune recognition in tumor progression. Ovarian cancer cells can regulate the composition of their stroma to promote the formation of ascitic fluid rich in cytokines and bioactive lipids such as PGE2, and to stimulate the differentiation of stromal cells into a pro-tumoral phenotype. In response, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, tumor-associated macrophages, and other peritoneal cells can act through direct and indirect mechanisms to regulate tumor growth, chemoresistance via alteration of class III β‎ tubulin, angiogenesis and dissemination. This chapter deciphers the current knowledge about the role of stromal cells, associated secreted factors, and the immune system on tumor progression. This suggests that targeting the microenvironment holds great potential to improve the prognosis of patients with ovarian adenocarcinoma.
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Book chapters on the topic "Tumor chemoresistance"

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Kalir, Tamara A., and D. Stave Kohtz. "Chemoresistance, Dormancy and Recurrence in Platinum Drug Therapy of Ovarian Cancers." In Tumor Dormancy, Quiescence, and Senescence, Vol. 3, 79–97. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9325-4_7.

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Bregenzer, Michael, Eric Horst, Pooja Mehta, Catherine Snyder, Taylor Repetto, and Geeta Mehta. "The Role of the Tumor Microenvironment in CSC Enrichment and Chemoresistance: 3D Co-culture Methods." In Methods in Molecular Biology, 217–45. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1956-8_15.

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Camaj, P., I. Ischenko, H. Seeliger, G. Arnold, K. W. Jauch, and C. J. Bruns. "Overexpression of the gene IFIT3 enhances tumor growth, angiogenesis, metastasing and chemoresistance of the pancreas carcinoma cells." In Deutsche Gesellschaft für Chirurgie, 17–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_7.

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Ischenko, I., A. Renner, H. Seeliger, A. Kleespies, J. W. Ellwart, P. Camaj, M. E. Eichhorn, K. W. Jauch, and C. J. Bruns. "Tumor stem cell targeted therapy with mTOR inhibitor RAD001 and hedgehog signalling inhibitor Cyclopamine reverts chemoresistance towards 5-Fluorouracil in human pancreatic carcinoma cells." In Deutsche Gesellschaft für Chirurgie, 55–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00625-8_22.

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Fabi, François, Pascal Adam, and Eric Asselin. "Par-4 in Chemoresistant Ovarian and Endometrial Cancers." In Tumor Suppressor Par-4, 41–58. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-80558-6_3.

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Sée, Violaine, Barry Pizer, and Daniel Meley. "Molecular Mechanisms of Chemoresistance in Medulloblastoma." In Tumors of the Central Nervous System, Volume 8, 59–69. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4213-0_6.

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Lefranc, Florence, and Robert Kiss. "Glioblastoma: Role of Galectin-1 in Chemoresistance." In Tumors of the Central Nervous System, Volume 2, 261–67. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0618-7_27.

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Shapiro, Joan R., Bipin M. Mehta, Salah A. D. Ebrahim, Adrienne C. Scheck, Paul L. Moots, and Martin R. Fiola. "Tumor Heterogeneity and Intrinsically Chemoresistant Subpopulations in Freshly Resected Human Malignant Gliomas." In Boundaries between Promotion and Progression during Carcinogenesis, 243–62. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5994-4_22.

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Thews, Oliver, Martin Nowak, Christoph Sauvant, and Michael Gekle. "Hypoxia-Induced Extracellular Acidosis Increases p-Glycoprotein Activity and Chemoresistance in Tumors in Vivo via p38 Signaling Pathway." In Oxygen Transport to Tissue XXXII, 115–22. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7756-4_16.

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Aigner, Karl Reinhard, and Emir Selak. "Isolated Thoracic Perfusion with Carotid Artery Infusion for Advanced and Chemoresistant Tumors of the Parotid Gland." In Induction Chemotherapy, 119–25. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-18173-3_8.

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Conference papers on the topic "Tumor chemoresistance"

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Lichtenfels, Martina, Camila Alves Silva, Caroline Brunetto Farias, Alessandra Borba Anton Souza, and Antônio Luiz Frasson. "TIN VITRO BREAST CANCER CHEMORESISTANCE TEST." In Scientifc papers of XXIII Brazilian Breast Congress - 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s1058.

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Introduction: Tumor resistance is the main cause of treatment failure leading to cancer progression and is classified into intrinsic and acquired resistance. Intrinsic resistance is related to a preexisting condition and acquired resistance is induced by a drug. Some methods are already available worldwide to assess drug resistance, however, in Brazil no in vitro chemoresistance test for cancer is validated for clinic use. Objectives: The aim of our study was to validate the in vitro chemoresistance test Chemobiogram for the drugs used in breast cancer (BC) treatment. An incomplete response to neoadjuvant treatment was used to validate the results at a short-term follow-up and treatment after primary BC will be used to validate the test in a long-term follow-up. Methods: Patients with invasive breast cancer were included in this initial report. Fresh tumor samples were collected during surgery and subsequently dissociated to obtain tumor cells. The tumor cells were cultured in a 96 well plate with the several drugs used for BC treatment, including cytotoxic, hormonal, antiHER2, and target therapies, and after 72 hours, cell viability was evaluated. The test result is defined based on cell viability as low (60%) resistance. The test result is compared to the patient`s response to the treatment. Results: To validate the dissociation and BC primary culture techniques we collected samples from six patients with in situ and invasive tumors. These samples were not tested in Chemobiogram. Samples from five BC patients undergoing neoadjuvant treatment and from three patients with primary BC were tested in the Chemobiogram. Of the five patients who underwent neoadjuvant treatment, two performed hormone therapy and three underwent chemotherapy. Four patients presented incomplete response to the treatment and one patient who underwent neoadjuvant chemotherapy presented disease progression during treatment. The chemoresistance test was able to demonstrate medium to high resistance for the drugs used in the neoadjuvant treatments (acquired resistance). The three patients with primary BC were diagnosed with Luminal tumors-HER2 negative. In the chemoresistance test all samples presented medium to high resistance to anti-HER2 drugs (intrinsic resistance) and low to medium resistance to cytotoxic drugs. These patients will be followed in the long term to compare patient outcomes with the test results. Conclusions: The primary culture of breast tumors was efficiently established and the preliminary result of the chemoresistance test was in accordance with the outcomes from five patients who underwent neoadjuvant treatment. This preliminary finding showed the capacity of the Chemobriogram to demonstrate drug resistance in accordance with the clinic and highlighted the importance of the in vitro chemoresistance test to avoid the use of inefficient drugs, improving and personalizing breast cancer treatment.
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Bai, Mingfeng, Yang Liu, Jing Cui, Meng Su, and Dawei Zhang. "Overcoming chemoresistance using tumor mitochondria-targeted photodynamic therapy." In Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXVIII, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2019. http://dx.doi.org/10.1117/12.2508085.

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Kikuchi, Ryota, Takao Tsuji, Yuki Iwai, Hiroyuki Nakamura, and Kazutetsu Aoshiba. "High CO2 tumor microenvironment confers chemoresistance in lung cancer cells." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.oa4865.

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Yu, F., J. Wu, C. Gong, F. Su, and E. Song. "Let-7 Inverts the Chemoresistance of Breast Tumor-Initiating Cells." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-1136.

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Orzechowski, Amanda, and Haidong Dong. "Abstract 5026: B7-H1 confers tumor chemoresistance by regulating MAPK/ERK activation." 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.am2014-5026.

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Lima, Paula Marynella Alves Pereira, Douglas Cardoso Brandão, Raquel Pereira Cruz, Priscila Capelari Orsolin, Wendell Guerra, Luiz Ricardo Goulart, Robson José de Oliveira Júnior, and Thaise Gonçalves Araújo. "A NEW COPPER TERNARY COMPLEX IS A PROMISED COMPOUND FOR THE TREATMENT OF TRIPLE-NEGATIVE BREAST CANCER." In Abstracts from the Brazilian Breast Cancer Symposium - BBCS 2021. Mastology, 2021. http://dx.doi.org/10.29289/259453942021v31s2011.

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Objectives: Triple-negative breast cancer (TNBC) is a biologically aggressive tumor with poor prognosis due to the lack of effective therapeutic strategies. Although chemotherapy is widely employed, chemoresistance and severe side effects remain a challenge in controlling this breast cancer subtype. Doxorrubicin (DOX) and platinum-based drugs are commonly used in oncological regimens but with limitations. In this scenario, metallodrugs based on copper element have been emerged as novel and promised compounds, due to the presenting mechanisms of action and biodistribution different from the platinum drugs already used, and may be effective against tumors that are resistant to conventional chemotherapy. This study focuses on assessing the cytotoxic effect of new copper ternary metal complex (CBP-01) on breast cancer tumor cells. Methodology: Cell viability of human breast cell lines, MCF 10A (non-neoplastic) and neoplastic cells, MCF7, T-47D, and MDA-MB-231, was evaluated by 3-[4,5-dimethylthiazole-2-yl]2,5-diphenyltetra-zolium bromide — MTT methodology. CBP-01 was tested in different concentrations (1, 5, 10, 12.5, 25, and 50 μM) for 24, 48, and 72 h, and the cellular responses were compared with Carboplatin (CARB), Cisplatin (CIS), and DOX. Results: The dose-dependent profile was identified for the four drugs and the cell viability differed between the times of treatment. CBP-01 was effective against the tumor cell lines. Regarding the triple-negative cell line (MDA-MB231), CBP-01 was clearly more effective with lower IC50 (2.05) and higher SI (3.10) than the other compounds. Conclusion: Our data provide new prospects for TNBC treatment and may yield new directions for tumor management.
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Rizvi, Imran, Emma A. Briars, Anne-Laure Bulin, Sriram R. Anbil, Daniela Vecchio, Ahmed Alkhateeb, William R. Hanna, Jonathan P. Celli, and Tayyaba Hasan. "Designing PDT-based combinations to overcome chemoresistance in heterocellular 3D tumor models (Conference Presentation)." In Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXV, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2016. http://dx.doi.org/10.1117/12.2213436.

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Kyle, Alastair H., Jennifer H. E. Baker, and Andrew I. Minchinton. "Abstract PR-7: Overcoming chemoresistance in solid cancers by targeting quiescent tumor cells." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-pr-7.

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Chaudhuri, Arnab Ray, Elsa Callen, Xia Ding, Ewa Gogola, Alexandra A. Duarte, Ji-Eun Lee, Nancy Wong, et al. "Abstract IA09: Replication fork stability confers chemoresistance in BRCA-deficient cells." In Abstracts: AACR Special Conference on DNA Repair: Tumor Development and Therapeutic Response; November 2-5, 2016; Montreal, QC, Canada. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1557-3125.dnarepair16-ia09.

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Rizvi, Imran, Anne-Laure Bulin, Sriram R. Anbil, Emma A. Briars, Daniela Vecchio, Jonathan P. Celli, Mans Broekgaarden, and Tayyaba Hasan. "PDT-based combinations in overcoming chemoresistance from stromal and heterotypic cellular communication (Conference Presentation)." In Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXVI, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2017. http://dx.doi.org/10.1117/12.2252685.

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Reports on the topic "Tumor chemoresistance"

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Park, Jae-Hyun. Influence of the Tumor Microenvironment on Genomic Changes Conferring Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2013. http://dx.doi.org/10.21236/ada580419.

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